VIRTUAL GRAND ROUNDS IN DERMATOLOGY 2.0

Atypical Diaper Dermatitis

2012-01-26T22:50:00.009Z

Abstract: 9 week old infant with recalcitrant diaper dermatitis.

HPI: This child has had a dermatitis which began in the napkin area at ~ 1 month of age. He has been treated with topical Nystatin, clotrimazole cream, Aquaphor and Maalox. No response. New lesions have appeared around umbilicus and neck. His paternal grandfather may have psoriasis.

O/E: There is a sharply demarcated erythematous dermatitis in the pubic, perineal and perirectal area. The umbilicus is involved and there are a few patches in the neck folds. The child is otherwise healthy in appearance.

Clinical Photos:

Diagnosis: I am suspicious of psoriasis or a psoriasiform diaper dermatitis here. This is so well-demarcated and the umbilical lesion may be a clue. I have started him on triamcinalone 0.1% ointment after bath and will reevaluate in a week.

Questions: What alternative diagnoses would you suggest? What may I be missing? Would biopsy be helpful?

References:

2012-01-20T09:52:00.004Z

Abstract: 80 yo man with scalp erosions following micrographic surgery.

HPI: The patient is an otherwise healthy 80 yo man who underwent Mohs surgery on November 16, 2011 for a basal cell carcinoma of the mid-parietal area of the scalp. The large defect needed a complex closure. Within a few days there was some evidence of inflammation and a wound culture grew out staph aureus sensitive to methicillin but resistant to penicillin, clincamycin and erythromycin. He was treated with cephalexin and seemed to do well, but presented on January 19, 2012 with thick crusts along a portion of the scar (unfortunately not photographed). He feels well otherwise.

O/E: 1/19/2012. There were thick honey-colored crusts in a linear distribution over ~ 1/2 of the "S" closure. The crusts were lifted off with a number 15 blade and the base was covered with creamy pus which was cultured and cleansed. The base was glistening granulation tissue, in some areas eroded in others raised.

Clinical Photo after very gentle debridement

Culture Report: Pending

Diagnosis: Erosions secondary to subacute infection. Role of subcuticular sutures may be key. Possible erosive pustular dermatosis of the scalp secondary to inadequately treated infected Mohs wound.

Plan: At this time will wait for culture report and then treat with an appropriate antibiotic. I will debride the hypergranulation tissue and consider using a topical steroid as recommended for erosive pustular dermatosis of the scalp.

Your Comments will be appreciated.

Puzzling Purpura

2012-01-10T22:58:00.015Z

Abstract: 11 yo with three week history of localized purpura

HPI: This is a healthy, stable 11 year old who has had two episodes of purpura on the upper arms. Mildly pruritic. Her pediatrician reported the family to social services. She's on no meds.

O/E: There are purpuric bruises on both upper arms. The remainder of the cutaneous examination if unremarkable.

Laboratory: All hematologic studies are normal

Pathology: A biopsy was performed. Results pending

Impression: Puzzling Purpura. Her pediatricians were concerned about child-abuse and referred her to social services. Their report found no evidence of this. It is likely that this is due to some kind of intentional or unintentional trauma. See a similar case "Diagnostic Challenge" presented by Dr. Amanda Oakley in 2007. I am also considering Gardner-Diamond syndrome (whatever that really is). Further reading raises the question of a purpuric contact dermatitis from azo and other clothing dyes.

Question: What are your thoughts?
One Week Follow-up:

Note: Cleared completely after one week. This argues for factitial disease (as our readers' felt)

Reference:
1. Rasmussen JE. Puzzling purpuras in children and young adults. J Am Acad Dermatol. 1982 Jan;6(1):67-72.
2. Meeder R, Bannister S. Gardner-Diamond syndrome: Difficulties in the management of patients with unexplained medical symptoms. Paediatr Child Health. 2006 Sep;11(7):416-9. Available full text.

Keratosis Follicularis

2011-12-17T20:16:00.024Z

Presented by DJ Elpern
Photomicrographs by Jag Bhawan

Abstract: 10 yo girl with 4 month history of a dermatosis on the neck

HPI: The patient is a pleasant 10 year old who presents for evaluation of a symmetrical papular eruption on the sides of the neck which has been present for about 4-5 months. She has been treated with a number of different topicals by her pediatrician without relief. The patient lives with a grandmother and there is no pertinent family history.

O/E: The examination show somewhat rough, 1 - 2 mm in diameter, keratotic micropapules on the lower folds of the neck. The remainder of the cutaneous examination is unremarkable.

Clinical Photos:

Biopsy: Focal acantholysis, multiple dyskeratotic cells, corps ronds and grains consistent with Darier's disease.

10 x and 20 x

40 x

Diagnosis: Keratosis follicularis (Darier's disease). It's unusual to see keratosis follicularis when it first appears. This is a sweet 10 year old and it's sad to contemplate what this may turn into. After "reviewing the literature" I decided to try pimecrolimus cream as there have been some reports of success.

Questions: How would you treat this child? Have you seen forme-frustes of keratosis follicularis?

References:

1. Good Overview: Darier's Disease eMedicine

2. Pérez-Carmona L, et. al. Successful treatment of Darier's disease with topical pimecrolimus. Eur J Dermatol. 2011 Mar-Apr;21(2):301-2.

3. (supplied by Yoon Cohen) Rubegni P, Poggiali S, Sbano P, Risulo M, Fimiani M. A case of Darier's disease successfully treated with topical tacrolimus. J Eur Acad Dermatol Venereol. 2006 Jan;20(1):84-7.
Abstract: Tacrolimus is a macrolide that inhibits T-cell activation. The most extensive experience with topical tacrolimus has been in treating atopic dermatitis but it has been used in various skin diseases, including Hailey-Hailey disease, with encouraging results. We report a case of extensive Darier's disease successfully treated with topical tacrolimus, after suspension of oral isotretrinoin due to major depression.

Facial flush in a pregnant woman

2011-12-11T14:59:00.010Z

Presented by Henry Foong

Ipoh, Malaysia

A 37 year old restaurant waitress had these rashes on the face for several years, but worse recently since her pregnancy. She is G2P1 at the end of her first trimester. The rash was described as itching, burning. She had seen a dermatologist in Japan and was diagnosed as rosacea. There was no fever or polyarthralgia. Family history was insignificant. Drug history nil.

She feels very uncomfortable. Examination was unremarkable except facial flushing with for bilateral and symmetrical erythematous papules on both cheeks with a mild involvement of the bridge of nose. There was no comedones. Her scalp was normal.
What do you think of the diagnosis? Do you think this is rosacea? What other differentials would you consider - lupus erythematosus, seborrheic dermatitis? How would you manage her remembering that she 3 months pregnant? Would you use topical metrondazole?

Neurotic Excoriations

2011-12-09T01:49:00.002Z

Abstract: 37 yo woman with few year history of excoriations

HPI: The patient is a disabled 37 yo woman who has suffered with painful sores on face, arms, buttocks, upper back for a few years. She was a trainer of race horses till a few years ago. She has a history of alcoholism. A few years back, she was diagnosed with alcoholic hepatitis and hemochromatosis (she gets regular phlebotomies). There is a history of sexual abuse starting at age 14 or 15 which continued for ten years. Thereafter she was in a physically abusive relationship. She is on a Fentanyl patch.

O/E: Fresh and healing excoriations on face, upper back, left earlobe, buttocks.

Diagnosis: Neurotic Excotiations (NE).

Discussion: In my experience, most women who excoriate their faces and bodies in this way have experienced sexual or physical abuse. This is similar to "cutting behavior." NE may be a minor varient of cutting. Adverse Childhood Experiences can manifest themselves in this kind of self-destructive behavior. Her alcoholism may be another expression.

Treatment: These patients are very diffuclt to reach. I started with clobetasol ointment and mupirocin ointment -- these are sometime helpful although one has to be careful not to use for too long on the face. Psychotrophic medications may be helpful. Cognitive behavioral therapy can help but is rarely available for poor patients. The ones who need it the most are those least likely to find a therapist who will help. Patients with NE like this woman are very needy. It can take months to reach them.

Cheilitis Oscura

2011-12-06T00:30:00.010Z

The patient is a 59 yo woman with a four month history of a pruritic dermatitis of the upper lip. It is spreading to the lower lip. She uses Crest toothpaste, a white ceramic nasal irrigator, dental floss, a WaterPic and a Sonic Dental Care apparatus on a daily basis. She has used Desonide ointment for three to four weeks with minimal help.

Presumably, this is an allergic contact dermatitis.
She was patch tested today. If this is negative, I will probably do a biopsy and if that is not helpful refer her to a center that does more in-depth patch testing. I suspect that part of her regimen is the culprit. In children, lip licking should be considered (lick eczema) but the history here does not support that diagnosis.

Question?: Have you encountered similar cases? What are your thoughts?

Painful Red Scrotum

2011-11-14T10:30:00.008Z

Over the past twenty years, we have seen a few patients a year with scrotal burning and/or redness (erythema). Some of these individuals had used topical steroids for prolonged periods, some only for a few weeks. I don't recall if any had not used steroid creams. The condition is called scrotodynia, scrotopyrosis, and red scrotum syndrome. The medical literature gives few clues to its etiology, except that topical steroids can play a significant role in some (or many) of these patients. There is a condition called "vulvodynia" which is similar in some ways. This post tells one patient's story and is a call for information from physicians, other care givers and, importantly, from individuals who suffer with this disorder. It is anonymous. Hopefully as practitioners and patients collaborate we will reach some clarity and start to help those who suffer. If you are a patient making a comment please give your age, occupation and any other information you may consider pertinent.

Patient's History: (November 2011)
I am a health 46-year-old man in the technology field who has suffered with a burning scrotum for past two months. I had knee surgery in May of 2011 which sidelined me from physical activity until September of this year. Upon resuming a workout regiment (primarily of basketball and running) I developed what was diagnosed as a fungal in my groin (tinea cruris - commonly referred to as “jock itch”), specifically in the creases of my thighs. The red scrotum seemed to appear along with the fungal issue, but being unfamiliar with tinea cruris (it was my first time with the condition) I assumed that the red scrotum was part of the same problem. My first attempt at resolving the issue came with a visit to a dermatologist (who I happened to be seeing for a minor skin condition on my hands). It was a “by-the-way can you prescribe something for this rash I have” which first turned our/my attention to the red scrotum.

Initially the dermatologist prescribed Hydrocortisone ointment USP 2.5% for the redness/inflamation and Ketoconazole cream 2% for the fungal issue. The instructions were to first apply the Hydrocortisone to the inflamed area (the creases of my legs were rather red with a fungal rash) for one week to reduce the inflammation. Then apply the Ketoconazole for one week and return for evaluation. I applied the Hydrocortisone to the creases of my thighs and to my inflamed scrotum. The redness in the creases of my thighs subsided marginally but there was no change to the red scrotum. I then applied the Ketoconazole for one week and did see relief of the jock itch. Upon my return to the dermatologist I reported that the fungal treatment was working but there was no change in my scrotum. It was here where I first heard the term “Red Scrotum Syndrome” as a possible diagnosis. I was then prescribed Triamcinalone Acetonide ointment USP 0.1% (a topical steroid) and instructed to apply it to the scrotum for one more week, twice daily, (which I did) and report back. After one week of applying the Triamcinalone ointment to my scrotum there was no change in my condition. I was told by the dermatologist that she was out of ideas and to report to my primary care physician for further treatment.

The visit to my Primary Care Physician began with a careful review of the notes from my dermatologist coupled with a detailed description of what was happening by me. Upon examination my PCP admitted that he had never seen a case like this before. He stated that his medical references offered little help but he did find some info by doing an internet search. The research suggested a treatment of Doxycycline (an antibiotic) 100 mg, twice per day for 10 days. I promptly began taking the oral dose of Doxycycline but after 10 days again there was no change in my condition.

During my initial visit with my PCP I asked if I should stop using the Ketoconazole even though there was still remnants of the tinea cruris. The doctor said to stop all ointment treatment to the groin and instead take an oral anti-fungal medicine to kill the jock itch once and for all. Not knowing the dosage his office requested advice from another dermatologist who upon contacting prescribed Fluconazole (one pill one time). I have taken the Fluconazole and coupled with the Ketoconazole I seem to have the tinea cruris under control.

Next my PCP referred me to a urologist who, like my first Dermatologist and Primary Care Physician, admitted that he had never seen this condition before. He checked my prostate (normal) and gave me a urine test (which also came back normal). The urologist wished me luck and apologized for not being more helpful.

It is here where my luck changed as the second Dermatologist recognized the symptoms and suggested I pay him a visit. Upon examination he too diagnosed the condition as Red Scrotum Syndrome (RSS) or in some circles known as “Great Balls of Fire”. He knew of two doctors (one in Boston and one in Sweden) that have had experience with RSS. Pictures and a description were emailed to each and we await feedback. From prior cases and research the dermatologist advised me to take gabapentin (300 mg 3 times per day). Gabapentin was originally developed for the treatment of epilepsy, and currently is also used to relieve neuropathic pain. I am on day three of the medication and I do not feel any change in the condition.

Hopefully some relief is in sight as the pain is annoying. Some days are significantly worse than others. In fact on some days I continue my normal family and work routine and barely notice the RSS. On other days it’s more pronounced and sitting for any length of time at my desk is uncomfortable. Walking and sitting seem to aggravate the sensation. Having had the shingles (Herpes zoster) at the age of 44 I liken the pain to having scrotal shingles. Perhaps there is something neurological in the equation because I’ve been told that 44 years old is unusually young for shingles. A final note is that high levels of stress (mostly caused by work) occurred during my shingles and when the RSS manifested. A psychological component to the condition cannot be ruled out.

Unfortunately I’ve been told that I am what the medical field calls an “orphan” patient. That RSS exists in a medical space between Dermatology and Neurology and neither discipline is really focused on the condition. I know there are others out there who are suffering with the same pain and that have possibly found a solution to this annoying problem. Hopefully, this post is seen by others, offers helpful information and lets them know that they are not alone. I also hope that any sufferers out there who have had Red Scrotum Syndrome and discovered a remedy reply back and give us a helpful start.

References:
1. Gabapentin for Neuropathic Pain

20 y.o. man with multisystem disease

2011-11-14T09:25:00.008Z

Presented by Henry B.B. Foong
Foong Skin Clinic, Ipoh, Malaysia

Abstract: 20 yo man with mouth ulcers, arthralgias, skin nodules

HPI: The patient is a 20 yr old student who presented with a 3 year history of recurrent mouth ulcers, polyarthralgia (knee, ankles), fever and tender nodules over the shoulders, elbows and legs. The attacks occur about every 6 months and responded to oral prednisolone. Apparently the nodules run a predictable course - initial erythema, then tender nodule then ulcerate and then subside leaving behind post inflammatory hyperpigmentation – all over 3-4 weeks. There is no photosensitivity, alopecia or cough. There is a family history of similar illness.

O/E: Multiple erythematous tender nodules over the elbows, legs , upper shoulders and scrotum. Those on the scrotum – severe, multiple tender nodules, of which ulcerated with scab formation. Multiple tender ulcers were also noted on the inner mouth.

Clinical Photos: (taken with iPhone)

LAB: (Some pending)
TWBC 11, 700 (N 67% L 18% E 1% M 12% B1%) ESR 44 mm/hr
ANA
ANCA
Mycoplasma serology 1: 160 ( N<1:40)
LFT and renal normal
CXR

Pathology: Pending

Dignosis: Behcet’s? PAN? SLE?

Questions: What are your thoughts? Any further studies indicated?

Tumor in Vaccination Site

2011-11-02T09:15:00.000Z

Abstract: 59 yo woman with six month history of tumor l. arm
HPI: The patient, a kindergarten teacher, was bitten on the hand by a child on March 20, 2011. School policy did not allow the child to be tested for hepatitis or HIV. Therefore, it was recommended that she receive hepatitis B vaccination. She had three shots ( March, June and December 2010) in the left deltoid area. In late January or early February 2011 she developed a tumor at the site of the vaccination.
O/E: There is a 1.2 cm. slightly friable tumor in the above-mentioned area. Dermoscopic exam shows some arborizing blood vessels.

Clinical Photograph:

Pathology: Basal Cell Carcinoma: Nodular and Infiltrating. No epidermal connection is apparent in submitted specimens.

Diagnosis: Basal Cell Carcinoma in Vaccination site.

Discussion: There have been sporadic reports of skin cancer developing at the sites of vaccination, but never one in a hepatitis B site. The latent period here is short. It's unclear what the initiating factor is. Our patient is a light-complected Caucasian, so has another risk factor, too. We plan to investigate this area further and present a case report with a review of the literature. Your thoughts will be helpful.

Temple Bracelet Dermatitis

2011-10-18T10:00:00.014Z

Abstract: 20 yo woman with allergic contact dermatitis to a bracelet purchased at a temple in Beijing

HPI: This young woman purchased some prayer beads at a Beijing temple in early September, 2011. Within two - three weeks she developed a rash under the bracelet. She treated this with a number of topicals including a neomycin containing cream. She was seen in an ER a few days before she presented to my office and started on prednisone and Keflex.

O/E: A well-defined area of resolving dermatitis on left wrist. It appears to have been bullous.

Clinical Photos:
The clinical picture did not come out well. Second picture is of bracelet on unaffected wrist to show how she wore it.

Diagnosis and Discussion: This contact dermatitis is most likely secondary to wooden beads. There are a few pertinent references (see below). The patient also applied neosporin so we can't rule out that this may have played a role. She does not live near my office and is in college far away. My approach would be to treat with a topical corticosteroid and warn her about neomycin. If this recurs she can be patch tested. At this point, I do not know what kind of wood the bracelet is made of. The references I found were mostly about cocobolo wood. This may prove difficult to determine. Your comments will be welcome. Note: A number of our readers favor rosewood as the culprit (see reference # 3)

References:
1. Hausen BM. Allergic contact dermatitis from a wooden necklace. Am J Contact Dermat. 1997 Sep;8(3):185-7.
Abstract
A 36-year-old female kitchenworker twice developed eczematous lesions corresponding exactly to the area around her neck where she had worn a wooden necklace. Contact dermatitis lasted longer than 1 week. The necklace consisted of 42 brown wooden beads and 63 other wooden parts, 0.5 to 3 cm diameter. Most parts could be identified as Cocobolo wood, Brazilian and East Indian rosewood, and teak. Patch tests with the pure constituents gave +3-reactions to three dalbergions and obtusaquinone, which are known to be the sensitizers of Cocobolo and the above-mentioned rosewoods. Because of these test results, the identification of the species by eye examination could be corroborated. Further detailed questioning revealed that the patient had played a recorder, probably made from Cocobolo (Dalbergia retusa), when a child, to which she unknowingly became allergic.

2. Moratinos MM, Tevar E, Conde-Salazar L. Contact allergy to a cocobolo bracelet. Dermatitis. 2005 Sep;16(3):139-41.
Abstract
Tropical woods are highly valued because of their strength, hardness, and resistance to moisture. These characteristics make them easy to work with and extremely durable, and that is why they have been used in the manufacture of wooden jewelry, musical instruments, furniture, and handles of many different objects. We present a case of a 44-year-old man who developed pruritus, erythema, and blistering around his right wrist, corresponding exactly to the area where he had worn a wooden bracelet. Thin-layer chromatography performed with the extract of the shavings revealed (R)-4-methoxydalbergione and obtusaquinone (the main components of cocobolo wood) and (S)-4'-hydroxy-4-methoxydalbergione (in lower amounts). Patch-testing with sawdust from the bracelet resulted in a very strong reaction. Patch tests with the pure constituents yielded +++ reactions to the main sensitizers of cocobolo, including obtusaquinone, but also to sensitizers present in other rosewoods. This last fact can be explained by cross-reactivity between different dalbergiones. Contact dermatitis from tropical woods is more frequent than thought, owing to their high sensitizing properties. An exhaustive search can identify the allergen responsible in many cases.

3. Hausen BM. [Rosewood allergy due to an arm bracelet and a recorder]. Derm Beruf Umwelt. 1982;30(6):189-92. [Article in German]
Abstract
A 40-year-old woman developed dermatitis of the left forearm after wearing a bracelet manufactured from Brazilian rosewood (Dalbergia nigra All.). Swelling of the lips, itching and vesicles recurred when she played a recorder made from the same timber some years later. Epicutaneous tests were strongly positive after 120 h with 2 of the wood constituents: R-4-methoxydalbergione and S-4,4'-dimethoxydalbergione. The third quinone (S-4'-hydroxy-4-methoxydalbergione) only elicited a weak reaction. Shavings of the wooden bracelet extracted with benzene and ethanol and separation of the residues by thin layer chromatography yielded all 3 dalbergiones in remarkable amounts (congruent to 0,8%). Cross-reactions to the chemically near related R-3,4-dimethoxydalbergione, known as the strongest sensitiser of the dalbergione group, were not obtained, although guinea pig experiments had revealed cross-reactivities. Of the racemic

Lupus Erythematosus?

2011-10-13T15:29:00.010Z

presented by Henry Foong:

A case in progress... 14 year-old Malaysian boy with photosensitive eruption

HPI:The patient is a 14 year old student with one year history of erythematous patches on the face, made worse with sun exposure. He is otherwise healthy with no systemic complaints. He has been on no medications byh mouth.

Examination showed few discrete 2-4 cm erythematous plaques on the cheeks, nose, upper and lower eyelids. No alopecia. No scarring.

I Suspect this is lupus erythematous. Acute LE or Subacute LE ? ANA serology and biopsy done. Results pending. Differentials - Jessner's lymphocytic infiltrates

Questions: What are your thoughts pending the biopsy findings? Would you do anything different from what I have done so far?

Painful Brusing in a 29 yo Woman

2011-09-23T19:55:00.010Z

Presented by Hamish Dunwoodie, MBBS
Moncton, New Brunswick, Canada

Abstract: 29 yo woman with one week history of painful bruising on thighs

HPI: The patient is an otherwise healthy 29 yo woman with a one week history of painful bruises on her thighs. Five years ago she had leucocytoclastic vasculitis of her lower legs and very mild proteinuria. A renal consult felt she probably had mild IgA nephropathy. This has cleared. Her only medication is paroxetine, which she has been on for three months. She denies any trauma. The patient is a single mother of two children (11 and 3 years old) and lives alone with her kids. She was in school recently but is now on disability for "seizures" (although she is on no antiepileptic medications at present). She has been assaulted by a boyfriend in the past, but denies trauma this time.

O/E: There is purpura of the lateral thighs bilaterally. No evidence of LCV any longer. The remainder of the cutaneous examination is unremarkable.

Clinical Photo:

Lab: CBC, Chemistries, Urine Analysis all normal save for trace + rbcs. No proteinuria any longer.

Diagnosis: This is most likely traumatic purpura in a young woman who is reluctant todivulge an accurate history. Gardner Diamond Syndrome (autoerythrocyte sensitization syndrome, psychogenic purpura) was considered as well.

Questions: What are your thoughts?

References: (Full Text Online)
1. Gardner-Diamond syndrome: Difficulties in the management of patients with unexplained medical symptoms. Meeder R, Bannister S. Paediatr Child Health. 2006 Sep;11(7):416-9.

2. Gardner-Diamond Syndrome: bruising feeling. Bostwick JM, Imig MW. Mayo Clin Proc. 2008 May;83(5):572. (This is a short article)

Traumatic Ulcer

2011-09-21T09:33:00.008Z

Abstract: 40 year-old man with non-healing wound

HPI: The patient is a 40 yo man who sustained traumatic abrasions of his leg and arm from a motorcycle accident on May 31, 2011. He has a history of chronic vesicular dermatitis of hands and feet complicated by recurrent staphyloccal cellulitis of legs. The wound on his right knee became infected and he was hospitalized over the summer on two occasions for parenteral antibiotics and debridement. As a result of this wound he has lot his job and his family is living marginally.

O/E: September 14, 2011. There is a nine cm relatively clean ulcer over the right knee. It has shown no tendancy to heal over the past month.

Clinical Photograph:

Diagnosis: Ulcer right knee.

Questions: How would you approach this lesion so that the patient can heal and get back to work? At present, he is getting dressing changes a few times a week and there are no plans for further surgical interventions. It looks like this will take months to heal by secondary intention.

Follow-Up: 10/19/2011 I have seen the patient on two occasions since this posting. The ulcer is ~ 75% better with just daily dressing changes with Vaseline impregnated gauze. He has not needed any further antibiotics. I expect it will be completely re-epitheliazed in two to three weeks.

Insect Bite Lymphangitis

2011-09-11T21:03:00.000Z

Presented by Nai-Chien Yeat
Williams College, Williamstown, Massachusetts

Abstract: 20 year-old Malaysian college student with one day history of an itchy line on right arm.

Yeat's History:
I developed itchy welts all over my body shortly after moving into my new dorm room. A bite on my right wrist caused extensive swelling and intense itching within 24 hours of first discovery. Within 36 hours, a swollen, pruritic red streak extended from my wrist to my upper arm.
A bite on my left ring finger caused extensive swelling and intense itching within 24 hours. Within 36 hours, the swelling and itching had spread to the back of my hand.
After bumping into Dr. Elpern on the street, I started a course of antibiotics (Augmentin) and took antihistamines (Clarityne and Benadryl) to relieve the pruritus.

O/E: (DJE) I bumped into Mr. Yeat on Sunday morning, September 4th on the Williams College campus and he showed me his hands and arms. There were erythematous papules with some superficial crusts on the hands and a lymphangitic streak on the volar right arm extending towards the elbow. Other than pruritus, he felt well and had no fever.

Clinical Photos taken by Mr. Yeat

Diagnosis: Although initially I was concerned about a bacterial lymphangitis, I now think this is most consistent with lymphangitis secondary to insect bite rather than a sign of a bacterial etiology. Yeat knows the initial lesions are bites and he feels well otherwise. I suppose a bite could have been superinfected with strep, so the Augmentin makes sense; but it could also be based on another mechanism. There are a few pertinent references including one from the BMJ which Mr. Yeat found (# 2). I am not convinced this is from bedbugs as many types of arthropod bites apparently can cause lymphangitis. It's curious that so few cases have been reported. This may be because the patients appear to have a bacterial process, are treated with antibiotics and get better as they would over a few days even without the medications. It would be important to know if bed bugs have been found in his dormitory.

(Note from Yeat one week after onset: "The swelling has completely subsided, and you can barely see the red streak that the lymphangitis left behind."

Questions: Mr. Yeat and I will appreciate your thoughts. Do you feel the Augmentin was necessary? Have any of you seen similar cases?

Reference: Superficial lymphangitis after arthropod bite: a distinctive but underrecognized entity?
1. Marque M, Girard C, Guillot B, Bessis D. myriammarque@yahoo.fr
Dermatology. 2008;217(3):262-7. Epub 2008 Aug 6.
Abstract
BACKGROUND: Acute bacterial lymphangitis is a common occurrence after skin damage. This diagnosis is often made in case of red linear streaks after arthropod bites, leading to the prescription of oral antibiotics. In this setting, noninfectious superficial lymphangitis after arthropod bites, an eruption rarely mentioned in the medical literature, appears as a diagnostic challenge.
OBJECTIVE: Our purpose was to study the clinical and histopathological features of this underrecognized condition.
METHODS: We collected the observations of six consecutive patients seen between the years 2003 and 2006, who developed an acute linear erythematous eruption along lymphatic vessels, mimicking common bacterial lymphangitis. Standard histological examinations were completed by immunopathological staining using the monoclonal antibody D2-40, a highly selective marker of lymphatic endothelium. Extensive review of the literature about acute noninfectious superficial lymphangitis was performed. Results: The clinical presentation and histological findings excluded an infectious etiology and suggested superficial lymphangitis after an arthropod bite in all the observations.
CONCLUSIONS: This article analyzes the clinical and histological features of noninfectious superficial lymphangitis after arthropod bite, a benign underrecognized condition mimicking common bacterial lymphangitis. Physicians should be aware of this benign reaction to avoid the useless prescription of antibiotics.

2. BMJ Case Reports 2010; doi:10.1136/bcr.09.2010.3310
Acute superficial lymphangitis following pigeon mite bite
Parvaiz A Koul, Syed Mudassir Qadri Full Text Online.

Erythema multiforme major

2011-09-06T11:19:00.013Z

Presented by: Dr. Henry Foong
Ipoh, Malaysia

Abstract: Five Year-old boy with E. multiforme

The patient is a 5 year old boy presented with 3 day history of fever and generalised skin eruptions. Apparently it started with superficial lower lip erosion and the next day he had high fever and generalised skin eruptions on trunk, the upper and lower extremities. There was no family history of similar skin problems.

O/E he was afebrile. Generalised erythematous macules and plaques were noted on the face, trunk and extremities. The lesions were distributed acrally. Some of the macules had sharp margin round shape with concentric rings within it. A vesicle was noted on the centre of the macules. Few typical round macules were noted on the palms and soles. Clinically he has erythema multiforme major

TWBC 14, 900 (N11.4% L75.4% E2%) ESR 19. Mycoplasma antibody is negative. He is now empirically on oral acyclovir and oral clarithromycin.

The most likely cause of the EM is HSV infection in this patient. Wonder if you would use systemic corticosteroids in this patient?

Raccoon Purpura

2011-08-31T19:31:00.004Z

I received this email from an otherwise healthy 23 yo woman who I saw a month ago for an unrelated problem: "I was wondering if you might have any insight to another skin problem I am having. After receiving some terrible news, I have popped a number of blood vessels around my eyes and face to the the point of having dark purple bruises around and on my eyes. I do not know what to do. I look like a victim of abuse and would like to heal my face as soon as possible."

Discussion: One can see eyelid purpura and petechiae with a number of pathologic processes (amyloidosis, coagulopathy) but also after valsalva maneuver, violent vomiting, coughing. I suspect the latter and need more information from the patient. Any thoughts?

Reference: Anesth Analg. 2007 Dec;105(6):1561-3, table of contents.
Periorbital ecchymoses during general anesthesia in a patient with primary amyloidosis: a harbinger for bleeding? Available Free Full Text Online
Weingarten TN, Hall BA, Richardson BF, Hofer RE, Sprung J.
Source
Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.
Abstract: Primary amyloidosis is a result of proliferation of a population of plasma cells that leads to an increased secretion of monoclonal immunoglobulins (amyloid). Amyloid protein infiltrates increase capillary fragility. Such capillaries can burst, even after minor stress, resulting in periorbital hemorrhage. We describe a 64-yr-old man with primary amyloidosis who underwent general anesthesia. His eyes were gently closed with tape. Upon removal of the tape bilateral periorbital purpura was noted. All coagulation studies were normal. The periorbital hemorrhage was attributed to amyloidosis-induced capillary fragility.

Post-Operative Contact Dermatitis

2011-08-24T19:11:00.011Z

Abstract: 63 yo woman with 5 day history of a dermatitis

HPI: A 63 yo woman developed a dermatitis 2 d post surgery. An arterial line had been placed in the L. radial artery pre-op. The area was first prepped with chlorhexidine, the line was placed, and the area covered with 6 x 7 cm Tegaderm Film. A venous line was placed in the R. external jugular vein and covered with Tegaderm w/o dermatitis.

O/E: An 8 x 8 cm erythematous vesicular and hemorrhagic plaque is seen in the area under the Tegaderm. Island of sparing in center of patch is where angiocath resided. This plaque is cool to touch. Neck completely clear.

Clinical Photos:

Lab and Pathology: Not deemed necessary at this time.

Diagnosis: Irritant vs. Allergic Contact Dermatitis. Not likely Tegaderm since area under patch on neck is clear. I am considering a toxic burn from chlorhexidine under wrist patch. (see Addendum)

Questions: What are your thoughts?

Addendum: The anesthesiologist reviewed his notes and found that he applied Tincture of Benzoin to the area around the arterial line to help keep the Tegaderm in place, but not on the neck for the venous line. Allergic Contact Dermatitis to Benzoin is well-reported. This seems to be the culprit here. Hopefully, wet compresses followed by clobetasol 0.05% ointment will be helpful. We are indebted to the anesthesiologist for reviewing the operative record and educating us! We will patch test her once her eruption has quieted down.

References: (Free Full Text)
1. Indian J Dermatol Venereol Leprol. 2006 Jan-Feb;72(1):62-3.
Contact dermatitis to compound tincture of benzoin applied under occlusion.
Lakshmi C, Srinivas CR.

2. BMC Dermatol. 2004 Mar 31;4:1.
Severe facial dermatitis as a late complication of aesthetic rhinoplasty; a case report.
Rajabian MH, Sodaify M, Aghaei S.
Department of Plastic Surgery Shiraz University of Medical Sciences, Shiraz

Congenital Hypopigmented Macules

2011-08-06T16:38:00.011Z

Presented by Henry Foong, Ipoh, Malaysia
A healthy 16 year old girl complains of asymptomatic 1-2 mm in diameter hypopigmented macules on both shins since birth. There are similar, but to a lesser extent, macules on the arms. Her elder sister has similar lesions. In an older individual with later onset I would have thought of idiopathic guttate hypomelanosis. However, these lesions were congenital and her sister is similarly affected. It does not look like a form of dyschromia but plain hypopigmentation. so unlikely to be dyschromatosis symmetrical hereditaria? or dyschromia cutis amyloidosis? Does not look like pigmentary mosaicism either. Any suggestions? Click images to enlarge.

Impression: Congenital Hypopigmented Macules. Has anyone seen a similar case?

References:
1. Fukai K, et.al. Monozygotic twins with congenital guttate leukoderma. Osaka City Med J. 2005 Jun;51(1):33-6. fukai@msic.med.osaka-cu.ac.jp
Abstract: We report here two cases of congenital guttate hypomelanotic macules observed in monozygotic twins. They both have had discrete leukoderma regions in the axillae, inguinal region and lower abdomen since birth. The size and the shape did not change until at least the age of nine. Development of both patients was otherwise normal. The split-DOPA reaction revealed no DOPA-positive melanocytes in the hypomelanotic skin, but electron microscopy revealed melanocytes that were regular but decreased in number. Cytogenetic analysis of the peripheral leukocytes revealed normal female karyotype in both cases. Considering the unique pattern of the leukoderma lesions which occurred in both monozygotic twins, this might be a new clinical entity.

2. Grosshans E, Sengel D, Heid E. White lentiginosis [ in French] Ann Dermatol Venereol. 1994;121(1):7-10.
Abstract
INTRODUCTION: A congenital guttate hypomelanosis is an unusual feature not yet mentioned in the dermatologic literature.
CASE REPORT: We observed 1982 in a 28 y. female patient numerous guttate lesions, which were flat and pigmented on the light-exposed areas of her limbs, flat or papulokeratotic and depigmented on her trunk. These lesions disclosed a particular histological aspect characterized by a lentiginous hyperplasia of the epidermis, with elongated club-shaped rete ridges, and an unusual loss of pigmentation without disturbance of the keratinization. Further electronmicroscopical and immunohistochemical data were not available. The patient emphasized the congenital occurrence of these lesions, whose fixity could be assessed during a 4 year-follow up time.
COMMENTS: The unusual histological aspect allows the differentiation of these depigmented spots and other known similar conditions: macular leucoderma as sequellae of previous inflammatory diseases, hypomelanotic macules associated with genodermatoses, idiopathic guttate hypomelanoses.
CONCLUSION: This seems to be a not yet described entity which we propose to denominate "white lentiginosis".

KS in Renal Transplant Patient

2011-07-31T11:24:00.005Z

Omid Zargari, a dermatologist from Rasht, Iran, is asking for your help regarding a 74 year old man with extensive Kaposi's sarcoma after renal transplantation. The disease began about two years ago, when he was on Cyclosporine (plus prednisolone). At that time, I asked the nephrologist to change CsA with Sirolimus. Now, he's on Pred+cellcept+sirolimus.
I've seen several cases of post-transplant KS. All of them regressed after discontinuing CsA and haven't seen a case with such extent. HHV8 screening is not available here. I referred him to an oncologist, but he refused to start any chemotherapy because he believed this is not a life-threatening condition....considering the amount of impact the disease has put on the QOL of this gentleman, he is seeking for any help...at least a palliation.
What do you suggest?

Smart Phone Fingers?

2011-07-01T09:43:00.005Z

The patient is a 15 yo girl with a 2-3 year history of painful thumbs. The palmar surface of her thumbs were glazed with decreased fingerprint markings. She has mild hyperhidrosis palmaris. One great toe has mild plantar hyperkeratosis but is not glazed like the thumbs. I noticed a cell phone in her back pocket and asked her to show me how she uses it (see below). She's had this for three years. Her father said she's on the smart phone for hours a day.
Is this a new entity? Contact? Irritant? Repetitive Trauma? Comments?

BCC Tip Nose

2011-04-29T17:53:00.003Z

The patient is a 70 yo woman who had a nasal bulb lesion biopsied in September 2010. This was an ill-defined area and two, 2-mm biopsies were taken. One showed a superficial and nodular BCC ang the other a melanocytic nevus. This was probably a collision lesion. The patient elected to wait and see what developed.

Today, April 29, 2010, the exam shows a residual lesion with arborizing blood vessels on dermoscopy. This lesion requires definitive treatment either with micrographic surgery or radiotherapy and the patient is leaning towards the former.

Question: With re: Moh's surgery, what kind of closure you you recommend?

Melanonychia Totalis

2011-04-22T00:45:00.007Z

Abstract: 70 yo African-American woman with black toe-nails for many years.

HPI: This otherwise healthy 70 yo woman was seen for lichen simplex chronicus of the dorsum of the feet. An incidental finding was that of black toe nails. Anamnesis reveals that this has been present for greater than ten years. She is was on no meds by mouth when this developed.

O/E: Most of her toe-nails are black. One or two have longitudinal melanocytic striae. Her finger nails are normal. The toe nails are thickened with subungual hyperkeratosis.

Clinical Photos:

Lab: The KOH was negative and a fungal culture was obtained on April 21, 2011

Diagnosis: Melanonychia. Is this a dermatophyte, a yeast or a saprophyte? We will wait to see what culture shows. What are your thoughts?

Reference:
A case of melanonychia due to Candida albicans
Lee SW, et. al. Clin Exp Dermatol. 2006 May;31(3):398-400.
Abstract: Melanonychia is characterized by tan, brown, or black pigmentation within the nail plate. Fungal melanonychia is rare and may simulate longitudinal melanonychia caused by melanocytic lesions. We report six cases of fungal melanonychia which were confirmed histopathologically or mycologically. On culture, Candida and/or Aspergillus species were isolated in four patients. The nail pigmentation improved after treatment with antifungal agents in all cases, but one patient experienced a new lesion on another nail after cessation of treatment. Fungal infection should be considered as a cause of melanonychia, and fungal melanonychia should be differentiated from the melanonychia caused by melanocytic lesions, particularly by subungual melanoma.

Amelanotic Acral Lentiginous Melanoma

2011-04-13T01:19:00.013Z

Abstract: 61 yo man with 4 - 5 year hx of a tumor on foot.

HPI: The patient is a healthy 61 year old man with a 4 - 5 year history of a slowly growing lesion on the plantar aspect of his right foot. On a recent trip to Jamaica it bled, leading him to consult a podiatrist who astutely did a biopsy. The patient has sarcoidosis which has been treated with weekly i.m. methotrexate for the past two years. (I do not know the dose byt presume it is around 15 mg).

O/E: 2 x 1 cm flesh-colored nodule. Crust in photo is from punch biopsy. Remainder of cutaneous exam unremarkable. No palpable regional lymph nodes. Dermatoscopic exam was not rewarding.

Photo:

Dermoscopic Images:

Lab: Mild leucopenia 3700. Otherwise all chemistries and LDH normal

Pathology: ALM 3.68 (at least) mm thick, (at least) Level IV.
Tumor thickness may be deeper tumor is present at the base of the specimen.
Regression: Not Present
Vascular/lymphatic invasion: Not identified
Mitotic Activity: 7/10 HPF
Tumor Infiltrating Lymphocytes: Non-brisk
Vertical Growth Phase: Present

Discussion: Although this tumor is called "acral lentiginous melanoma" it clearly is a nodular lesion. Might it better be called "acral nodular melanoma?" The patient will need staging and the, depending on findings of staging studies, a wide-local excision with lymph node mapping . He is being referred to the melanoma clinic at Dartmouth Mary Hitchcock Medical Center.

This is an amelanotic acral melanoma that has been present 4 - 5 years by history. Amelanotic acral melanoma are scary lesions as clinically and dermoscopically they do not appear to be worrisome.
It is well-recognized that these can fool practitioners, as they are only rarely seen even by dermatologists and a high index of suspicion is needed. The podiatrist who saw the patient was astute to biopsy the lesion on his first visit.

References:
1. Acral lentiginous melanoma: a clinicoprognostic study of 126 cases.
Phan A, Touzet S, Dalle S, Ronger-Savlé S, Balme B, Thomas L.
Br J Dermatol. 2006 Sep;155(3):561-9.
Department of Dermatology, Hôtel Dieu, Claude Bernard University, 69288 Lyon cedex 02, France.
Abstract:
BACKGROUND: Although the histopathological subtype of melanoma has not been clearly proven to carry independent prognostic significance, acral lentiginous melanoma (ALM) seems to confer a poorer prognosis mainly because disease is often more advanced at the time of diagnosis.
OBJECTIVES: To investigate the distinctive epidemiological and clinical characteristics of ALM, a peculiar histological entity, and to identify prognostic factors.
METHODS: We performed a register-based review of cases from a single large referral centre, the University Hospital Department of Dermatology, Lyons, France. We reviewed patient demographics, the initial presentation of the lesion, and clinical outcome. ALM-specific and disease-free survival were estimated using the KaplanMeier method and compared using the log-rank test. A Cox model was used to identify prognostic factors.
RESULTS: One hundred and twenty-six patients were identified as having histopathology-proven ALM in our melanoma patient register from 1996 to 2004. There were 46 (37%) subungual ALM and 80 (63%) ALM on soles, palms and nonvolar sites. The mean age at diagnosis was 63 years. There were 44 (35%) men and 82 (65%) women, sex ratio M/F 1 : 1.86. The mean Breslow thickness was 2.51 mm (range: in situ to 20 mm). There was no evidence of overexposure to ultraviolet radiation, nor was there found a predisposing genetic trait. Only 16 (13%) patients recalled a history of trauma. Thirty-four ALM (28%) were unpigmented. The median ALM-specific and disease-free survival were 13.5 and 10.1 years, respectively. The 5-year survival rate was 76%. Multivariate analysis identified tumour thickness, male gender and amelanosis as independent clinical prognostic factors for both ALM-specific and disease-free survival.
CONCLUSIONS: Our study provides specific information on the clinical characteristics and outcome of this uncommon histological subtype of melanoma. However, the pathogenesis remains unknown. Breslow thickness, male gender and amelanosis were significantly associated with a poorer prognosis.

2. Acral lentiginous melanoma mimicking benign disease: the Emory experience.
Soon SL, Solomon AR Jr, Papadopoulos D, Murray DR, McAlpine B, Washington CV.
J Am Acad Dermatol. 2003 Feb;48(2):183-8.
Abstract
BACKGROUND: Plantar and subungual melanoma exhibits a higher misdiagnosis rate relative to other anatomic sites. Misdiagnosis and delay in diagnosis are statistically associated with poorer patient outcome. Awareness of atypical presentations of acral melanoma may, thus, be important to decrease misdiagnosis rates and improve patient outcome.
METHODS: We conducted a retrospective case review of plantar or lower-extremity subungual melanoma performed at Winship Cancer Center, a tertiary care, referral center affiliated with Emory University, between 1985 and 2001.
RESULTS: A total of 53 cases of plantar or lower-extremity subungual melanoma were identified. Of 53 cases with a final diagnosis of melanoma, 18 were initially misdiagnosed. Misdiagnoses included wart, callous, fungal disorder, foreign body, crusty lesion, sweat gland condition, blister, nonhealing wound, mole, keratoacanthoma, subungual hematoma, onychomycosis, ingrown toenail, and defective/infected toenail. Of the 18 misdiagnosed cases, 9 were clinically amelanotic.
CONCLUSION: Awareness that amelanotic variants of acral melanoma may assume the morphology of benign hyperkeratotic dermatoses may increase the rate of correct diagnosis and improve patient outcome.

A Complex Patient

2011-04-08T01:27:00.012Z

The patient is a 61 year-old woman with long-standing insulin-dependent diabetes, rheumatoid arthritis and insulin-dependent diabetes. Her rheumatologist has treated her with methotrexate which she stopped b/c of side-effects. She has also had side-effects (mostly urticaria) with Humira and Remicaide. She was referred for her psoriasis by another dermatologist. Her meds include insulin and prednisone 10 mg per day.

O/E: The patient appears older than her stated age. She appears to have mild facial lipoatrophy. The stigmata of RA is seen in her hands. Her psoriasis is limited to plaques on her back.

Discussion: Given her infirmities and reaction to standard RA and psoriasis meds, I elected to start her on narrow band UVB and clobetasol ointment 0.05% applied after a bath (Soak and Smear protocol).

Questions: Is this real facial lipoatrophy? Is it related to the DM or RA. The patient has not risk factors for HIV or history of abnormal hemograms to suggest immunodeficiency.

Dermatomyositis?

2011-04-05T11:45:00.007Z

Abstract: 84 yo man with three week history of erythema dorsa hands

HPI: The patient is an 84 yo man who presents with a three week history of a mostly painless eruption on the dorsal hands (left more than right). I have taken care of his skin for over a decade as he's had a thin melanoma and a number of non-melanoma skin cancers. In addition, he has Parkinson's disease and his only medication is carbodopa. Fourteen years ago, he had prostate Ca successfully treated with seeds. Although mentally alert, the patient has been somewhat frail for years and muscle weakness is difficult to evaluate. There are no other skin findings, no heliotrope, no poikioldermatous changes.

O/E: Dusky erythema on dorsum of left hand with a predilection for the MCP joints. Some crusting. Periungual erythema of proximal nail folds, two fingers, right hand.

Clinical Photos (April 4, 2011)

Lab: The patient saw a rheumatologist who did a thorough w/u for collagen vascular disease with a focus on dermatomyositis. All serologies, chemistries and the hemogram were completely normal. CPK was not done.

Impression: The dermatitis is suggestive of dermatomyositis (DM). It's early spring here and he may have been more exposed to light. At this point, I am considering an early and evolving DM. Amyopathic or hypomyopathic DM takes six months to confirm. Considering his age, a thorough evaluation for malignancy might be considered. This appears to be photo-located, so I considered PCT but will hold off on urinary porphyrins for the time being.

Questions: Your thoughts will be appreciated.

Addendum: Two colleagues (Amanda Oakley from NZ and Fran Storrs from Portland, OR, USA) suggested chilblains. I called the patient and asked him if he might have been out more recently without gloves. He told me his hands are usually cold and he has a 200 yard (~ 200 mtr) walk to his mailbox. He hasn't been wearing gloves recently. It's been a cold spring here -- I think chilblains is a more likely diagnosis and I asked him to wear gloves outside when it's < 50 F (10 C) and get back to me in a week. The extend of his involvement is more than we usually see with chilblains, but the dx makes good sense. I'll affix a f/u in a couple of weeks.

Alopecia Universalis

2011-03-30T10:03:00.006Z

HPI: The patient is a 77-year-old woman who was seen for alopecia, which has been present for about eight months now. This followed chemotherapy for nonhodgkin’s lymphoma. She has a history of alopecia areata decades ago which resolved on its own.

O/E: The examination shows that this patient has alopecia universalis. She has a few eyelashes but no eyebrows, no body hair, no scalp hair.

DX: Alopecia universalis following chemotherapy. This is unusual. There is one report of alopecia universalis following treatment for hepatitis C with ribavirin and interferon.

PLAN: I am going to get a list from her of the medications she was treated with for NHL and see if there are any reports on this. I will also run this be some colleagues.

Question: Has anyone seen a similar patient?

References:

Unusual Nail Bed Tumor

2011-02-02T10:26:00.013Z

Abstract: 67 yo man with 1 - 2 month hx of a nail bed tumor.

HPI: 67 yo man with 1 - 2 month hx of a nail bed tumor. The overlying nail has been destroyed. Lesion is asymptomatic.

O/E: 8 mm diameter flesh-colored tumor left thumb nail. No pigment. Lesion is solid, not friable.

Clinical Photos

Pathology: Hyperkeratosis, parakeratosis, epidermal hyperplasis. There are ectatic blood vessels in an edematous and fibrotic stroma. Iin the DDx is an unusual traumatized hemangioma or subungual fibroma.

Microscopic Photos courtesy of Deon Wolpowitz, Boston University SkinPath

Diagnosis: Benign nail bed tumor, not otherwise specified. Presented for ideas.

Questions: What is your diagnosis, and how would you approach this lesion?

Plan: The patient has been referred for defintive surgery to a Mohs surgeon.

Dermatitis and Failure to Thrive

2011-01-29T12:29:00.009Z

Abstract: 3.5 month old male infant with Failure to Thrive and Dermatitis

HPI: This 3.5 mo old infant male is the product of a normal pregnancy and delivery. He has had a severe dermatitis since shortly after birth. The process is most prevalent on head and neck and torso. He has lost weight on 150 kcal/kg per day. On visits seems happy and content. Three older siblings are all normal.

O/E: Widespread scaly patches on trunk and scalp. Thick cradle cap, greasy scale scalp and face. Background erythema. Red excoriated napkin area.

Photos: Taken when child was 9 weeks old.

Labs: Hi K+ and NA on hospital admission for FTT (but since normalized). Mild eosiniophilia and increased plts. Normal: CBC, ZN, IgE, IgM, IgA, IgG, amino acids. Normal karyotype, negative FISH for Williams Syndrome. Complement levels will be done and hair will be looked at for trichorhexis invagninata.

Diagnosis: Unclear. Initially I thought this child had infantile seborrheic dermatitis, but that usually responds well to treatment. At this point, Leiner's and Netherton's syndromes need to be ruled out. While neglect was initially considered, the child's pediatrician feels at this time that the mother is competent and has raised three other normal children.

Discussion: I saw this child once six weeks ago and because of transportation problems they could not keep f/u appointments. The eruption was originally treated with HC valerate 0.2% cream. Scalp hygiene was discussed. At this point a systemic process is considered.

Questions: In addition to considering Netherton's and complement deficiency syndromes like Leiner's what else would you recommend?

Follow-Up: The patient saw a pediatric gastroenterologist who changed her formula to one that excluded all milk proteins -- the eruption cleared completely in a few days and weight gain ensued. This was a milk allergy that masqueraded as a serious underlying disorder.

Brachioradial Pruritus

2011-01-09T10:53:00.011Z

I have had an interest in Brachioradial Pruritus (BRP) for over 25 years and published a paper on it in 1985 and co-wrote a chapter on BRP for eMedicine.com. (Actually, the lion's share of the writing was done by Julianne Mann, then a dermatology resident at Oregon Health Sciences University.) As a result of the eMedicine.com chapter, I receive a few requests for information each year. Two came in recently and, with their permission, are presented here. Perhaps, some of our readers have suggestions for management of this annoying and occasionally disabling problem. Note: It is amazing how many comments have been made by people who suffer with BRP. Around 55 at this time. If you wish to leave a comment, and would like us to acknowledge it, please send me your name and email address. It will not appear anywhere on this site; but if you want me to relpy to you I need your contact information. Thank you, DJ Elpern.

1. This is from a 32 y.o. equestrian
I am an otherwise healthy woman desperately searching for a doctor who may be able to discuss some treatment options for my very itchy arms! I am 32 year old, 110 lb, active, female resident of New England and have been suffering with itchy arms (without rash) for at least four years now. When I finally sought treatment- I was referred by my primary MD to a dermatologist who informed me that I had dry, sensitive skin, and prescribed a topical cream and an oral steroid - I carefully followed his advice for 2 years - with absolutely no relief from the itch. The only thing that relieved the symptoms (which flare more intensely in the evening hours) was ice packs. I was often woken from sleep by the itch.

The itch occurs in cyclical pattern- symptomatic for months, followed by a month or two of none or very mild symptoms, then followed by another flare. it is present in sunny months as well as winter.

Finally, frustrated by the unresolved symptoms, at my own expense, I had one visit with a dermatologist in a nearby large city who very quickly diagnosed brachioradial pruritus and prescribed topical Capsaicin. Capsaicin works - sort of. But, it is a total pain in the butt for minimal relief. I am seeking alternative treatment.....acupuncture, chiropractic, anything ... ? Do I need an X-ray? What do I do? I am on my own out here in a sea of medical professionals who seem unwilling to take this condition seriously or look for possible causes that may be an underlying cause for this condition of itchy arms....

It may also be of interest that I have a large amount of muscle/ligament type tension in my neck and shoulders- it's pretty severe, some of this tension is a manifestation of stress, some results from my very physical occupation as an Equestrian.... I am personally tempted to think that all the tension in my neck and shoulders may have something to do with the arm itch - but this conflicts with the cyclical nature of the itch. Has the tension is chronic?
To me, BRP it's a big deal!

2. This is from a 37 yo health care professional:
I have suffered with this for no less than 5 years. Until about a year ago it was sporadic, but has been substantially worse and constant for the last year or so. Nights are particularly difficult, as the itching becomes intolerable and uncontrollable. I have recently found some comfort with ice packs, but naturally having to traipse off to the kitchen several times a night is inconvenient and exhausting. The most recent prescriptions I have tried are 10mg cetirizide for daytime and 25mg doxepin (1-2 at bedtime), and also betamethosone cream. The cetirizide helps with other allergy issues I have, but doesn't offer any relief to the itchy arms. Also, the doxepin helps me get a few solid hours of sleep, if I take 2, but, as with hydroxizine, I feel "hungover" the next morning... AND insatiably hungry.
I do LOVE the sun, and have always found that I feel better through the cold months if I go tanning a couple times a week. In the winter months, I spend a bit of time tanning prior to spending any significant time outside in the summer. I have fair skin, and it helps prevent burning before spending a day at the beach. (which I do, ALL day, as often as possible.) I do not, however notice any increase or decrease in the itching based on exposure to sun/tanning. In the last year, however, I HAVE starting being a bit more careful and use a minimum of SPF 30 during peak hours at the beach. Here is a recent picture:
(Editor's note: This shows some typical findings. The skin looks a bit dry and lichenified and there is evidence of excoriation. Not all cases show these changes, some are more subtle.)

I have seen several doctors, including a dermatologist, regarding this debilitating itch and NOTHING has helped enough to warrant the side effects. I cannot seem to get anyone to understand that it isn't like a skin itch, it feels like its UNDER my skin. I scratch so much, especially at night, that I bleed. I am not a crazy, irrational person.... but the loss of sleep and inability to find anything that relieves this itching probably makes me seem as though I am.

Comment: Both of these patients appear to have chronic BRP. I see a similar patient once or twice a year. While most patients with BRP have episodic, relatively easy to treat disease, there are a few patients who have disabling symptoms. There is an aphorism, "It is often more important to treat the patient who has the disease than the disease the patient has." I think this applies to persons with chronic BRP. In a real way, these are orphan patients. Few dermatologists have the expertise, and fewer the time, to adequately evaluate and treat these patient. If you have suggestions, they would be most appreciated.

ULE?

2010-12-31T19:20:00.013Z

Abstract: 4 yo girl with 3 week hx of papular eruption left axilla
HPI: This otherwise healthy four year old girl has had a mildly pruritic papular eruption which began in the left axilla with a dermatitic appearance and spread centrifugally where it appeared more papular. There was no antecedent illness. The eruption was first seen on 12/23/2010, cleared after a few days and they reoccurred. The child is not bothered by it. No animals at home and no other family members similarly affected.
O/E: Discrete erythematous papules in the left axilla and surrounding areas. The individual lesions are 3 - 5 mm in diameter. The right axilla and thoracic area are clear. There is left axcillary adenopathy
Clinical Photos: 12/31/2010
Left Axilla

Right Axilla
Lab: none

Diagnosis: Unilateral Laterothoracic Exanthem.

DDx: The lesions look like bites. Against that is the lack of symptoms, the unilateral location, and no likely cause of bites. Contact dermatitis seems unlikely.

Discussion: This is an unusual entity but the child seems well otherwise and I have recommended no treatment for present. I have not seen ULE before (to my knowledge); yet this seems the likely diagnosis. Unfortunately, the pictures in the textbooks are not very good. I suspect, that like Gianotti-Crosti, ULE may be caused by a number of viruses and that it will be difficult to come up with an etiology. The clinical appearance seems to be protean, but the distribution aids in making a diagnosis.

Reference:
1. Emedicine.com has a good chapter, however, they use the name "Asymmetric Periflexural Exanthem of Childhood."

2. McCuaig CC, et. al. Unilateral laterothoracic exanthem. A clinicopathologic study of forty-eight patients. J Am Acad Dermatol. 1996 Jun;34(6):979-84.
Department of Pediatrics, Hôpital Sainte-Justine, Montreal, Quebec, Canada.
Abstract
BACKGROUND: Four years ago, we began seeing young children with an unusual, predominantly unilateral, morbilliform and eczematous, self-limited cutaneous eruption. It appeared to correspond to unilateral laterothoracic exanthem (ULE) reported from France and to an eruption described as "a new papular erythema of childhood" in the United States.
OBJECTIVE: We conducted a prospective study of ULE to define its clinical evolution, pathology, and therapy. In addition, we performed epidemiologic and microbiologic investigations in an attempt to determine the cause of ULE.
METHOD: We studied 48 children with ULE. In some patients, blood, urine, stool, as well as skin biopsy specimens were analyzed.
RESULTS: ULE is a morbilliform, eczematous eruption that often begins close to the axilla and spreads to become bilateral, although it usually retains a unilateral predominance. Patients' mean age at onset is 24.3 months, with a female predominance (2:1) and mean duration of 5 weeks, followed by spontaneous resolution that may or may not be improved with topical corticosteroids. It is characterized by a unique eccrine lymphocytic infiltration. Although signs of infection were reported by most patients, no one infectious agent was identified. No significant epidemiologic factor was found.
CONCLUSION: ULE, in young children, is a self-limited morbilliform and scarlatiniform eruption that may represent a specific skin reaction to one or more infectious agents.

Follow-up Note: The patient's symptoms continued to wax and wane and she was seen by a pediatric dermatologist. At that time, there was just one lesion in the left axilla ( see picture) and a diagnosis of psoriasis was made. There were no other stigmata for psoriasis. If this is the case, the initial picture did not suggest that. Since the sole lesion present now is a plaque in the left axilla, if this turns out difficult to control with topical steroids, consideration to using tacrolimus should be given.

References:
Tacrolimus ointment is effective for psoriasis on the face and intertriginous areas in pediatric patients.
Brune A, Miller DW, Lin P, Cotrim-Russi D, Paller AS. Pediatr Dermatol. 2007 Jan-Feb;24(1):76-80.
Abstract
Children with psoriasis often have involvement of the face and intertriginous areas. While corticosteroids have been the mainstay of treatment for plaque-type psoriasis, the face and intertriginous areas are more sensitive to local effects of topical steroid use such as cutaneous atrophy. Topical tacrolimus has shown promise in adult patients as an alternative antiinflammatory without the cutaneous side effects of steroids. Eleven patients between 6 and 15 years of age with facial or inverse psoriasis were evaluated in a 6-month, single-center, open-label trial. Clinical evaluations were made at baseline and days 30, 90, and 180. Severity was assessed using the physician's global assessment of improvement relative to baseline, a 6-point rating scale for signs of disease (erythema, infiltration, desquamation), and an overall severity score. Within the first 30 days of treatment, every patient had cleared or achieved excellent improvement with the use of tacrolimus ointment. Statistically significant improvement was achieved in each sign of disease and the overall severity score. The only adverse event reported in 6 months of observation was significant pruritus in one patient. We therefore conclude that tacrolimus ointment is an effective treatment for psoriasis on the face or intertriginous areas in children.

Dermatomal Eruption

2010-12-22T20:34:00.018Z

Abstract: 39 yo man with two month history of dermatomal eruption.
HPI: This 39 yo man developed a dermatomal vesicular eruption 2 months ago. He was seen by his GP and treated with valcyclovir and it cleared somewhat but not completely. The eruption continues to evolve. He complains of pain and pruritus. Feels well otherwise. No underlying diseases known of.
O/E: There is a dermatomal process extending from T-10 to L 2 on the right side. The lesions are scaly patches. There are no vesicles. The lesions do not cross the mid-line. Area biopsied today is only a couple of days old, by history.
Photos:

Diagnosis: Atypical Herpes Zoster. H.z. progressing over a two month period (especially after valcyclovir) is quite unusual in a healthy, immunocompetent person.

Plan: I did a biopsy and checked his chemistries and CBC. I have seen patients with HIV/AIDS and a patient with angioimmunoblastic lymphadenopathy with atypical HSV and HZ; but never a patient like this. Perhaps, this is something I am not thinking about. I will post a photomic when path is reported and lab results. For the time being, I prescribed acyclovir 800 mg 5 times a day.

Addendum: Fran Storrs felt this was an eczematous process, possibly a contact dermatitis. The pathology showed no multinucleated giant cells and had features of a "dermatitis." So, was this a dermatitis secondary to H.Z., an atypical contact dermatitis, or factitial (the patient did ask for pain meds when first seen, which were not given)? He is now being treated with a topical corticosteroid now and we'll see how he does. When seen for suture removal sight days after biopsy, the eruption looked a bit better, was less symptomatic and had not spread beyond the dermatomes first involved.

The Power of BLINCK

2010-10-17T15:16:00.016Z

Presented by Yoon Cohen MS IV, University of New England, Biddeford, Maine and David Elpern MD, Williamstown, Massachusetts

Abstract: 68 yo woman with 4-6 months history of an atypical melanocytic lesion.

HPI: This healthy 68 yo woman with type II skin presented to the clinic with 4-6 months history of an atypical melanocytic lesion on the left knee. She had noticed an increase in size and change in color and was concerned about these changes in the lesion.

O/E: There was a 7 mm in a diameter asymmetrical brownish macule on the left knee. The lesion showed an irregular border with varied colors.

Clinical photographs:

Dermoscopic images:

Microscopic images:

Dermatopathology report:

The specimen exhibits a proliferation of moderate to severely atypical melanocytes distribubted in irregular nests, as well as singly at and above the dermal epidermal junction, with pagetoid spread to the granular layer and near confluence over at least three rete ridges. These findings support the histologic diagnosis of melanoma-in-situ.

Our appreciation to Dr. Deon Wolpowitz, MD from Boston Univeresity, Dermatopathology, for providing these photomicrographs for the case.

10X

20X

Diagnosis:

Malignant melanoma in situ

Discussion:

The BLINCK approach:

We followed the BLINCK checklist, introduced by Dr. Peter Bourne, a founder of the Skin Cancer College of Australia and New Zealand (SCCANZ). The score for the lesion was added up to 4 by criteria as following.

1. B. The lesion was not clearly benign at our first initial evaluation

2. L. The lesion appeared to be lonely without any other similar melanocytic lesion near by

3. I. The lesion appeared to be irregular outline and color on our dermoscopic exam

4. N & C. The patient was nervous about the change in color in past 4-6 months

5. K. The lesion exhibited known clues when viewed with a dermatoscope. See "Chaos and Clues" reference below.
BLINCK Score = 4

According to the BLINCK approach, a lesion should be biopsied if the BLINCK score is 2 or more out of a possible 4. Therefore, the we excised this lesion and sent for a pathologic evaluation.

According to Dr. Bourne, the BLINCK approach is presented as a simple method to assist the clinician with the decision of whether to biopsy a skin lesion or not. The use of this algorithm will improve the pickup rate of potentially serious skin cancers as well as reduce the number of unnecessary benign lesion excisions. BLINCK may be especially helpful to clinicians who have only basic or intermediate dermoscopy skills but who are regularly called upon to assess skin lesions in their practices.

Questions:

1. Would you consider using the BLINCK approach at your practice?

2. If you already have adapted the BLINCK approach, how have your experiences been?

References:

1. McColl I. BLINCK. http://idsblinck.blogspot.com/2009/11/blinck.html. Updated November 19, 2009. Accessed September 7, 2010

2. Rosendahl C, Kittler H, Cameron A, et al. CHAOS & CLUES - The Algorithm. http://www.chaosandclues.blogspot.com. Updated November 19, 2009. Accessed September 7, 2010

Palmoplantar Erythrodysesthesia Syndrome

2010-09-22T01:06:00.029Z

Presented by Yoon Cohen, MS IV
University of New England College of Osteopathic Medicine

Abstract: 45 yo woman with a metastatic breast cancer and a painful hand/foot dermatitis.

HPI: This is a 45 yo woman who was diagnosed with a metastatic breast cancer a few years ago. She has developed "atopic dermatitis" like symptoms on her hands and feet since starting capecitabine. She has completed 5 cycles of Xeloda (capecitabine) and has had to reduce the dose because of this condition. The lesions started as dry edematous, erythematous areas on palms and soles with a tingling sensation.

O/E: The examination reveals general areas of desquamation and hyperlinearity with mild erythema on both palms. This is best shown on the first photograph.

Clinical photographs:

Diagnosis: Palmoplantar erythrodysesthesia syndrome, hand-foot syndrome, chemotherapy-induced acral erythema

Discussion:

Chemotherapy-induced acral erythema or palmoplantar erythrodysesthesia syndrome is a well-defined reaction to some of the chemotherapeutic agents such as methotrexate, cytarabine, doxorubicin, fluorouracil, cytosine arabinoside, and bleomycin. This reaction is characterized by symmetric, well-demarcated, painful erythema of the palms and soles, which may progress to desquamation or blisters. It appears to be dose dependent, and is likely a direct toxic effect of the drug. Tingling on the palms and soles is followed in a few days by painful, symmetric, well-defined swelling and erythema [4].

Questions:

1. Please feel free to share your experiences with treatment options.

References:

1. Marini A, Hengge UR. Hand-foot syndrome with capecitabine therapy. Hautarzt. 2007 June; 58(6):532-6

Abstract: A 72-year-old patient with esophageal carcinoma developed a severe hand-foot syndrome during second-line therapy with the oral fluoropyrimidine capecitabine. We also summarize the current knowledge with regard to the hand-foot syndrome and distinguish it from palmoplantar erythrodysesthesia.

2. Degen A, Alter M, Satzger I, et al. The hand-foot-syndrome associated with medical tumor therapy- classification and management. J Dtsch Dermatol Ges. 2010 Sep; 8(9):652-61

Abstract: The hand-foot-syndrome (HFS, palmoplantar erythrodysesthesia, chemotherapy-associated acral erythema) is characterized by painful predominantly palmo-plantar lesions. The association with different chemotherapeutic agents has been known for over 20 years. More recently, HFS has been reported in association with regimens using targeted agents, in particular the multikinase inhibitors (MKI) sorafenib and sunitinib. The HFS associated with MKI has a different distribution and clinical appearance than the traditional disorder. In this review, similarities and differences between chemotherapy- and MKI-associated HFS are discussed and current recommendations for their prophylaxis and management are summarized.

3. Janusch M, Fischer M, Marsch WCh, et al. The hand-foot syndrome - a frequent secondary manifestation in antineoplastic chemotherapy. Eur J Dermatol. 2006 Sep-Oct; 16(5): 494-9

Abstract: The hand-foot syndrome (HFS) (palmoplantar erythrodysesthesia) designates acute, painful erythemas of the palms and soles of the feet caused by antineoplastic chemotherapies. The most frequent trigger substances are 5-fluoruracil and its derivates. At maximum severity, the HFS is bullous to erosive or ulcerous in character. The pathogenesis has not yet been clarified. Histologically, the HFS is characterized by a toxic keratinocyte reaction. Furthermore, there is sub-basal edema with a tendency to bullae, dilated blood and lymph capillaries and usually only mild perivascular lymphocytic infiltration. Early recognition and delineation from other differential diagnoses is prerequisite to targeted management of the disease. Depending on the severity, HFS requires dose reduction, interruption or switch in the antineoplastic chemotherapy. (You can access to the article at http://www.john-libbey-eurotext.fr/e-docs/00/04/26/D7/vers_alt/VersionPDF.pdf)

4. Habif TP. Clinical Dermatology. 5th edition. USA: Elsevier Science 2010

Keratolysis exfoliativa

2010-08-29T16:51:00.002Z

HPI: The patient is a 27 yo medical assistant who was seen on August 27, 2010 with a six day history of slightly pruritic scaling of the palms. She is well otherwise and has had no recent illnesses.

O/E: The examination reveals discrete areas of desquamation on both palms. No vesicles. Soles are normal and remainder of cutaneous exam is unremarkable.

Photos:

Diagnosis: The clinical picture is consistent with Keratolysis exfoliativa. Strangely, PubMed has only three references to this relatively common disorder, and only one is helpful (see below). Most dermatologists are familiar with this entity. There's a brief description on DermNet.

A throat culture taken to r/o post-streptococcal desquamation of the palms was negative.

Refererence:
Recurrent focal palmar peeling.
Lee YC, Rycroft RJ, White IR, McFadden JP.
Australas J Dermatol. 1996 Aug;37(3):143-4.
St John's Institute of Dermatology, St Thomas' Hospital, London, United Kingdom.
Abstract
Recurrent focal palmar peeling, previously known as keratolysis exfoliativa, is an idiopathic condition characterized by chronic palmar and occasionally plantar peeling. It can be exacerbated by environmental factors, and may be misdiagnosed as chronic contact dermatitis. Accurate diagnosis is from the history and examination. It is supported by a negative patch test result. Three cases of recurrent focal palmar peeling are presented, of which two were misdiagnosed as chronic dermatitis. Although there are few references on recurrent focal palmar peeling, it is likely to be a common condition that rarely presents to dermatologists because it is largely asymptomatic. A correct diagnosis is essential due to the social, occupational and legal implications if misdiagnosed.

Atypical Lymphocytic Infiltrate

2010-07-30T12:53:00.055Z

Presented by:
Ron Yaar, Boston University Skin Path and D.J. Elpern

Abstract: 50 yo man with few month history of an asymptomatic nodule on the scalp.

HPI: This 50 yo man has had a slowly enlarging tumor of the mid parietal scalp for three to four months. No other similar lesions. He has Type II diabetes and hypertension. Meds: furosemide, metformin, Diovan, atenolol.

O/E: 15/6/2010 6-7 mm papule w/o diagnostic features mid-parietal
15/7/2010 (reevaluation) 8 mm firm pink papule. Difficult to see because covered with hair.

Clinical Photo:

Pathology:

Image HE – 20x - Dense, pandermal lymphocytic infiltrate. Focal crush cell artifact at edges.
Image HE – 100x – A mixed population of cells. A clear Grenz zone is present.
Image HE – 400x – Smaller lymphocytes mixed with highly pleomorphic cells.
Photos courtesy of Ron Yaar, M.D.

CD3 – Numerous T lymphocytes present. Higher mag shows that most are smaller cells.
CD20 – Numerous B lymphocytes present. Higher mag shows many of them correspond to the larger, pleormorphic cells.

H & E 20x

H & E 100x

H & E 400 x

CD 3 40x

CD 3 400x

CD 20 40x

CD 20 400x

Lab: At this point we don't have any lab results. Will check on his latest CBC.

Diagnosis: Solitary Atypical Lymphoid Infiltrate. Benign or Malignant?

Questions: Have you seen a similar case? Could this be a reaction to a bite? How would you approach this?

References:
1. Talpur R, Duvic M. Atypical lymphoid infiltration occurring at the site of a healed varicella zoster infection. Clin Lymphoma. 2003 Mar;3(4):253-6.
Abstract: Herpes zoster infection has been associated with a number of cutaneous reactions. The authors report the first case of a patient with an atypical epidermotropic lymphoid infiltrate that arose within skin previously affected by herpes varicella zoster. The differential diagnosis of such lesions and review of literature on previous cutaneous infiltrates occurring at sites of zoster infection are discussed.

Facial Excoriations in a 22 yo woman

2010-07-02T10:00:00.002Z

Presented by Dr. Euan Coig
The Pass, Manitoba

Abstract: Twenty-two yo homemaker with three to four year history of excoriations on face, arms and chest.

HPI: This woman's chief complaint was "itching and pimples." She grew up in a dysfunctional family ~ 100 miles from where she now lives . Her father was an alcoholic who was physically and verbally abusive to her mother, her younger sister and herself. She denies sexual abuse. She was diagnosed with ADHD at age eight and has been treated for that since then with Ritalin. The also suffers from migraines. The patient went to college for two years and was studying sociology but ran out of money and dropped out. She is now married with an 18 month old child and her husband is deployed in Afghanistan with the Canadian forces.

O/E: The patient is an obese somewhat unkempt young woman. She has excoriations on her face, arms and chest. Many (mostly atrophic) scars on arms and chest. Back spared. Many of the excoriations have serous crusts.

Photographs:

Diagnosis: Excoriations in a young woman. This is more serious than acne excoriee. These type of lesions are self-inflicted but the patient is often not aware of doing this or will deny having done so. Many of these patients (who are almost always woman) have a history or abusive childhoods (physical and/or sexual). This is a form of "self-harm" behavior. These patients often fall into a no-man's zone between dermatology and psychiatry and prove difficult to treat.

Questions: How would you approach a similar patient?

Special Comments: Here are in-depth comments from two experts in this area, Drs. Anna Luise Kirkengen and Caroline Koblenzer.

References:
1. Shenefelt PD. Using hypnosis to facilitate resolution of psychogenic excoriations in acne excoriée. Am J Clin Hypn. 2004 Jan;46(3):239-45. pshenefe@hsc.usf.edu
Abstract: Hypnotic suggestion successfully alleviated the behavioral picking aspect of acne excoriée des juenes filles in a pregnant woman who had been picking at the acne lesions on her face for 15 years. Acne excoriée is a subset of psychogenic or neurotic excoriation. Conventional topical antibiotic treatment was used to treat the acne. Compared with other treatments for uncomplicated acne excoriée, hypnosis is relatively brief and cost-effective and is non-toxic in pregnancy.

2. Arnold LM, Auchenbach MB, McElroy SL. Psychogenic excoriation. Clinical features, proposed diagnostic criteria, epidemiology and approaches to treatment. CNS Drugs. 2001;15(5):351-9.
Women's Health Research Program, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. arnoldlm@email.uc.edu
Abstract: Psychogenic excoriation (also called neurotic excoriation, acne excoriée, pathological or compulsive skin picking, and dermatotillomania) is characterised by excessive scratching or picking of normal skin or skin with minor surface irregularities. It is estimated to occur in 2% of dermatology clinic patients and is associated with functional impairment, medical complications (e.g. infection) or substantial distress. Psychogenic excoriation is not yet recognised in the DSM. We propose preliminary operational criteria for its diagnosis that take into account the heterogeneity of behaviour associated with psychogenic excoriation and allow for subtyping along a compulsivity-impulsivity spectrum. Psychiatric comorbidity in patients with psychogenic excoriation, particularly mood and anxiety disorders, is common. Patients with psychogenic excoriation frequently have comorbid disorders in the compulsivity-impulsivity spectrum, including obsessive-compulsive disorder, body dysmorphic disorder, substance use disorders, eating disorders, trichotillomania, kleptomania, compulsive buying, obsessive-compulsive personality disorder, and borderline personality disorder. There are few studies of the pharmacological treatment of patients with psychogenic excoriation. Case studies, open trials and small double-blind studies have demonstrated the efficacy of selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors in psychogenic excoriation. Other pharmacological treatments that have been successful in case reports include doxepin, clomipramine, naltrexone, pimozide and olanzapine. There are no controlled trials of behavioural or psychotherapeutic treatment for psychogenic excoriation. Treatments found to be effective in case reports include a behavioural technique called 'habit reversal'; a multicomponent programme consisting of self-monitoring, recording of episodes of scratching, and procedures that produce alternative responses to scratching; and an 'eclectic' psychotherapy programme with insight-oriented and behavioural components.

3. Arnold LM, McElroy SL, et. al. Characteristics of 34 adults with psychogenic excoriation. J Clin Psychiatry. 1998 Oct;59(10):509-14.
Biological Psychiatry Program, University of Cincinnati Medical Center, Ohio 45267-0559, USA.
Abstract: BACKGROUND: Psychogenic excoriation, characterized by excessive scratching or picking of the skin, is not yet recognized as a symptom of a distinct DSM-IV disorder. The purpose of this study was to provide data regarding the demographics, phenomenology, course of illness, associated psychiatric comorbidity, and family history of subjects with psychogenic excoriation. METHOD: Thirty-four consecutive subjects were recruited from an outpatient dermatology practice and by advertisement. Subjects completed the Structured Clinical Interview for DSM-IV augmented with impulse control disorder modules, the Yale-Brown Obsessive Compulsive Scale, and a semistructured interview for family history, demographic data, and clinical features. RESULTS: Most subjects were women who described a mean age at onset of 38 years and a chronic course. Subjects excoriated multiple sites, most frequently the face. The behavior caused substantial distress and dysfunction. All 34 subjects met criteria for at least 1 comorbid psychiatric disorder, with a mood disorder the most common. Family histories were notable for depressive disorders and psychoactive substance use disorders. Most subjects experienced both mounting tension before excoriation and relief after excoriation as in impulse control disorders. A minority of subjects excoriated skin as part of obsessive-compulsive disorder. Body dysmorphic disorder with preoccupation about the skin's appearance precipitated excoriation in about a third of subjects. CONCLUSION: Psychogenic excoriation is chronic, involves multiple sites, and is associated with a high rate of psychiatric comorbidity. The behavior associated with the excoriation is heterogeneous and spans a compulsive-impulsive spectrum. Most subjects in this sample described features of an impulse control disorder.

4. Mohammad Jafferany, M.D. Psychodermatology: A Guide to Understanding Common Psychocutaneous Disorders. Prim Care Companion J Clin Psychiatry. 2007; 9(3): 203–213.
Abstract: More than just a cosmetic disfigurement, dermatologic disorders are associated with a variety of psychopathologic problems that can affect the patient, his or her family, and society together. Increased understanding of biopsychosocial approaches and liaison among primary care physicians, psychiatrists, and dermatologists could be very useful and highly beneficial. This article is available free Full Text.

Neuropathy Dermatitis

2010-06-22T09:22:00.004Z

Presented by Professor Khalifa Sharqie
Chief of Dermatology
University of Baghdad, Iraq

Abstract: Sixty year-old woman with neuropathy dermatitis at the right side of incision scar following right knee-joint replacement.

History: This 60 year-old woman had a right knee joint replacement on 7 Jan 2010. About three months post-op, she noticed non-itchy rash on the right side of the incision scar which has gradually enlarged in size. No other important medical history.

O/E: I saw the patient on 9 June 2010 with the slightly scaly erythematous rash forming a plaque on the front of the right knee joint, on the right side of the incisional scar only. It does not cross to other side. The rash is completely anesthetic as confirmed by neurological assessment, while there is normal sensation on the left side of the scar.

Clinical Photo:

Diagnosis: Neuropathy dermatitis

Comment and question: This is similar to post-bypass dermatitis along one side of the saphenous vein harvesting scar on the front of the leg at the site of sensory neuropaphy. This rash also does not cross to the other side. The present case seems to confirm that many skin diseases might follow the course of neuropathy like vitiligo and dermatitis.

I would like to ask my colleagues about any similar observations simulating the present case and await their fruitful comments.

References:
1. Sharquie KE. Post-Bypass dermatitis. October 10, 2009 VGRD Blog

2. Logue EJ 3rd, Drez D Jr. Dermatitis complicating saphenous nerve injury after arthroscopic debridement of a medial meniscal cyst. Arthroscopy. 1996 Apr;12(2):228-31
Abstract: We report the case of a patient who developed hypesthesia in the distribution of the saphenous nerve after an arthroscopic debridement of a medial meniscal cyst. Dermatitis developed in the area of the hypesthesia 3 months later, Both complications responded to symptomatic treatment. A review of the literature confirms the unusual nature of these complications.

3. Satku K, Fong PH, Kumar VP, Lee YS. Dermatitis complicating operatively induced anesthetic regions around the knee. A report of four cases. J Bone Joint Surg Am. 1993 Jan;75(1):116-8. No Abstract available

4. Mathias CG. Post-traumatic eczema. Dermatol Clin. 1988 Jan;6(1):35-42.
Abstract:
Thirteen cases of eczema that followed acute cutaneous trauma were observed. On the basis of the present case series, the following conclusions may be drawn: 1. Cutaneous trauma may precipitate eczema. 2. The trauma is sufficient to cause obvious tissue damage accompanied by an inflammatory or regenerative response. 3. Eczema usually begins within a few weeks of acute injury at the site of the cutaneous trauma. 4. Eczema may occur as an isolated idiopathic reaction or as an isomorphic reaction either preceding or following the appearance of an endogenous eczematous condition in nontraumatized skin. 5. Individual lesions of post-traumatic eczema may persist or recur for long periods of time. 6. The occurrence of post-traumatic eczema following occupational injury has important medicolegal implications.

.

35 yo woman with short history of urticarial vasculitis

2010-06-15T06:00:00.000Z

Abstract: 35 yo woman with three day history of an atypical urticarial eruption

HPI: This 35 yo woman developed an urticarial eruption 8 - 10 days after starting amoxicillin for a dental infection. At first the lesions blanched with pressure but over the last few days before her office visit the some of the lesions looked hemorrhagic. She had mild arthralgias but no fever or malaise.

O/E: There was a wide-spread eruption mostly on legs and arms. On her thighs the lesions appeared hemorrhagic. The torso, head and neck were mostly spared.

Clinical Photos:

Pathology: Two 4 mm punch biopsies were obtained from the thighs. There was a superficial and mid dermal mixed inflammatory infiltrate composed mostly of neutrophils and eosinophils with a few lymphocytes. The pathology was read as leucocytoclastic vasculitis vs. urticarial vasculitis.
Photomicrographs are 10x, 20x, 40x and courtesy of Dr. Jag Bhawan

Lab: CBC nl; Chem panel nl; UA nl

Diagnosis: Most consistent with Drug-Induced Urticarial Vasculitis (UV).

Discussion: While UV is recognized to present as a cutaneous drug eruption, MEDLINE has no reports of UV from amoxicillin. In this otherwise healthy woman, this seems to be the best diagnosis. She was treated with prednisone 20 mg b.i.d. and at one week her skin lesions had completely resolved. The dose was dropped to 20 mg per day for the second week and then she will stop. We are aware of cases of presumably drug-induced UV which can last for weeks to months and be associated with hypocomplementemia and positive ANA and antihistone antibodies. Since this woman did well and her process resolved quickly more specialized tests were not done.

Questions:
I don't feel any further work-up is indicated at this point. If she stays clear the case is probably closed. If she continues to have UV-like lesions once prednisone is discontinued, a more in-depth work-up will be initiated. Does anyone feel we should be more aggressive?

Reference:
1. eMedicine.com Urticarial Vasculitis
2. There are no reports of UV from amoxicillin and only one with ampicillin but it is very vague.

Note: I will ask the patient to add her comments.

64 Year-old Man with dysesthesia and alopecia

2010-05-26T15:40:00.001Z

Abstract: 64 yo man with abnormal sensation and localized alopecia on the left thigh.

History: This 64 yo business man has experienced dysesthesia on the lateral aspect of his left thigh for the past few years. He has noticed alopecia at the site of his symptoms. His health is good and he takes no medications by mouth. For the past 30 years, he has done business in Indonesia and spends two to three months a year there. There is a history of lower back pain, but no diabetes and no history of trauma.
O/E: On the left lateral thigh there is a side, 7 cm in diameter area of mild lichenification and alopecia. The findings are subtle but real. I am not sure how convincing the photos are.
Clinical Photos:

IMPRESSION: This is most likely merlagia paresthetica.

Questions:
The findings are subtle. Do you accept this diagnosis? Would a referral to a neurologist be appropriate? Should the patient just be reassured?

References:
1. Nabavi DG, et. al.. [Meralgia paresthetica. A rare differential diagnosis of circumscribed alopecia] Dtsch Med Wochenschr. 1996 Jun 21;121(25-26):834-8. ([Article in German])
Klinik und Poliklinik für Neurologie, Universität Münster.
Abstract
HISTORY AND CLINICAL FINDINGS: Two patients with circumscribed alopecia on the lateral aspect of the thigh underwent a neurological investigation after medical and dermatological examinations had failed to establish the cause. Patient 1 also had neuralgia of the genitofemoral nerve after osteotomy of the iliac crest; patient 2 had insulin-dependent diabetes mellitus. Within the affected part of the skin both patients had sensory dysfunctions over the area of distribution of the cutaneous lateral femoral nerve. Patient 2 additionally had sensory dysfunctions in other areas of innervation. INVESTIGATIONS: Neurogram and recordings of sensory evoked potentials revealed decreased amplitudes on the affected side, establishing the diagnosis of meralgia paresthetica. TREATMENT AND COURSE: The painful neuropathy was successfully treated in both patients with carbamazepine (patient 1: 1.600 mg daily; patient 2: 900 mg daily). CONCLUSION: Circumscribed alopecia can be caused by peripheral nerve lesions. It should be considered in the differential diagnosis, particularly as the cause can be easily established.

2. Harney D, Patijn J. Meralgia paresthetica: diagnosis and management strategies. Pain Med. 2007 Nov-Dec;8(8):669-77.
Department of Anesthesiology and Pain Management, University Hospital Maastricht, Maastricht, The Netherlands. dharney@hotmail.com
Abstract
Meralgia paresthetica (MP), coined from the Greek words meros (thigh and algos), meaning pain, is a neurological disorder characterized by a localized area of paresthesia and numbness on the anterolateral aspect of the thigh. The incidence of MP is more common than often reported in the literature. The etiology of MP includes mechanical factors such as obesity, pregnancy, and other conditions associated with increased intrabdominal pressure, surgery of the spine, and pelvic osteotomy. A coherent history and pertinent physical examination is essential in making the diagnosis; however, red flags such as tumor and lumbar disk herniations must be recognized and appropriately treated. While the diagnosis of MP is essentially a clinical diagnosis, sensory nerve conduction velocity studies are a useful adjunctive diagnostic tool. The management of MP includes treating the underlying cause (if any) and conservative management. Surgery should only be adopted when all nonoperative therapies have failed to manage the condition in an effective manner.

Facial erythema Secondary to Topical Corticosteroids

2010-05-21T09:18:00.002Z

Abstract: 37 yo man with marked facial erythema who has been using hydrocortisone valerate 0.2% cream (HC valerate) for 20 years.

HPI: HC valerate was prescribed for a facial eruption when the patient was a teenager. He's been using it ever since. Over time, he has developed marked painful facial erythema.

O/E: There is fiery erythema over the malar eminences, periorbital areas and portions of forehead. Three weeks after stopping the HC valerate, using cool compresses b.i.d. and minocycline 100 mg b.i.d. the process persists.

Clinical Photo: May 20, 2010 (three weeks after stopping HC valerate

Diagnosis: Red Face Syndrome. Facial addiction to topical corticosteroid.

Questions: Other than abstinence and cold compresses, are there any other treatments you have had success with? What about topical tacrolimus ointment?

Reference: The most helpful reference I have found is:
Papaport MJ, Rapaport V. Eyelid dermatitis to red face syndrome to cure: clinical experience in 100 cases. J Am Acad Dermatol. 1999 Sep;41(3 Pt 1):435-42.
Abstract:
A retrospective review of all eyelid dermatitis patients seen over an 18-year period revealed a large subgroup of patients who had, as the basis for their ongoing problem, an addiction to the use of topical or systemic corticosteroids. This group of 100 patients often sought many consultations with various physicians. Unrelenting eyelid or facial dermatitis often resulted in the use of increasing amounts of corticosteroids for longer periods of time. Soon the skin became addicted. Once the work-up ruled out other causes, the remedy for the problem was absolute total cessation of corticosteroid usage. This article describes the typical history of the problem, the evaluation of these patients, and the distinctive pattern of flaring erythema that ensued when the corticosteroids were ceased. We stress the absolute necessity of total cessation of corticosteroid use as the only treatment for corticosteroid addiction. We also demonstrate that no additional therapy or further consultations were necessary once remission was obtained after topical corticosteroid abuse was halted.

This may be worth a trial:
Goldman D. Tacrolimus ointment for the treatment of steroid-induced rosacea: a preliminary report. J Am Acad Dermatol. 2001 Jun;44(6):995-8
BACKGROUND: Excessive topical corticosteroid application to facial areas commonly leads to steroid-induced rosacea. This may be a recalcitrant problem that requires months of antibiotic and anti-inflammatory therapy before it resolves. OBJECTIVE: The purpose of this article is to review the use of tacrolimus ointment, a macrolide anti-inflammatory ointment for the treatment of 3 patients with steroid-induced rosacea. METHODS: Three patients with steroid-induced rosacea applied tacrolimus ointment, 0.075% twice daily for 7 to 10 days. Patients were also instructed to avoid topical corticosteroid use and other rosacea-aggravating substances including caffeine, spicy foods, alcohol, hot fluids, and fluoride. Patients were observed for tenderness, erythema, and relief of pruritus. RESULTS: Pruritus, tenderness, and erythema were resolved in all 3 patients after 7 to 10 consecutive days' use of tacrolimus 0.075% ointment in conjunction with avoidance of topical steroids, caffeine, spicy food, alcohol, hot fluids, and fluoride. CONCLUSION: This preliminary study demonstrates that tacrolimus 0.075% ointment may be effective for patients with steroid-induced rosacea, when combined with avoidance of topical steroid use, as well as avoidance of other agents known to aggravate rosacea (caffeine, spicy foods, alcohol, hot fluids, and fluoride).

14 yo boy with a genodermatosis

2010-05-07T10:24:00.011Z

Presented by:
Drs Israa Al Shawi, FICMS, & Ali Al Hilaly, DVD
Al_Hashmia Hospital
Babylon,Iraq

Abstract: 14 to boy with photosensitivity and verrucous skin lesions.

HPI: This 14 yo boy's story started when he was two months old. He developed many bullae on scalp and extremities which healed spontaneously leaving a thickened skin. Over the years, he also developed many dark brown lesions in a generalized distribution. He has two sisters (age three and five) and two young cousins (male and female) with the same features. His parents are cousins and they are unaffected. There are a sister and brother who are normal

O/E: Large numbers of brown-black verrucous papules and plaques distributed all over the body. These lesions resemble seborrheic keratosis. He has erythema of sun-exposed areas and thick brown scales of scalp and sides of the face with alopecia. His body hair is coarse and is reported to sometimes improve spontaneously.

Clinical Photos:

Lab: None available at present

Pathology: One verrucous papule showed hyperkeratosis, acanthosis, papillomatosis and intranuclear inclusions consistent with verruca vulgaris.

Diagnosis: Not clear

Questions: This appears to be an autosomal recessive disorder.
If we consider it as Epidermodysplasia verruciformis, what is the explanation for scarring alopecia, photosensitivity and hypertrichosis?
Could this be a patient with Rothmund-Thompson Syndrome?
What are your opinions about the diagnosis?
What further studies can be done to establish the diagnosis, or can this be made clinically?
If genetic testing is indicated, what tests should be done and what kind of samples would they need?

References:
Rothmund-Thomson Syndrome [Internet].
Wang LL, Plon SE.
In: Pagon RA, Bird TC, Dolan CR, Stephens K, editors. GeneReviews [Internet]. Seattle (WA): University of Washington, Seattle; 1993-.
1999 Oct 06 [updated 2009 Apr 07].

Excerpt

Disease characteristics. Rothmund-Thomson syndrome (RTS) is characterized by poikiloderma; sparse hair, eyelashes, and/or eyebrows/lashes; small stature; skeletal and dental abnormalities; cataracts; and an increased risk for cancer, especially osteosarcoma. The skin is typically normal at birth; the rash of RTS develops between age three and six months as erythema, swelling, and blistering on the face and subsequently spreads to the buttocks and extremities. The rash evolves over months to years into the chronic pattern of reticulated hypo- and hyperpigmentation, punctate atrophy, and telangiectases, collectively known as poikiloderma. Hyperkeratotic lesions occur in approximately one-third of individuals. Skeletal abnormalities include dysplasias, absent or malformed bones (such as absent radii), osteopenia, and delayed bone formation. Diagnosis/testing. The diagnosis of RTS is established by clinical findings — in particular, the characteristic rash. Routine cytogenetic studies of lymphocytes or skin fibroblasts may reveal mosaic abnormalities of chromosome 8, such as trisomy 8, partial 8q duplication, and tetrasomy 8q, which have been seen in individuals with RTS but are not diagnostic. Skin biopsy may show poikilodermatous changes, which are nonspecific but consistent with RTS. RECQL4 is the only gene associated with RTS to date; although evidence suggests genetic heterogeneity, no other locus for RTS has been identified. Molecular testing of RECQL4 is clinically available. Management. Treatment of manifestations: pulsed dye laser to treat the telangiectatic component of the rash; surgical removal of cataracts; and standard treatment for cancer. Prevention of secondary complications: use of sunscreens with both UVA and UVB protection to prevent skin cancer. Surveillance: annual physical and eye examination, monitoring of skin for lesions with unusual color or texture, screening for osteosarcoma. Agents/circumstances to avoid: excessive sun exposure. Genetic counseling. RTS is inherited in an autosomal recessive manner. At conception, each sib of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier. Once an at-risk sib is known to be unaffected, the risk of his/her being a carrier is 2/3. Carrier testing for at-risk relatives and prenatal testing for pregnancies at increased risk are possible if the disease-causing mutations in the family are known.

12 yo Boy with Chest Pain and Skin Lesions

2010-04-26T23:26:00.013Z

From the Department of Medicine
People's College of Medical Sciences
Bhopal, India

Abstract: 12 year old boy with shortness of breath, intermittent chest pains and skin lesions.

History: This 12 year-old boy was admitted to the pediatric service with a three month history of shortness of breath. He has been having sleepless nights and we witnessed his distress in the echo room when he developed severe chest pain ( no sweating etc) and it remarkably subsided after 5 minutes of standing up after the echo examination! He has had skin lesions since the age of four.

O/E: We saw him in the echocardiography room. On examination he had these remarkable cutaneous lesions in the elbows, legs and perianal region and over the Achilles tendons. There were reddish-yellow nodules over the extensor aspects of the knees and elbows and discrete subcutaneous nodules over the Achilles tendons.

Clinical Photos:

Lab: Serum cholesterol 641 mg%. His echo showed a global hyopkinesia with dilated left atrium and ventricles.

Diagnosis: Familial Hypercholesterolemia with Tuberous and Tendon Xanthomas.

Questions:
1. What further diagnostic studies are needed?
2. Do you think this is the homozygous variant?
3. We have yet to find a suitable explanation for his variable chest pain that aggravates only on lying down and subsides on standing. Could it be due to a myxomatous tissue near the coronary ostia?
3. What is the evidence surrounding the efficacy of drugs and even LDL apheresis for familial hypercholesterolemia?
5. What are the chances of failure to respond to therapy and what is the long term prognosis?

References:
1. Christopher Sibley and Neil J Stone . Familial hypercholesterolemia: a challenge of diagnosis and therapy. Cleve Clin J Med. 2006 Jan;73(1):57-64
Abstract
People with familial hypercholesterolemia (FH) have dramatically high levels of low-density lipoprotein cholesterol (LDL-C), which can lead to accelerated atherosclerosis and, if untreated, early cardiovascular death. Although the heterozygous form of FH is often unrecognized, detecting it early can enable risk reduction before premature coronary heart disease occurs. Available Free Full Text on PubMed

2. Beigel R, Beigel Y. Homozygous familial hypercholesterolemia: long term clinical course and plasma exchange therapy for two individual patients and review of the literature. J Clin Apher. 2009;24(6):219-24
Heart Institute, Chaim Sheba Medical Center, Tel-Hashomer, Israel. beigelr@yahoo.com
Abstract
Familial hypercholesterolemia (FH) is an autosomal dominant disease. Homozygous FH (HFH) manifests with severe hypercholesterolemia since birth (cholesterol levels >5-6 the upper normal limit), which, if untreated, leads to early onset accelerated atherosclerosis and premature coronary death, usually before the 2nd or 3rd decades of life. Various invasive procedures (iliocecal bypass, porto-caval shunt, liver transplant, and gene therapy) have been introduced for lowering low density lipoprotein (LDL) aiming at reducing atherosclerosis and improving survival of HFH patients. Of all the various methods, LDL apheresis has become the most attractive. Although its impressive effect on LDL-C reduction is well established, its long-term (of more than 10 year) effect on the atherosclerotic process and specifically cardiac end-points in HFH is hardly documented. We herewith report on the longest term lipophoresis so far reported in two HFH patients, each treated with plasma-exchange and LDL-apheresis for more than 20 years. The observations provide an opportunity to focus on various aspects regarding not only the procedure itself but also its effect on various clinical endpoints. By this description together with reviewing the literature, we discuss several issues, some of them are generalized while others are individualized, dealing with the approach of long term LDL apheresis in HFH.

STUMP vs. Melanoma

2010-04-15T00:22:00.037Z

presented by DJ Elpern and Jag Bhawan

Abstract: 20 yo woman with two month hx of an aggressive melanocytic neoplasm.

HPI: This otherwise healthy 20 yo college student noticed a papule on her right upper back two months before her dermatology visit. It rubbed on her bra and that is how she found it.

O/E: There was a 5 mm diameter brownish papule on the right upper back. It had no play of color, no asymmetry, and the border was fairly sharp. Dermoscopically it was not diagnositic of benign melanocytic neoplasm or melanoma. It was definitely and "outlier" lesion and was rapidly growing. She had an excisional biopsy the next week.

Clinical Photo:.

Pathology:
Excisional biopsy revealed an atypical cellular lesion with a nesting pattern, especially in the upper part of the lesion ( Fig 1,2). The deeper part showed infiltration of reticular dermis (Fig 3 ) as well as arrector pili ( Fig 4 )by islands of atypical cells. The cells were epithelioid, pleomorphic, large with atypical nuclei and several mitoses including in deep dermis ( Fig 5). Focal pigmentation was seen. There was mild epidermal hyperplasia, but no confluence or pagetoid spread of atypical melanocytes was observed. No radial growth phase was noted. These findings were interpreted as malignant melanoma with a depth of 3.5 mm. Lack of inflammatory response, confluence and pagetoid spread raised the possibility of melanocytic tumors of uncertain malignant potential ( MEL-TUMP ).
Two of the 5 sentinel lymph nodes were positive with atypical nests of melanocytes confirmed by MART-1 within the parenchyma of the lymph nodes.

Figures 1 - 5 in sequential order (Courtesy of Jag Bhawan)

Surgery. A wide-local excision and SLN biopsy was done and this showed the tumor was completely excised by the first excision and two of 5 nodes were positive. She will have a PET scan in a few days.

Questions for Panel:
1. Is this a MELTUMP -- Melanocytic tumor of uncertain malignant potential -- also called STUMP Spitzoid tumor of uncertain malignant potential?
2. Does this impart a better prognosis than if this is a MM? Is thickness less important for these lesions as a prognostic tool?
3. Do MELTUMPs have a different biological behaviors than MMs?
4. If PET scan is negative, would you recommend ELND?
5. Should her care be managed at this point by an oncologist with an interest in chemotherapy. Role for interferon? Can this be cured by chemotherapy or is pharmacologic therapy just palliative?
6. Many more questions. Your thoughts are most welcome.

References:
1. Balch CM, et al. Multivariate Analysis of Prognostic Factors Among 2,313 Patients With Stage III Melanoma: Comparison of Nodal Micrometastases Versus Macrometastases. J Clin Oncol. 2010 Apr 5.
Abstract PURPOSE: To determine the survival rates and independent predictors of survival using a contemporary international cohort of patients with stage III melanoma. PATIENTS AND METHODS: Complete clinicopathologic and follow-up data were available for 2,313 patients with stage III disease in an updated and expanded American Joint Committee on Cancer (AJCC) melanoma staging database. Kaplan-Meier and Cox multivariate survival analyses were performed. RESULTS: Among all 2,313 patients with stage III disease, 81% had micrometastases, and 19% had clinically detectable macrometastases. The 5-year overall survival was 63%; it was 67% for patients with nodal micrometastases, and it was 43% for those with nodal macrometastases (P < .001). Tremendous heterogeneity in survival was observed, particularly in the microscopically detected nodal metastasis subset (from 23% to 87% for 5-year survival). Multivariate analysis demonstrated that in patients with nodal micrometastases, number of tumor-containing lymph nodes, primary tumor thickness, patient age, ulceration, and anatomic site of the primary independently predicted survival (all P < .01). When added to the model, primary tumor mitotic rate was the second-most powerful predictor of survival after the number of tumor-containing nodes. In contrast, for patients with nodal macrometastases, the number of tumor-containing nodes, primary ulceration, and patient age independently predicted survival (P < .01). CONCLUSION: In this multi-institutional analysis, we demonstrated remarkable heterogeneity of prognosis among patients with stage III melanoma, especially among those with nodal micrometastases. These results should be incorporated into the design and interpretation of future clinical trials involving patients with stage III melanoma.

2. Soonh SJ etc. Predicting Survival Outcome of Localized Melanoma: An Electronic Prediction Tool Based on the AJCC Melanoma Database. Ann Surg Oncol. 2010 Apr 9. [Epub ahead of print]
Abstract:
BACKGROUND: We sought to develop a reliable and reproducible statistical model to predict the survival outcome of patients with localized melanoma. METHODS: A total of 25,734 patients with localized melanoma from the 2008 American Joint Committee on Cancer (AJCC) Melanoma Database were used for the model development and validation. The predictive model was developed from the model development data set (n = 14,760) contributed by nine major institutions and study groups and was validated on an independent model validation data set (n = 10,974) consisting of patients from a separate melanoma center. Multivariate analyses based on the Cox model were performed for the model development, and the concordance correlation coefficients were calculated to assess the adequacy of the predictive model. RESULTS: Patient characteristics in both data sets were virtually identical, and tumor thickness was the single most important prognostic factor. Other key prognostic factors identified by stratified analyses included ulceration, lesion site, and patient age. Direct comparisons of the predicted 5- and 10-year survival rates calculated from the predictive model and the observed Kaplan-Meier 5- and 10-year survival rates estimated from the validation data set yielded high concordance correlation coefficients of 0.90 and 0.93, respectively. A Web-based electronic prediction tool was also developed ( http://www.melanomaprognosis.org/ ). CONCLUSIONS: This is the first predictive model for localized melanoma that was developed based on a very large data set and was successfully validated on an independent data set. The high concordance correlation coefficients demonstrated the accuracy of the predicted model. This predictive model provides a clinically useful tool for making treatment decisions, for assessing patient risk, and for planning and analyzing clinical trials.

Nail Dystrophy in an Eight Year-Old Girl

2010-04-06T23:59:00.002Z

Introduction: In the past, we published a case of localized acrodermatitis continua. The father of a child with this diagnosis in the U.S. came across our post on VGRD and asked our advice for his daughter. Your opinions may help with the diagnosis and management of this child. One can only imagine how this disorder impacts on a young child. Perhaps, one of us has had a favorable outcome with a similar patient.

History: Please help with an opinion on our eight year-old daughter who has had an acral dermatitis for the past 5 years. The swelling started at the cuticle and slowly moved back towards the first knuckle over the years and was associated with itching. Initially it was diagnosed as insect bites. About a year ago her fingers became more swollen and a doctor made a clinical diagnosis of fungus (no tests were done). She was treated first with vinegar soaks, then triamcinalone cream then Grifulvin 125mg/tsp. None was effective and we then saw a new dermatologist who referred us to a pediatric dermatologist who she made a diagnosis: Acrodermatitis Continua of Hallopeau. She did a fungal culture which grew out a soil contaminant that was not felt to be significant. Our daughter is presently on clobetasol ointment. The nail looks a bit better but not the skin. Treatment discussions so far have included Thalidomide, Psoralen plus UVA or UVB, Acitretin, Methotrexate and others. We know that these medications can have serious side-effects and that this disease can be resistant to treatment. Our daughter has a lot of finger pain and can't pick up thing with her fingers. She is only a child and we'd appreciate your thoughts.

Clinical Photos:

Questions:
1) Are there alternative diagnoses?
2) What therapies have you had success within similar cases?
3) Any further work-up?

Case for Diagnosis

2010-03-10T21:24:00.002Z

Abstract: 11 y.o. girl with 6 month history of facial eruption
HPI: This almost 12 yo girl has had a recurring facial eruption for ~ 6 months. In her mother's words: "At first it looked like hives. It was itchy and stung. Each day the rash changed in appearance and lasted almost 3-4 weeks. It traveled behind her ears and neck, then on to her hands and arms and finally to her chest and back. The pediatrician put her on oral steroids which did not seem to help at all. We went to 2 dermatologists, 3 pediatricians, and an allergist/immunologist. Their opinions varied from poison ivy, to a virus, to having absolutely no idea. The only thing that seemed to work was hydroxyzine.
The second occurrence happened in February 2010. I gave the hydroxyzine immediately and the symptoms began to disappear within 24 hours.
The next occurrence happened on March 7, 2010. She has had 3 doses of the hydroxyzine and the rash seems to be almost gone.
The patient is on no other medication and has no known allergies. We have racked our brains about everything she eats and all the products we use at home but cannot come up with any rhyme or reason.
Our pediatrician wonders if it is related to the sun......She was outside for recess yesterday and it was the first nice sunny day we have had."

Clinical Photo

Lab: Consider obtaining parvovirus B19-specific antibodies if this has not been done. CBC was done a few months back. This and an ANA panel will be obtained.

Questions: What are your thoughts as to possible diagnoses? The erythema of the cheeks suggests Erythema infectiosum, but this is almost never recurrent.

Diagnosis: This child's case was presented for ideas. She was not seen and her parents have had problems getting an appointment with a pediatric dermatologist. Based on the history and photograph I would consider an atypical erythema infectiosum, urticaria, a collagen vascular disease.

References:
Musiani M, et. al. Recurrent erythema in patients with long-term parvovirus B19 infection. Clin Infect Dis. 2005 Jun 15;40(12):e117-9. Epub 2005 May 11.
Department of Clinical and Experimental Medicine, University of Bologna, Bologna, Italy. monica.musiani@unibo.it
We describe 3 patients with long-term parvovirus B19 infection (defined as detectable parvovirus B19 DNA load for >6 months after the onset of symptoms), which we monitored by serial testing for parvovirus B19 load and the presence of parvovirus B19-specific antibodies in blood. The patients showed recurrent erythema at intervals of several months.

Note: Informed consent to present this patient's history and photograph was obtained from her parents.

An Orphan Patient

2010-03-03T21:25:00.015Z

Abstract: 44 yo man with a 10 year history of a progressive and disabling dermatitis if the feet.
HPI: This 44 yo professional was first seen 10 years ago with a dermatitis of both feet and nails. KOH prep from toe nails was positive for hyphae and he was treated with 3 months of Lamisil p.o. Nails and feet improved at that time. He was next seen in 2004 with dermatitis of both feet located on plantar areas which was predominantly hyperkeratotic with areas of excoriation. He had developed a cellulitis of the right leg which required hospitalization. KOH from affected aeas was negative in 2004. Treated with betamethasone diproprionate 0.05% ointment and wet compresses and was "80%" improved in two weeks. At that time a diagnosis of "keratoderma" and possible "dyshidrosis" was considered. The process recurred and he asked his PCP to place him on prednisone which was done and seemed to help for a while. From 2004 - 2010 he saw a number of other dermatologists and podiatrists both locally and at a large university center where a number of other therapies were tried, including Castelanni's paint. None worked for very long and he was seen back at my office in March 2010. The patient is at the end of his wits with this. It dominates his life and is the cause of pain which interferes with his ability to stand at work.

O/E: March 1, 2010: Symmetrical hyperkeratosis of the plantar aspects of both feet with areas of excoriation. Nails look normal. Palms normal. KOH prep from plantar dermatosis is negative for hyphae and a fungal culture was plated.

Photos March 2010:

Diagnosis: Is this keratoderma, tylosis or an unusual contact dermatitis? Could this have begun with tinea pedis nine years ago or was than an incidental finding?

Plan: Patch testing needs to be considered to r/o occult contact. I doubt biopsy will help. Will start therapy with Salex Cream (6% salycilic acid) as we await fungal culture.

Questions: Does anyone have strong feelings about a diagnosis here? If so, what therapy should be tried?

Reference:
1. Shelley WB, Shelley ED. The orphan patient. N Engl J Med. 1988 Mar 10;318(10):646. In this important letter to the NEJM, the Shelleys define the orphan as an individual “with a unique, inchoate, baffling and often disabling disease and yet clearly not discernable in the medical literature.” While the patient described here is not strictly an "orphan patient" his 10 year unsuccessful quest for control or cure, puts him in that unfortunate category. Your help will be appreciated.

2. Brian Maurer sent us an important review of "Shoe Dermatitis" by Robert Adams which appeared in California Medicine in 1972. It is still valuable.

Digital Cameras for Clinical Photography

2010-02-06T11:59:00.008Z

All one needs for teledermatology is the ability to take good quality digital photos. A fine and timely review of inexpensive digital cameras appeared in the NY Times on February 4, 2010. If you are in the market for a new camera for your office, David Pogue's 2010 Review of Digital Cameras will be helpful. The Canon Power Shot, Fuji FinePix or Nikon Coolpix described in the article seem appropriate, but I'd suspect any of the cameras reviewed will serve the average physician's needs. Be sure to see the multimedia and video attachments to this article.

Henry or I will be happy to answer specific questions.

Traction Alopecia

2010-01-30T10:25:00.012Z

Abstract: 15 yo girl with one year history of alopecia
HPI: This 15 yo African-American girl has noted progressive alopecia for the past year or so. Earlier in her life her hair was in corn-rows for one to two years. She has used "relaxers" for many years but stopped ~ a year ago. Her hair was pulled back for many years. Her mother has been applying "fish oil" to the area which they think may be helping.
O/E: There is marked thinning of the hair at the temporal and occipital areas. Much less involvement on frontal and parietal areas. No inflammation, scaling or scarring is appreciated.
Photos:

Diagnosis: This is most likely " Marginal Traction Alopecia"
Questions: What would you offer this young woman as for treatment. I told her to leave her hair natural, avoid relaxers or any tension on hair.
References:
1. eMedicine.com has a good chapter on Traction Alopecia: Here is an excerpt: "Traction alopecia is a common cause of hair loss due to pulling forces exerted on the scalp hair. This excessive tension leads to breakage in the outermost hairs. This condition is seen in children and adults, but it most commonly affects African American women. The 2 types of traction alopecia are marginal and nonmarginal. Unlike trichotillomania, a psychiatric disorder of compulsive hair pulling that leads to patchy hair loss, traction alopecia is unintentionally induced by various hairstyling practices (eg, use of braids, hair rollers, weaves, twists, locks, or "cornrows"). In the initial stages, this hair loss is reversible. With prolonged traction, alopecia can be permanent. Physicians, especially dermatologists, must recognize this condition early to prevent irreversible hair loss."

2. I would recommend renting Chris Rock's documentary "Good Hair" when it is available.

Cheilitis in a Young Woman

2010-01-27T15:07:00.016Z

Abstract: 1.5 year history of cheilitis in a 26 yo woman
HPI: This is a a 23 yo esthetician who first developed cheilitis on her honeymoon in Mexico. She was using many lip balms at the time. These were discontinued and she found toothpaste without cinnamates. The process continued to flare. While initially on upper and lower lips, it is now just on the lower lip. She has read a lot on the subject and has many concerns. The patient has had a problem with anxiety since her father's death when she was 14 and sees a therapist. Cool compresses and fluocinalone 0.025% ointment control the problem fairly well; but it flares when she stops this. At one point, a KOH prep was positive for Candida (but that was when she'd been using a optical corticosteroid and this resolved quickly with ketoconazole cream).
O/E: Recently, the process is located on the lower lip. Here there is erythema, some induaation and scaling.
Clinical Photos: 1/10/1010

This photo was taken on Feb. 8, 2010 after a month off usual lip products and use of Vaseline and/or fluocinalone ointment.

Pathology: A 3 mm punch biopsy was taken from the lower lip.
This shows "confluent scale crust containing neutrophils, acanthosis with spongiosis and a dense lichenoid infiltrate. No granulomatous changes. The pathologist felt that these changes were non-diagnostic but "consistent with cheilitis glandularis."
Diagnosis: Cheilitis. In the ddx is contact, cheilitis glandularis and factitial cheilitis.
Discussion: I am not comfortable with a disgnosis of cheilitis glandularis here. Contact and factitial etiologies could still play a role. Patch testing will be done, but if negative and the problem persists consideration to having more in-depth patch testing may be given. We are also working with patient to stop licking and chewing lips.
Questions: What are your thoughts re: 00etiology here?
Addendum: A few months after this case was presented, the patient recalled that she had received a new dental retainer shortly befor the cheilitis began. Her old retainer was plastic and the new one was metal. She stopped using this new retainer and her cheilitis disappeared. Thus, a metal sensitivity (most likely nickel) was the culprit.
References:
1. Nico MM, Nakano de Melo J, Lourenço SV. Cheilitis glandularis: A clinicopathological study in 22 patients. J Am Acad Dermatol.. [Epub ahead of print]
Department of Dermatology, Medical School, São Paulo, Brazil.
BACKGROUND: Cheilitis glandularis (CG) is a condition in which thick saliva is secreted by minor labial salivary glands and adheres to a swollen lip causing discomfort to the patient. Most publications refer to single case reports or small case series. OBJECTIVE: We sought to report and to analyze clinical, pathological, and therapeutic data on 22 patients with CG seen at the department of dermatology at our university. METHOD: Retrospective data about 22 patients with CG are reviewed and presented. RESULTS: Seventeen patients were male and 5 were female. All were fair skinned, including 6 albino individuals. Several of them presented significant signs of photodamage on the lips. Surgical treatment was performed in 10 severely affected patients and consisted of a vermilionectomy followed by minor salivary gland removal. Histopathological study revealed various degrees of chronic sialadenitis and vermilion epithelial changes. Superficially invasive and in situ squamous cell carcinoma of the vermilion was detected in 3 cases. LIMITATIONS: Biopsy and surgery were not performed in all patients. CONCLUSIONS: CG is strongly related to sun sensitivity and may be more severe in albino patients. The swollen, sun-exposed lip may become more susceptible to the occurrence of squamous cell carcinoma.

2. Aydin E, Gokoglu O, Ozcurumez G, Aydin H. Factitious cheilitis: a case report. J Med Case Reports. 2008 Jan 29;2:29.
Baskent University Department of Otolaryngology, Ankara, Turkey. erdinca@baskent-ank.edu.tr
INTRODUCTION: Factitious cheilitis is a chronic condition characterized by crusting and ulceration that is probably secondary to chewing and sucking of the lips. Atopy, actinic damage, exfoliative cheilitis, cheilitis granulomatosa or glandularis, contact dermatitis, photosensitivity reactions and neoplasia should be considered in the differential diagnosis of crusted and ulcerated lesions of the lip. CASE PRESENTATION: We present a 56 year-old female with an ulcerated and crusted lesion on her lower lip. The biopsy showed granulation tissue and associated inflammation but no malignancy. Based on the tissue examination and through clinical evaluation the diagnosis of factitious cheilitis was rendered. CONCLUSION: Thorough clinical history, utilization of basic laboratory tests and histopathologic evaluation are required to exclude other diseases and a thoruough psychiatric evaluation and treatment is vital for successful management of these patients.

3. Torgerson RR, Davis MD, Bruce AJ, Farmer SA, Rogers RS 3rd. Contact allergy in oral disease. J Am Acad Dermatol. 2007 Aug;57(2):315-21. Epub 2007 May 25.
Department of Dermatology, Mayo Clinic, Rochester, MN 55905, USA.
BACKGROUND: The role of contact allergy in oral cavity disease processes is unknown. OBJECTIVE: We sought to determine the prevalence of contact allergy to flavorings, preservatives, dental acrylates, medications, and metals in patients with oral disease. METHODS: Patients were tested with an 85-item oral antigen screening series. Data were analyzed retrospectively. RESULTS: We evaluated 331 patients with burning mouth syndrome, lichenoid tissue reaction, cheilitis, stomatitis, gingivitis, orofacial granulomatosis, perioral dermatitis, and recurrent aphthous stomatitis. Positive patch test results were identified in 148 of the 331 patients; 90 patients had two or more positive reactions. Allergens with the highest positive reaction rates were potassium dicyanoaurate, nickel sulfate, and gold sodium thiosulfate. Of the 341 positive patch test reactions, 221 were clinically relevant. LIMITATIONS: No follow-up data were available in this retrospective analysis. CONCLUSION: The positive and relevant allergic reactions to metals, fragrances, and preservatives indicated that contact allergy may affect oral disease.
.

Pityrosporon Folliculitis

2010-01-05T18:22:00.017Z

Abstract: 32 yo woman with 4 day history of folliculitis chest and back
HPI: This 32 year-0ld woman has had a folliculitis for 3 - 4 days. She has a history of ulcerative colitis and had been on prednisone for a few weeks and the dosage was recently increased. She is also on Apriso and Cipro.
O/E: This is a healthy-appearing woman with scores of erythematous papules admixed with a few pustules on upper chest and back. No other findings.
Clinical Photos:

Diagnosis: Steroid acne vs. Pityrosporon folliculitis.

Biopsy: There are dilated follicles with basophilic debris and numerous PAS positive spores (no hyphae). This is P. folliculitis.

Discussion: She was treated with ketoconazole 200 mg daily for a month. Will put a f/u after she is seen back. Although it seems obvious that the prednisone played a role, there is scant support for this in the literature. We will have to see how the patient does with treatment and whether she suffers recurrences.

Reference:
Lévy A, Feuilhade de Chauvin M, Dubertret L, Morel P, Flageul B. [Malassezia folliculitis: characteristics and therapeutic response in 26 patients] Ann Dermatol Venereol. 2007 Nov;134(11):823-8.

[Article in French]

Service de Dermatologie I, Hôpital Saint-Louis, Paris.

BACKGROUND: Malassezia folliculitis is most often described in patients living in hot and humid countries or in immunocompromised patients. Its frequency in France is unknown. We report 26 cases diagnosed at Saint-Louis Hospital between May 2002 and April 2004. The clinical features, the contributing factors, the results of direct mycological examination and/or histology and the efficacy of antifungal treatments were compared to the literature. PATIENTS AND METHODS: The inclusion criteria were the presence of folliculitis on the trunk confirmed by direct microscopy and/or histopathology showing abundant yeast cells in the follicles. RESULTS: Patients comprised 22 men and 4 women (M/F sex ratio: 5: 5) with a mean age of 46 years. Five patients (19%) were immunocompromised. In normal patients, the duration of folliculitis was long with a mean of 61 months. The eruption was typical, with follicular papules and superficial pustules distributed predominantly on the trunk. Itching was frequent (70%). Direct microscopy was more often positive than histology (89% vs 33%). Some sixty-five percent of the patients had been previously treated by topical or systemic antibiotics or anti-acne drugs, which was ineffective in all cases. Cure with topical ketoconazole, oral ketoconazole alone or in combination with topical ketoconazole occurred respectively in 12%, 75% and 75% of patients, but with consistent recurrence within 3 to 4 months after cessation of treatment. DISCUSSION: Malassezia folliculitis is probably misdiagnosed, as suggested by the long time between onset and diagnosis and the high frequency of non-antifungal treatments prescribed. In our study, direct mycological examination provided more effective diagnosis than histology. Treatment is difficult especially because of the high frequency of relapses. CONCLUSION: A diagnosis of Malassezia folliculitis should be considered in young adults or immunocompromised patients with an itching follicular eruption. Further therapeutic trials are needed due to the frequency of relapse.

Follicular Mucinosis?

2009-12-20T18:34:00.011Z

Abstract: 27 yo woman with 6 month history of plaques face
HPI: This 27 year-old baker has asymptomatic plaques on the right cheek for six months. She has not been treated as yet.
O/E: Two ill-defined plaques on right cheek. There is a suggestion that follicular openings are dilated.
Clinical Photos:
One can compare the right and left cheeks. Dermoscopic image as well.
Normal left cheek on left, affected right cheek on right.

The image to the right is taken through a dermoscope.
I believe it shows dilated follicular openings.
I am not sure this has been reported.

Diagnosis: Possible Follicular mucinosis

Questions: Do you think this young woman should have a biopsy? Should she be observed? Treated?

Reference:
Gorpelioglu C, Sarifakioglu E, Bayrak R. A case of follicular mucinosis treated successfully with pimecrolimus. Clin Exp Dermatol. 2009 Jan;34(1):86-7.
This paper describes a 24 yo man with biopsy proven follicular mucinosis who was successfully treated with pimecrolimus.

Acneiform Eruption in an 11 year-old boy

2009-12-11T18:06:00.020Z

Abstract: 11 y.o. boy with localized papular dermatitis of face

HPI: This 11 yo boy has a 2 month history of a facial eruption. Initially, his mother applied Bacitracin ointment. It was not effective and they then used a prescription "hydrocortisone" ointment for a few weeks which was similarly unhelpful. Good general health. He takes Adderal for ADHD.

O/E: There are erythematous acneiform papules around the right alar groove. Face is otherwise clear.

Clinical Photos

Labs: N/A

Clinical Diagnosis: My first thought is that this may be a variant of perioral dermatitis. Prior to puberty, P.O.D. is seen in both sexes. We see women with "perialar dermatitis" which is usually bilateral but can look like this. In the differential diagnosis one would consider Demodicois and atypical acne. Perhaps, I should have done a scraping for demodex mites.
Alternatively, this could be the onset of acne vulgaris, localized at this early stage. Perhaps, I jumped at a zebra when this is just common acne.

Therapy: The patient was given a prescription for doxycycline 100 mg b.i.d. and ketoconazole cream which I have found to be effective for perialar dermatiis. He will be reevaluated in a month.

Questions: Do you think this is periorificial dermatitis, demodicosis, or atypical acne? Your comments will be appreciated.

References:
1. Nguyen V, Eichenfield LF. Periorificial dermatitis in children and adolescents. Volume 55, Issue 5, Pages 781-785 (November 2006)
There has been very little evaluation of the history, morphology, or disease course of perioral/periorificial dermatitis in children.
Objective: We sought to elucidate the clinical manifestations and treatment outcomes in this condition.Methods A retrospective chart review with telephone follow-up was used to study 79 children and adolescents. Results: Patients ranged from 6 months to 18 years of age. The average duration of the rash at presentation was 8 months. Seventy-two percent had a history of topical, inhaled, or systemic steroid exposure. Seventy percent of patients had perioral involvement, 43% perinasal, and 25% periocular involvement. A perivulvar rash was reported in 1% of patients. Treatment with topical metronidazole was associated with clearing on follow-up examination.
Limitations: This is a retrospective study without case controls and is subject to interviewer and memory bias. Conclusion: Perioral dermatitis appears at all ages in childhood and adolescence and may be associated with topical corticosteroid use. It may be responsive to topical metronidazole in children and adolescents and is more appropriately termed periorificial dermatitis.

2. Hsu CK, Hsu MM, Lee JY. Demodicosis: a clinicopathological study. J Am Acad Dermatol. 2009 Mar;60(3):453-62.
Department of Dermatology, College of Medicine, University Hospital, Tainan, Taiwan.
BACKGROUND: Demodex mites are common commensal organisms of the pilosebaceous unit in human beings and have been implicated in pityriasis folliculorum, rosacea-like demodicosis, and demodicosis gravis. OBJECTIVE: We sought to describe the spectrum of clinicopathological findings and therapeutic responses of demodicosis in Taiwanese patients. METHODS: We conducted a retrospective study to review clinicopathologic findings and therapeutic responses of 34 cases of diagnosed demodicosis. RESULTS: Fifteen cases with positive results of potassium hydroxide examination, standardized skin surface biopsy specimen, and/or skin biopsy specimen, and resolution of skin lesions after anti-Demodex treatment were included for final analysis. Nineteen cases were excluded because of insufficient positive data to make a definite diagnosis. There were 4 male and 11 female patients (age 1-64 years, mean age 38.7 years). The disease was recurrent or chronic with a duration ranging from 2 months to 5 years (mean 15.7 months). The skin lesions were acne rosacea-like (n = 8), perioral dermatitis-like (n = 5), granulomatous rosacea-like (n = 1), and pityriasis folliculorum (n = 1). Skin biopsy was performed in 7 patients. Overall, the histopathology was characterized by: (1) dense perivascular and perifollicular lymphohistiocytic infiltrates, often with abundant neutrophils and occasionally with multinucleated histiocytes; (2) excessive Demodex mites in follicular infundibula; and (3) infundibular pustules containing mites or mites in perifollicular inflammatory infiltrate. The skin lesions resolved after treatment including systemic metronidazole, topical metronidazole, crotamiton, or gamma benzene hexachloride. LIMITATIONS: Small sample size and a fraction of patients without long-term follow-up are limitations. CONCLUSION: Demodicosis should be considered in the differential diagnosis of recurrent or recalcitrant rosacea-like, granulomatous rosacea-like, and perioral dermatitis-like eruptions of the face. Potassium hydroxide examination, standardized skin surface biopsy, skin biopsy, or a combination of these are essential to establish the diagnosis.

Does this ring a bell?

2009-11-10T00:16:00.012Z

HPI: The patient is a 36 yo woman on home hemodialysis after a failed renal transplant for membraneous glomerulonephtritis who was referred by her rheumatologist for a "stat" skin biopsy. She sees the rheumatologist for amyloid nephropathy.

Shs is having the second episode of a painful erythematous eruption on the dorsum of the left foot. The first episode, two months ago, resolved after two weeks of Keflex and Bactrim.

Meds: Oxycontin, prednisone 20 mg daily, Keflex (x 4 days)

O/E: This is an upbeat but chronically ill woman. The pertinent findings are on the legs. There is dusky erythema on the dorsum of the left foot. In addition, there are petechaie on both lower extremities. She has a 2/6 pansystolic murmur which the rheumatologist feels is cardiac but her nephrologist feels radiates from her dialysis shunt (left arm).

Clinical Photos:

Labs: CBC: WBC 8900 normal differential. Creatinine 11.32 (normal < 1.2 mg%")
Biopsy: Performed today

Impression: Second episode of an erythematous process left foot. Although this was treated initially as "cellulitis" no real evidence of infection. This does not look infectious to me. I wonder about an embolic phenomenon. I know I have not seen this before.

Questions:
What is your presumptive diagnosis?
What more would you do at this time?
(On thinking about this patient, and the recurrence, the question of Fixed Drug Eruption arose. I will question her about intermittent prescription and OTC drug use.)

I will give F/U re: bx findings.

Post-Bypass Dermatitis

2009-10-10T01:16:00.014Z

Presented by Professor Khalifa Sharquie
Baghdad, Iraq

HPI: A 58 year old patient developed sudden heart infarction that needed urgent bypass heart surgery in March of 2009. Left saphenous vein was used as graft. The patient was otherwise healthy apart from developed a rash on the left leg along the incision scar. The rash is nonpruritic and red in color ranging in size from pinpoint to 2 cm in diameter. This gradually enlarges in size and stop, then slowly resolves without therapy leaving residual pigmentation or scar within few weeks. The rash appear only on one side of the incision but never cross. The patient's medications include simvastatin and lisinopril therapy.

On examination: 2 red patches appeared 15 days ago. They were scaly and psoriasiform from about 1 cm to 2 cm in diameter. Within 2 days they started to resolve, losing their scales and becoming dusky red in color. In addition,there are numerous small varicosities along the legs and feet.

Biopsy could not be done for fear of developing a leg ulcer.
Lab: All investigations are normal including blood picture,ESR and biochemistry.

Clinical Photos:

Discussion: I have not seen any case similar to this patient. So I wonder if this is what has been rarely reported in the literature. (see reference) I am waiting my colleagues comments.

Reference:

Arch Dermatol. 1993 May;129(5):609-12.
Saphenous vein graft donor site dermatitis. Case reports and literature review. Hruza LL, Hruza GJ.Division of Dermatology, Washington University School of Medicine, St Louis, Mo.BACKGROUND--Coronary artery bypass grafting for atherosclerotic heart disease is commonly performed throughout the world. Complications of coronary artery bypass grafting include saphenous neuralgia due to injury to the saphenous nerve duringharvest of the saphenous vein. Dermatologic complications of coronaryrevascularization are infrequently reported and include an eruption overlying the vein donor-site scar. OBSERVATIONS--We describe two cases of saphenous vein donorsite dermatitis associated with sensory peripheral neuropathy in the distributionof the dermatitis. Histopathologic studies revealed a subacute spongiotic dermatitis. The course of the eruption was characterized by exacerbations and remissions with gradual resolution of both the dermatitis and neuropathy over a1- to 2-year period. CONCLUSIONS--Our cases are unique because the dermatitis developed in the area of the neurologic changes. We propose that the dermatitis may be a trophic change secondary to saphenous neuralgia.

Atypical plaque on the hand

2009-09-30T14:55:00.008Z

Submitted by Dr Henry Foong, Ipoh, Malaysia

An 80-year-old retired goldsmith presented with 4-month history of an ulcerated plaque on the left hand. It had gradually increased in size. His past medical history included hypertension, diabetes mellitus, and ischemic heart disease. His medications included norvasc, zocor, ticlid and amaryl.

Examination of the skin showed a localized ulcerated verrucous plaque 6 x 6 cm on the dorsum of the left hand. Closer examination showed slough and blackish dots on the surface of the plaque. Regional nodes were not enlarged.

Our presumptive diagnosis is either atypical mycobacterium infection or chromoblastomycosis.

The epithelium shows pseudoepitheliomatous hyperplasia. The upper dermis is densely infiltrated by acute and chronic inflammatory cells. Neutrophils are also noted in the lining epithelium. No granulomas or Langhan's giant cells are seen. No microorganisms are noted. Negative for dysplasia and malignancy. Ziehl-Neelsen stain for acid fast bacilli is negative. Periodic acid Schiff stain for fungi is negative. Culture for AFB and fungal organism were negative

He was initially treated with itraconazole 100mg bd and after 2 weeks there was no improvement at all. Bactrim 2 tab daily was added and this time it showed improvement after 2 weeks of the combination.

One of the differential that was considered is pustular vasculitis or neutrophilic dermatosis of the dorsum of the hands. Points supporting this diagnosis include pseudoepitheliomatous hyperplasia and the absences of granuloma on histology examination.

I suspect this could be atypical mycobacterium infection based on the empirical therapeutic response to bactrim. I wonder what your views are with regard to this case?

Annals of Puzzling Purpuras

2009-09-03T10:09:00.016Z

Percussion Purpura -- Taiko Purpura
Submitted by Trudi Shim, San Antonio, Texas

History: The patient is a 63 year-old Japanese-Hawaiian woman who plays Taiko drums as a hobby. She has a past history of porphyria cutanea tarda (PCT) from estrogens which is now quiescent. A few years back, she developed tendonitis of her wrists and received cortisone injections near each wrist from two different physicians. When she developed a hypopigmented patch of skin on her right forearm she attributed it to the cortisone injection. The patch was characterized by an large, flat, smooth area of hypopigmentation, and occasionally some round, bright red spots appeared in the hypopigmented area. They would disappear after a week or two. She consulted a dermatologist a year ago because she worried that this might be contagious. He diagnosed tinea, but did no KOH prep and she has been faithfully applying clotrimazole ever since, but without relief. The dermatologist also raised the spectre of Hansen's Disease which worried the patient, a retired public health nurse, greatly. She does not have any known skin problems elsewhere on her body at this time.

On Examination: The patch is now predominately reddish in color, with sharp irregular borders. The skin is fragile in the sense that if she hits her arm against something, it will break and take a while to heal. - similar to what used to happen way back when she had PCT. This only occurs in the localized area of hypopigmentation.

Clinical Photos:
Patient and Taiko

Discussion: This case presentation contains some interesting points. The patient is a late middle-aged Japanese-Hawaiian woman who has lived in the sub-tropics for her entire life. Thus, she has a fair amount of solar elastosis. The intra-articular corticosteroid most likely caused more localized atrophy and the trauma the arm experienced doing heavy drumming was all she needed to cause purpura. The diagnosis of tinea without a KOH prep showed a certain cavalier approach on the part of her practitioner; and the suggestion of the possibility of Hansen's Disease should not have been made unless a biopsy followed. Leprosy in economically comfortable people born in Hawaii is very unusual. Most cases seen in the Hawaiian Islands today are in immigrants from the Philippines, Oceania and Southeast Asia. Purpura is not a usual finding, but rather a hypopigmented anesthetic plaque (tuberculoid leprosy). Lepromatous leprosy would often appear more dramatically. The patient's PCT is likely not related, but she should have regular liver function studies and ferritin levels looked at. In the absence of other findings urinary porphyrins may not be necessary. "Percussion Purpura" while likely not super rare, has not been reported before.

Comments: Your thoughts and questions will be most welcome.

Parastomal Ulceration

2009-08-25T10:07:00.012Z

Presented by Amanda Oakley, Hamilton, NZ

The patient is a 44 year old man with parastomal ulceration over the last 12 months.
He had a stable stoma for 12 years, following colostomy to remove rectal tumour (carcinoid) and is healthy otherwise with no bowel problems and no skin disease elsewhere.

Last year he received IV antibiotics for peristomal cellulitis, with complete recovery. A month or so later the peristomal skin began ulcerating. Partial healing is followed by skin lifting off at bag changes alternate days, leaving painful ulceration. Meticulous hygiene resulted in no improvement with different devices or topical steroid for one month, applied as beclomethasone nasal spray. Now trying clobetasol solution on appliance, allowed to dry before fitting to skin. He is on no medications.

Swab: group G streptococcus on two swabs - no deep fungi or mycobacteria.
Blood screen: all normal - no sign carcinoid or other disease

Clinical Photos (July '09 (top) and February '09 bottom):

Histology: paucicellular; subepidermal clefting. Not diagnostic.

Dr. Oakley's Comments: Most stomal rashes are dealt with by stoma nurses and a dermatologist's opinion is rarely sought; so we don't see many of them. I see irritant dermatitis from time to time and it responds to topical steroids. He has no risk factors for pyoderma gangrenosum, and the histology is not typical of that.

Questions: Could group G streptococcus do this? There is no cellulitis or abscess formation and I have prescribed antibiotics without improvement.
Any suggestions re: diagnosis and treatment will be gratefully received! I am hoping some dermatologists have greater exposure to stomal disease and I can benefit from their experience.

Reference:
Yeo H, Abir F, Longo WE. Management of parastomal ulcers.
World J Gastroenterol. 2006 28;12(20):3133-7.
Management of surgically placed ostomies is an important aspect of any general surgical or colon and rectal surgery practice. Complications with surgically placed ostomies are common and their causes are multifactorial. Parastomal ulceration, although rare, is a particularly difficult management problem. We conducted a literature search using MD Consult, Science Direct, OVID, Medline, and Cochrane Databases to review the causes and management options of parastomal ulceration. Both the etiology and treatments are varied. Different physicians and ostomy specialists have used a large array of methods to manage parastomal ulcers; these including local wound care; steroid creams; systemic steroids; and, when conservative measures fail, surgery. Most patients with parastomal ulcers who do not have associated IBD or peristomal pyoderma gangrenosum (PPG) often respond quickly to local wound care and conservative management. Patients with PPG, IBD, or other systemic causes of their ulceration need both systemic and local care and are more likely to need long term treatment and possibly surgical revision of the ostomy. The treatment is complicated, but improved with the help of ostomy specialists. Note: This reference is available as free full text from the publisher.

Localized Bullae

2009-08-15T20:26:00.016Z

This healthy 83 year-old man has had a one year history of bullae and vesicles on the medial aspect of the left knee. They come and go. He is on no new medications and does not take any drugss on an as necessary or intermittent basis. His medications consist of valsartan (Diovan), simvastatin and omeprazole (Prilosec).

O/E: A collection of vesicles and bullae left knee.

Clinical Photo:

Lab and Path:
Bacterial Culture 8/14/o9 Negative
Biopsies were done by two other dermatologists (will try to get results). Apparently, no firm diagnosis was made.

Path Report: 9/30/08 Perivascular and interstitial dermatitis with mixed cell infiltrate including eosiniphils. Dermal hypersensitivity reaction. "These findings may be seen in the prebullous lesions of pemphigoid." DIF was negative.

Diagnosis:
Consider localized bullous pemphigoid.

Discussion: This is an 82 yo man with a one year history of a localized bullous disorder. The initial pathology showed an inflammatory process with eosinophils. The bullous process has stayed localized to the left knee. It seems likely that this is localized bullous pemphigoid. There is a "pretibial variant" and this may be related. Apparently, many of these patients have negative direct immunofluorescence (See ref. below)
Plan to treat initially with clobetasol ointment and if does well follow with tactolimus ointment 0.1%.

Questions: What do you think? What else is in your differential diagnosis? Therapeutic options?

Reference:

Kurzhals G, et. al. [Localized cicatricial bullous
pemphigoid of the Brunsting-Perry type] Hautartz.
1993 Feb;44(2):110-3 [Article in German]
Localized cicatricial pemphigoid of the Brunsting-
Perry type is a very rare bullous condition, which
has so far been reported in 51 cases. It is
characterized by scarring blisters confined to the
head, scalp and neck.  Diagnosis can be difficult
because of the discrete skin lesions, often repeatedly
false-negative direct immunofluorescence, and the
absence of circulating antibodies. We report on a
87-year-old male patient with the typical clinical
feature of a cicatricial pemphigoid of the Brunsting-
Perry type and give a reviewof the 51 cases published
in the world literature.

Follow-up Photo (08/21/09):  The patient was seen after a week for a second visit.  No
treatment had been rendered and the bullae had resolved.  One wonders
what triggers the bullae?  He's a tennis player, so could it be minor
trauma, UVL?

Tan Papules in a Child

2009-08-05T18:57:00.010Z

Abstract: Eight year old boy with six month hx of tan macules

HPI: This otherwise healthy boy has had a six-month history of asymptomatic tan macules on his torso. Takes no meds by mouth and is asymptomatic.

O/E: Six - eight smooth surfaced tan macules measuring from 5 mm to 15 mm in diameter on torso. After lesions are rubbed they urticate mildly and are faint pink. Dermographia is negative.

Photos:

Pathology:

Diagnosis:

Photodermatitis in a Teenage Girl

2009-07-17T01:56:00.006Z

Abstract: 8 yr history of photodermatitis in a 17 yo girl

HPI: This 17 yo student has an 8 year history of a summer eruption. She has a pruritic eruption of her hands and distal forearms starting in spring and lasting till late fall. In winter her skin is perfectly normal. She has used triamcinalone 0.1% ointment without relief and similarly has not been helped with sunscreens.

O/E: Mild lichenification and a fine micro-papular eruption on the dorsum of the hands. A few serum crusts. No vesicles or h/o vesicles.

Photos (7/16/09)

Note no facial lesions

Diagnosis: Atypical Photodermatitis in a teenaged girl. Consider PCT, Hydroa variant, photoactivated atopoic dermatitis (nothing fits perfectly at this time)

Plan: 24 hour urine for porphyrins. Broad spectrum sunscreen for hands and clobetasol ointment after a 20 minute soak. Not sure biopsy will be helpful, but will do at next visit. PCT would be unusual but the porphyrias need to be ruled out.

Comments and suggestions?

Recurrent Toxic Erythema vx. Cellulitis

2009-07-08T10:06:00.007Z

H.P.I. The patient is a 70 yo woman who has had ~ 10 episodes of a cellulitis-like picture of her legs over the past ten years. She has never had fever or constitutional signs. The process can affect one or both lower extremities. I saw her in 2001 for this and then she was referred by the emergency room yesterday with the same picture. It began with a fall two days ago. She hit her hip -- was in pain and took ibuprofen before this episode. She said she does not recall taking this before other episodes.

O/E: Patchy, fiery erythema of left lower extremity. Very mild erythems of right lower leg (mostly around the ankle).

Clinical Photos:

Labs: Biopsy obtained and CBC ordered

Diagnosis: Is this an atypical cellulitis, or toxic erythema secondary to and NSAID?

Discussion: If the patient remains afebrile and wbc is normal, I'd be inclined to just watch and wait.

Unusual Pigmentation of Legs

2009-07-03T21:28:00.012Z

The patient is a healthy 51 yo woman with a 5 - 6 year history of asymptomatic progressive hyperpigmentation of the legs. She is in good general health and takes no medications by mouth. The process started on the calves and has spread proximally to the knees. She has rosacea in addition. She thinks her father has a similar problem.

O/E: Both legs from just above the ankles to the knees show punctate hyperpigmentation. The skin here has a slightly pebbly feel. Other than erythematous papules on both cheeks, the remainder of the cutaneous exam is normal. (There is no sclerodactyly, telangiectasas or sclerotic changes).

Photos:
Affected skin

Digital Zoom

Normal Skin (adjacent)

Dermoscopic Image

Lab: Biopsies of affected and normal skin were taken.

Diagnosis: Punctate Hyperpigmentation of the Legs. This does not look like the "salt and pepper" picture of scleroderma. Could this be an unusual genodermatosis?

Plan: Present to VGRD. Perhaps get serologies for scleroderma.

References: Nothing helpful found on PubMed.

Amytrophic (?) Dermatomyositis

2009-06-24T17:42:00.008Z

Presented by Henry Foong
Ipoh, Malaysia

HPI: A 82 yr old housewife presented with 6 month history of skin eruptions on her face, neck and hands. They were aggravated with exposure to sun. She was diagnosed with carcinoma of the stomach in 2007 and completed chemotherapy about 3 months ago. While on chemotherapy she noticed weakness in getting up and putting on her shirt. She has improved since then. She has a history of diabetes mellitus, and IHD for more than 10 years.

O/E: Pertinent findings: bilateral and symmetrical erythematous macules and plaques on the dorsum of the PIP, DIO and MCP jpints. They have a violaceous hue and were non tender. Erythematous discoloration was noted
bilaterally and symmetrically around the eyes, nose and forehead.

Photos:

Lab:
TWBC 5,500
CK 41 U/l (<201) style="font-weight: bold;">Clinical Diagnosis: Dermatomyositis in Ca stomach
Could this be amytrophic dermatomyositis?
ANA + 1:320 Speckled and homogeneous

Questions: How would you proceed? Would you do a skin biopsy?
Would you treat her? Oral prednisolone or plaquenil alone?

Reference: (from eMedicine.com) Dr. Jeff Callen

Dermatomyositis sine myositis, also known as amyopathic dermatomyositis, is diagnosed in patients with typical cutaneous disease in whom no evidence of muscle weakness exists and in whom serum muscle enzyme levels are repeatedly normal for a 2-year period in the absence of disease-modifying therapies such as corticosteroids, immunosuppressive agents, or both. When studied, some patients with amyopathic dermatomyositis have abnormal ultrasound, MRI or magnetic resonance spectroscopy, or muscle biopsy findings. These patients have muscle involvement, and their condition may be better classified as hypomyopathic dermatomyositis. Patients with these variations may also reflect an underlying malignancy, and some develop severe pulmonary disease, particularly persons from Asian countries.
Patients exist in whom myositis resolves following therapy but whose skin disease remains as an active, important feature of the disease. These patients are not classified as having amyopathic dermatomyositis, despite the fact that, at this point in time, the skin is the major and often only manifestation of the disease. Sontheimer has suggested the term postmyopathic dermatomyositis for these patients.

Therapy for the cutaneous disease is often difficult. Patients who present primarily with skin disease (amyopathic dermatomyositis) and those in whom the muscle component is controlled but who still have significant skin disease exist. The first-line of therapy is recognizing that the patient is photosensitive and advising the patient to avoid sun exposure and to use sun protective measures, including broad-spectrum sunscreens. Hydroxychloroquine and chloroquine have been beneficial in small open-label case studies. Methotrexate is also useful. Mycophenolate mofetil has been reported to be useful. IvIg not only benefited the muscle but also cleared the skin lesions in the patients in whom it was used. Rituximab has been used for skin disease, but the results are mixed. Efalizumab has been used and may have some benefit. Efalizumab (Raptiva), a drug indicated for psoriasis, is being withdrawn from the US market and will no longer be available after June 8, 2009, because of potential risk for progressive multifocal leukoencephalopathy (PML). PML is a rapidly progressive infection of the central nervous system caused by the JC virus that leads to death or severe disability. Demyelination associated with PML is a result from the JC virus infection. JC virus belongs to the genus Polyomavirus of the Papovaviridae.

Lyme Tick

2009-06-22T23:17:00.007Z

This 60 yo man came in for a skin cancer check. He had a basal cell removed from his forehead two years ago. The exam was negative until I checked his leg and noted a funny looking lesion. On closer examination, I realized it was a tick. It's head was embedded in the patient's leg. I removed the tick and gave the patient 200 mg. of doxycycline. This latter might be unnecessary, but a study published in the NEJM gives support to this fairly benign prophylaxis.

Reference:
Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after
an Ixodes scapularis tick bite.

Nadelman RB, wt. al. Tick Bite Study Group.

Department of Medicine, New York Medical College, Valhalla 10595, USA.

BACKGROUND: It is unclear whether antimicrobial treatment after an Ixodes scapularis tick bite will prevent Lyme disease. METHODS: In an area of New York where Lyme disease is hyperendemic we conducted a randomized, double-blind, placebo-controlled trial of treatment with a single 200-mg dose of doxycycline in 482 subjects who had removed attached I. scapularis ticks from their bodies within the previous 72 hours. At base line, three weeks, and six weeks, subjects were interviewed and examined, and serum antibody tests were performed, along with blood cultures for Borrelia burgdorferi. Entomologists confirmed the species of the ticks and classified them according to sex, stage, and degree of engorgement. RESULTS: Erythema migrans developed at the site of the tick bite in a significantly smaller proportion of the subjects in the doxycycline group than of those in the placebo group (1 of 235 subjects [0.4 percent] vs. 8 of 247 subjects [3.2 percent], P<0.04). p="0.02)" p="0.02)." style="font-weight: bold;">CONCLUSIONS: A single 200-mg dose of doxycycline given within 72 hours after an I. scapularis tick bite can prevent the development of Lyme disease.

Abdominal Sinuses in a 23 yo Man

2009-06-09T17:51:00.008Z

Three month history of draining sinuses lower abdomen.

HPI: This college student developed abdominal pain and bloody diarrhea in August of 2008. A diagnosis of ulcerative colitis was made and a number of theapies were tried (including prednisone and Remicaid). All were ineffective and he had a subtotal colectomy and ileostomy performed in December of 2008. Subsequent to that he continues to have some pain in the rectal stump and is scheduled for a J-pouch procedure in a few weeks. Three months ago, he developed painful draining tracts in the lower abdomen.

O/E: The patient is a healthy-appearing 23 yo man. The cutaneous findings are 5 - 10 mm in diameter sinus tracts with sero-sanguinous drainage. There are four active lesions at this time. The remainder of the cutaneous exam is negative.

Photos: (June 9, 2009)

Lab and Path: Nil

Diagnosis: Could this be an extra-intestinal manifestation of inflammatory bowel disease? This is more common with Crohn's disease than U.C. My working diagnosis is sinus tracts or abdomino-cutaneous fistulae. The patient was referred for the question of pyoderma gangrenosum. If this is P.g., it is a very atypical case.

Questions:
Has anyone seen and treated a similar patient?
He is scheduled to have a resection of the rectal stump with a re-anastamosis of small bowel to the rectum allowing closure of his ileostomy (I am not sure of exact procedure). Perhaps this will help. Your thoughts are appreciated.

Trichoepithelioma

2009-06-03T10:34:00.010Z

A Dermatologic Vignette.

The patient is a 78 yo woman with a few year history of an enlarging lesion on the nasal tip. Excellent health.

Eight mm in diameter pearly papule nasal tip. Clinically and dermoscopically BCC.

Pathology shows this to be a trichoeoithelioma:

Question: Observe, refer to Mohs, radiate?
Would surgery be deforming in this site? vs. Is radiotherapy overkill?

Reference: There are very few references which address this type of lesion, unless we consider this to be like a BCC. But here is one.

Aygun C, Blum JE. Trichoepithelioma 100 years later: a case report supporting the use of radiotherapy. Dermatology. 1993;187(3):209-12.
Trichoepitheliomas are rare skin tumors which can cause significant cosmetic and functional impairment when they occur in the head and neck area. Multiple methods of treatment including plastic surgery, dermabrasion, cryosurgery and laser surgery have been reported in the literature. A 32-year-old male with multiple coalesced lesions in his ear canals was treated with radiation therapy after he failed more conventional methods of treatment. He is free of tumor in the radiated area 17.5 months after treatment with significant functional improvement. Various aspects of this tumor were reviewed. More data are still needed to define the proper place for radiation in the management of this disease.

Remember Dorinda and Walter Shelley's poem:
Who knows
Who's nose
Needs Mohs

Dissecting Cellulitis of the Scalp

2009-05-16T23:26:00.010Z

Abstract: 18 yo man with three year history of cystic lesions scalp, axillae, chin

HPI: This 18 year-old man has had dissecting cellulitis of the scalp for three years. He has been treated with doxycycline 100 mg b.i.d. and excisions of cysts and sinuses by a plastic surgeon. He presented in May of 2009 for another opinion. He has had a few cysts of the axillae and chin. The patient has observed that his scalp is worse after wearing a helmet for football.

O/E: The patient is a healthy, moderately obese African-American teenager. He has painful cysts, nodules and draining sinuses mostly on the occipital portion of the scalp and around the vertex. He has a hypertrophic scar at the site of an excision in the occipital region. He has a few hyperpigmented nodules in the axillae and some small acne cysts on his chin in the bearded area.

Clinical Photos:

Lab: Nil
Path: Nil

Diagnosis: Dissecting Cellulitis of the Scalp in the setting of Follicular Triad Syndrome. An older name for the scalp process is the hard to remember "Perifolliculitis Capitis Abscedens et Suffodiens

Treatment: To date, only doxycycline 100 mg b.i.d. and frequent excisions by a plastic surgeon. I injected some active lesions with triamcinalone acetonide 10 mg/cc and am considering following the rifampicin and isotretinoin protocol reported in the reference below.

Reason Presented: For therapeutic suggestions

References:
1. Georgala S, et al. Dissecting cellulitis of the scalp treated with rifampicin and isotretinoin: case reports. Cutis. 2008 Sep;82(3):195-8.

Dissecting cellulitis of the scalp, or perifolliculitis capitis abscedens et suffodiens, is an uncommon chronic suppurative disease of the scalp manifested by follicular and perifollicular inflammatory nodules that suppurate and undermine, forming intercommunicating sinuses, and leading to scarring alopecia. Treatment generally fails to obtain a permanently successful result; thus, many therapeutic options have been proposed. We report 4 cases of dissecting cellulitis of the scalp successfully treated with oral rifampicin and oral isotretinoin. To our knowledge, this is the first report of oral rifampicin used concomitantly with oral isotretinoin in this disease entity. We also present a brief review of the literature on the topic.

2. Dissecting Cellulitis of the Scalp Emedicine.com chapter

Teledermatology Rules: Vasculitis

2009-05-06T17:00:00.010Z

Abstract: 2o yo man with one week history of palpable purpura.
HPI: This 20 yo college student was started on isotretinoin for severe cystic acne a month before he developed a rash on his legs. He also had an upper respiratory infection two weeks before the eruption began. He is away at school (a two hour drive). His mother called the office and spoke to my secretary. Busy week. When I heard that he had a rash, I relayed the message that it was probably the common dermatitis we see with patients on isotretinoin and if worried to send me a photo. Two days later, this photo was sent:

The patient was then emailed and asked to come in the next day. Labs were ordered done before the visit.

O/E: Palpable purpura both L.E. Right ankle swollen and tender. Patient limping.

Lab: CBC normal, UA normal. Pending Labs: Throat culture, ANA, ASOT. (Hep C, Stool for OB, not ordered)

Path: Biopsy performed. Not back

Diagnosis: Leucocytoclastic vasculitis. Etiology: The URI, isotretinoin, idiopathic

Plan: Rest for a few days. No specific therapy at this time except stopping the isotretinoin. If he improves uneventfully without evidence of GI or renal involvement will offer a re-challenge with isotretinoin.

Discussion: A few cases of LCV have been reported with isotretinoin. This patient has severe cystic acne with scarring and it would be a shame to withhold drug if it were not putative for the LCV. I admit I did not pay proper attention to the first telephone call. This illustrates the power of teledermatology which can be almost standard in a few years as cell phone cameras become better and people know how to use them more adroitly.

Questions: What are your thoughts and suggestions?

Ear Keloids and Imiquimod

2009-03-30T17:07:00.015Z

We presented this patient around a year ago (she is patient # 2). The woman, now 19 years old, presented in March of 2008 for a keloidal scar in the left triangular fossa. On 12/18/08 based on suggestions and a report in MEDLINE, the lesion was shave excised and a week after surgery, imiquimod was applied nightly for six weeks. She is now one month out after stopping imiquimod. At this point, she looks very good. We will have to see if this is a long term solution.

Reference:
1. Berman B, Kaufman J. Pilot study of the effect of postoperative imiquimod 5% cream on the recurrence rate of excised keloids. J Am Acad Dermatol. 2002 Oct;47(4 Suppl):S209-11.
New adjunctive treatments are needed to reduce the high recurrence rates (50%) of excised keloids. Interferon alfa injections have been shown to decrease the size of stable keloids. This study examined the effects of postoperative imiquimod 5% cream on the recurrence of 13 keloids excised surgically from 12 patients.Starting on the night of surgery, imiquimod 5% cream was applied for 8 weeks. Patients were examined at weeks 4, 8, 16, and 24 for local erythema, edema,
erosions, pigment alteration, and/or recurrence of keloids. Of the 11 keloids evaluated at 24 weeks, none (0%) recurred. Incidences of hyperpigmentation were 63.6%. Two cases of mild irritation and superficial erosion cleared withtemporary discontinuation of imiquimod. Both patients completed the 8 weeks of topical therapy and the final 24-week assessment. At 24 weeks, the recurrence rate of excised keloids treated with postoperative imiquimod 5% cream was lower than recurrence rates previously reported in the literature.

Nodules in Search of a Diagnosis

2009-03-29T13:55:00.014Z

Presented by

J. Erin Reid, M.D. Dermatology Resident &
Stephen P. Stone, M.D. Professor of Dermatology
Southern Illinois School of Medicine

Abstract: 70 yo man with a five year history of exophytic nodules on the lower extremities.

HPI: A 70 year old white male presented with a five year history of exophytic nodules on the lower extremities. They were increasing in number. A few had been removed by shave excision, and the areas that were treated did not regrow.
Over the past few years he had numerous nodules measuring up to 4 cm in diameter. A few of them were excoriated and crusted. There was no lymphadenopathy. He also had extensive areas of erythema and scale on his forearms, upper arms, and thighs.
He had been in the Navy over 50 years ago and served in Japan. He also went to Bangkok and Hong Kong 20 years ago. No significant past medical history

O/E: On the pre-tibial area the patient has multiple nodular lesions, as well as some erythematous and hypopigmented scars where previous lesions have been removed by shave excision. The lesions range from 1 cm to 3-4 cm in diameter.

Photos:

Pathology: Many biopsies have been performed. In May, 2006, a biopsy showed “superficial perivascular dermatitis of the mixed type, with eosinophilic spongiosis and pustules consistent with an allergic etiology”.
In February, 2007, biopsies of the right anterior and lateral leg showed “marked epidermal hyperplasia, spongiosis, and mixed intraepidermal and superficial dermal inflammatory cell infiltrate”. There was no evidence of malignancy or infection at that time, but there was evidence of chronic venous stasis change.
In January, 2009, we excised another nodule. This was read as “marked epidermal hyperplasia with acute and chronic inflammation” and was negative for fungal, bacterial and acid fast bacilli stains. There is also no evidence of malignancy or carcinoma. Cultures for fungus, anaerobes and AFP were all negative. Flow cytometry was negative.

Diagnosis: What is your differential diagnosis?
Questions: What further information would you want? What additional studies? How would you treat this man?

References will be added when available.

Diseases Don't Read Textbooks

2009-02-28T12:20:00.013Z

Abstact: 5 yo girl with enlarging plaque on back.

HPI: The patient is a 5 year old girl seen on February 27, 2009 with a 10 day history of an enlarging plaque on the left back. She had a similar, but less dramatic lesion in April 2008 which was treated with cefuroxime for two weeks. Her family lives in a wooded area and her mother had Lyme Disease last year. The patient feels well, may have had some mild arthralgias according to her mother. No neurological symptoms. She is allergic to penicillin, amocicillin and sulfonamides.

O/E: 17 x 12 cm plaque left back. 2 x 2 cm plaque right arm. These lesions are somewhat urticarial in appearance. The center of the larger lesion is paler than the periphery.

Photos:

Lab: Lyme titers pending

Diagnosis: Presumptive Lyme Disease. She was started on cefuroxime by her pediatrician.
Questions:
1) What else would you consider in the differential diagnosis
2) Can one have ECM more than once? This child had something similar 10 months ago.
3) Presuming this is Lyme -- how long shoud she be treated?

Reasons Presented: Lyme Disease is unusual in the winter. Can one have "primary lesions" with a reoccurence? In a young patient where tetracyclines are contraindicated with a proven allergy to penicillins, what is the best third line drug and how long to administer.

Interesting Follow-up: Paronychia in a Child

2009-02-21T13:05:00.019Z

In October 2007, we presented the case of an eight year old girl with chronic paronychial inflammation located on the left index finger (Paronychia in a Child). She had no other dermatoses. The patient is adopted so we have no family history. We assumed this was some kind of localized psoriasis or acrodermatitis continua. Clobetasol ointment was prescribed which she has used since. (Photo above from 10/2007)

The patient was seen in follow-up recently. The paronycial inflammation had subsided but the finger tip was still abnormal, especially on the palmar surface and there is now hypopigmentation and atrophy distal to the area of inflammation. This latter is likely secondary to the clobetasol. Her topical therapy was switched to calcipotriene cream (the ointment is no longer available in the US.)

Photos:

Questions:
1) What do you think the diagnosis is?
2) Side-effects on the fingers from super-potent topical corticosteroids are rarely reported. One suspects that they are not that unusual. When does the treatment get worse than the disease? (I should have been more diligent in follow-up)
3) Who thinks that these preparations can cause bone changes?
Your comments will be appreciated.

References:
1. Deffer TA, Goette DK.. Distal phalangeal atrophy secondary to topical steroid therapy. Arch Dermatol. 1987 May;123(5):571-2.

2. Tosti A, Fanti PA, Morelli R, Bardazzi F. Psoriasiform acral dermatitis. Report of three cases. Acta Derm Venereol. 1992;72(3):206-7.
Department of Dermatology, University of Bologna, Italy.
The authors report 3 patients affected by psoriasiform acral dermatitis, a distinctive clinical entity characterized by a chronic dermatitis of the terminal phalanges, associated with marked shortening of the nail beds of the affected fingers. The skin biopsy showed in all cases the pathological features of a subacute spongiotic dermatitis. X-ray examination of affected fingers showed no bone or soft tissue changes. Differential diagnosis of psoriasiform acral dermatitis included psoriasis, atopic or contact dermatitis and corticosteroid-induced distal phalangeal atrophy.

3. Brill TJ, Elshorst-Schmidt T, Valesky EM, Kaufmann R, Thaçi D. Successful treatment of acrodermatitis continua of Hallopeau with sequential combination of calcipotriol and tacrolimus ointments. Dermatology. 2005;211(4):351-5.
Department of Dermatology, J.W. Goethe University, Frankfurt, Germany.
Acrodermatitis continua of Hallopeau (ACH) is a rare type of pustular psoriasis affecting the digits. We report on a 43-year-old female patient who had been suffering from ACH for more than 20 years. Despite the fact that the disease was localized on one finger during the whole period, several topical and systemic treatments resulted in only temporary or partial improvement of the lesion. Although the monotherapies with calcipotriol and tacrolimus ointments gave no satisfying results in the long-term management of the disease, the combination of both agents led to a continuous improvement of the patient's skin condition. Copyright 2005 S. Karger AG, Basel.

R/O Subungual Melanoma

2009-02-14T21:53:00.017Z

70 yo man referred for suspected subungual melanoma.

HPI: The patient is a retired engineer with a one month history of subungual pigmentation. He suffers from Waldenstrom's macroglobulinemia and peripheral neuropathy. If he had injured his toe, he would not know.

O/E: The left middle toenail shows brown-blackish subungual pigmentation. It was difficult to appreciate if this was melanin or blood both clinically or dermoscopically. Hutshinson's sign is negative.

Dermoscopy before 3 mm punch biopsy

Diagnosis: Probably subungual hematoma. Need to r/o melanoma.

Procedure: Modification of Haneke Technique.

1. Patient soaks foot in warm water for 20 - 30 minutes
2. Carefully drive a 3 mm punch through the nail with care not to cut into the nail bed.
3. Lift off the cut disk of nail and observe the nail bed.

Dermoscopy after 3 mm punch biopsy and H2O2 to defect

In this case, what appeared to be dried blood was present. The area was cleaned with hydrogen peroxide and a normal appearing nail bed was see. There was no pigment noted. Dr. Hanecke's technique utilizes a Hemocult stick to test scraping from underside of nail, however, our strips were outdated and not reliable.

Note: Dr. Eckhart Haneke pioneered this technique but is not acknowledged in the literature. Here are his comments to this case: "Thank you very much for your email and the links, which I saw for the first time. Thank you also for giving me the credit.
You are completely right that we do not even need the hemoccult test strip for the correct diagnosis, but it is very convincing and impresses the patient. And of course, it is one more proof.
Also clinically, as this is no streaky lesion a melanoma is improbable - however, a very fast growing melanoma can appear like this.
When you apply hydrogen peroxide and the pigment disappears this is due to the hemodestructive action of H2O2 on erythrocytes: hemoglobin has a pseudocatalase action splitting H202 into H2O and O. That is why hydrogen peroxide is also a very good disinfective agent and I use it to cleanse my dermatosurgery field from blood."

Pseudocyst of the Auricle

2009-01-21T10:41:00.006Z

The patient is a 20 yo college wrestler with a one week history of a painless swelling in the right ear. The area outlined is fluctuant but not inflamed.

This is an auricular pseudocyst. It is overly optimistic to think that simple drainage will ensure cure. A number of therapies have been proposed.

For an excellent (and reasonably succinct) review of this subject see eMedicine/Pseudocyst.

This patient was referred to a plastic surgeon -- I will put an addendum after I learn of the therapy. The problem is that most dermatologists do not have enough experience treating this entity. Inadequate treatment can result is a permanent deformity of the auricle.

Magic Cure?

2009-01-03T11:19:00.017Z

Abstract: 45 yo man with two year history of painful fingers
Posted by DJ Elpern
HPI: The patient is a 45 yo electrician and professional pianist who developed hyperkeratotic patches on his hands two years ago. Nothing new in exposures. After much questioning, he remembered that his mother-in-law moved in with them around that time. (not kidding). The fissures are very painful, especially when playing keyboard. He can use gloves doing electrical work. Patch testing has not been done but is planned.
O/E: Hyperkeratotic areas around thumb and middle finger tips bilaterally. Fissures are deep but clean. He has had similar areas on thenar and hypothenar eminences in past. Remainder of cutaneous exam is unremarkable.
Photos:

Diagnosis: Hyperkeratotic Hand Eczema, Psoriasis variant? Fristional Contact Dermatitis
Treatment: He has tried potent topical steroids with occlusion and with the Soak and Smear technique. Crazy glue for fissures. Intralesional triamcinalone 10 mg/cc helped the palmar keratoses. He has had one month of methotrexate 10 mg per week. Only the intralesional TAC has helped but he does not want finger tips injected at this time.
Questions:
1. What do you think the diagnosis is? The role of trauma may be key as he works with his hands as an electrician and his fingers are "traumatized" on the keyboard.
2. Do you have any magical therapeutic suggestions?
3. I have heard that X-ray treatment was used in the past. Any rational for Grenz?
4. Further work-up
Reason Presented: This man is at his wit's end with pain. He can't play the piano since every time he hits a key he has exquisite pain. I have had one or two similar patients -- they just got better over a few years seemingly not related to treatment.
Reference:
E. McMullen, D.J. Gawkrodger, Physical friction is under-recognized as an irritant that can cause or contribute to contact dermatitis. Br J Dermatol. 2006:154;154-156
Department of Dermatology, Royal Hallamshire Hospital, Sheffield U.K.
Full Text of Article
Background The role of physical friction as an irritant in the causation of contact dermatitis is under-recognized. Frictional dermatitis is defined as an eczematous process in which physical frictional trauma contributes to the induction of a dermatitis process.
Objectives To examine the clinical background of patients in whom friction was contributing to dermatitis.
Methods Over a 30-month period during which 2700 new patients were seen, frictional irritancy was identified as playing a role in the dermatosis in 31 cases: in 27 of these, case notes were evaluated for a range of parameters.
Results Physical friction was identified as causing or contributing to the dermatitis in 18 men and nine women, mean age at onset 42 years. The hands, usually the fingers of the dominant hand, were affected in all but two cases. Occupational frictional activities were found in 25 cases: commonly handling small metal components, paper, cardboard or fabric, and driving. Potential frictional activities in hobbies were noted in 12 cases. Wet work irritancy contributed in four cases (15%). Patch testing showed relevant contact allergies as cofactors in seven of 25 subjects tested (26%). Psoriasis was a cofactor in four (15%), and atopic dermatitis in 11. The study was selective, being based in a teaching hospital clinic with a special interest in contact dermatitis. Frictional irritancy is often one of several factors contributing to dermatitis.
Conclusions The contribution of friction to contact dermatitis is under-recognized probably because dermatologists do not think about the potential for physical forces to induce eczematous changes in the skin.

Onychomadesis

2008-12-24T22:59:00.019Z

The patient is a 21 yo college student who emailed me around a month ago. He was away at school at the time:
Nov. 15, 2008 Dear Dr. Elpern, I was wondering if you had any idea what this skin rash / irritation is being caused by. On my hands and feet I've got these little red dots scattered all over. They don't itch, but offer a mild pain when applying pressure. Most of them are plush (sic) with the skin, but some of them are raised up slightly. Also my taste buds are inflamed and red... but I think this is an unrelated condition. Any help you could offer would be greatly appreciated.
He wrote back on December 20, 2008: Shortly after writing you the dots seemed to go away, so I didn't bother setting up an appointment; however, although the red dots went away, I did notice that the white half circle, that are supposed to be at the bottom of the nail, seemed to become weird and displaced on both middle fingers. About two weeks went by and nothing really changed. Yesterday things got worse. Both my middle finger nails seem to be falling off at their roots. I'm not sure what's causing this, and I was wondering if you thought I should set up an appointment, or if you think that I should seek help elsewhere.

O/E: The patient was seen on December 23, 2008: At this time, he had a separation of the proximal nail fold of both middle fingers. No other abnormal findings.

Clinical Photos:

Diagnosis: Post viral onychomadesis. The illness he had was most likely Hand, Foot and Mouth Disease or a related enterovirus infection. I have never seen nail dystrophy after this, but onychomadesis has been reported at least three times after similar episodes. One report is of an outbreak in Spain. I wonder if this is not another enterovirus infection.
Question: Has anyone else seen this?
References:
1. Salazar A, et al. Onychomadesis outbreak in Valencia, Spain, June 2008. Euro Surveill. 2008 Jul 3;13(27). pii: 18917. Available Full Text
2. Bernier V, Labrèze C, Bury F, Taïeb A. Nail matrix arrest in the course of hand, foot and mouth disease. Eur J Pediatr. 2001 Nov;160(11):649-51
Onychomadesis describes complete nail shedding from the proximal portion; it is consecutive to a nail matrix arrest and can affect both fingernails and toenails. It is a rare disorder in children. Except for serious generalised diseases or inherited forms, most cases are considered to be idiopathic. Few reports in literature concern common triggering phenomena. We present four patients in whom the same benign viral condition in childhood appeared as a stressful event preceding onychomadesis. In each case, spontaneous complete healing of the nails was achieved within a few weeks. CONCLUSION: Onychomadesis and/or onycholysis is a newly recognised complication in the course of viral infections presenting clinically as hand, foot and mouth disease, and because of mild forms, is probably underestimated.
Clementz GC, Mancini AJ. Nail matrix arrest following hand-foot-mouth disease: a report of five children. Pediatr Dermatol. 2000 Jan-Feb;17(1):7-11.
Hand-foot-mouth disease (HFMD) is a contagious enteroviral infection occurring primarily in children and characterized by a vesicular palmoplantar eruption and erosive stomatitis. Nail matrix arrest has been associated with a variety of drug exposures and systemic illnesses, including infections, and may result in a variety of changes, including transverse ridging (Beau's lines) and nail shedding (onychomadesis). The association of HFMD with Beau's lines and onychomadesis has not been reported previously. Five children, ages 22 months-4 years, presented with Beau's lines and/or onychomadesis following physician-diagnosed HFMD by 3-8 weeks. Three of the five patients experienced fever with HFMD, and none had a history of nail trauma, periungual dermatitis, periungual vesicular lesions, or a significant medication intake history. All patients experienced HFMD within 4 weeks of one another, and all resided in the suburbs of the Chicago metropolitan area. In all patients the nail changes were temporary with spontaneous normal regrowth. The mechanism of the nail matrix arrest is unclear, but the timing and geographic clustering of the patients suggests an epidemic caused by the same viral strain.

Comment: It is likely that this young man's nails will regrow. However, it may take longer than in a young child. All other previous cases have been in children. It is also possible that this is a related virus and not the usual putative agent of HFAM Disease.

Retroauricular Dermatitis

2008-12-15T01:35:00.004Z

Abstract: 16 yo boy with 3-4 year history of retroauricular dermatitis
History: This 16-year-old boy was seen for evaluation of a retroauricular dermatitis that has been present for 3-4 years. He is in his usual state of health. He does not have a history of atopy. He does not wear glasses.
O/E: Honey-colored crusting in the superior retroauricular sulci bilaterally.
Clinical Photo:

click image to enlarge
Lab: Culture positive for many Staph. aureus with usual sensitivities.
Histopathology: N/A
Diagnosis or DDx: Retroauricular Dermatitis: This is felt to be a marker for atopic dermatitis or atopy. However, this boy is not atopic and the finding may not be all that specific. There is only one article has appeared on this subject (see Reference).
Treatment: The patient was given a sample tube of retapamulin ointment (Altabax) to use b.i.d. for one week. The next photo shows appearance after one week of use as monotherapy. I plan to now use fluocinalone 0.025% ointment daily for a week or two for the residual dermatitis. This may well recur. The natural history of retroauricular dermatitis is poorly defined. There is only one article in the medical literature that discusses this entity.

status post 0ne week of retapamulin ointment

Questions: Does anyone have any comments on this entity? How often do you see this? I see one or two cases a year.
Reason(s) Presented: For interest. It is curious that there are no more reports on this since it appears to be an entity.
References:
Marks MB, et. al. An unsuspected sign of cutaneous allergy. J Am Acad Dermatol. 1981 May;4(5):519-22.

An eczematous eruption in the superior retroauricular areas of the scalp and often
on the posterior aspects of the pinnas may be seen in about 30% of allergic
children. The eruption is not generally noticed because the overhanging hair covers
the affected areas. The dermatitis is seen mainly in those children afflicted with
bronchial asthma, perennial allergic rhinitis, or both. A previous history of atopic
or seborrheic dermatitis is, as a rule, not elicited.

Scalp Folliculitis in a Patient on Chemotherapy

2008-12-02T22:49:00.010Z

HPI: This 55 yo woman has had a folliculitis of her scalp for the past 2 - 3 weeks. She is receiving taxol and carboplatinum every three weeks for ovarian cancer and has had two infusions thus far. This eruption began after the second infusion.

O/E: Alopecia secondary to chemotherapy. Scattered over the scalp are erythematous papules and pustules. There are no other lesions other than on the scalp.

Clinical Photos:

Lab: Bacterial culture obtained.

Pathology: Can consider biopsy

Diagnosis: Folliculitis. Probably related to Taxol.

Discussion: A Medline search found one reference to Taxol and folliculitis. This was a case report of two men with folliculitis of the bearded areas and chests after Taxol infusions. Folliculitis is also reported in women on Taxol, but there is no literature available on the subject.

Reason Presented: I discussed her findings with her oncologist who said he sees this picture frequently. It's peculair that there are no case reports. Folliculitis can be bacterial, sterile, fungal or even eosinophilic pustular folliculitis. A biopsy might help. In the absence of guidelines, I started the patient on doxycycline 100 mg. bid. If anyone has seen and treated a similar patient, I would appreciate your insights and recommendations.