Recurrent Oro-labial HSV in a Four Year Old

The patient is a four year-old boy with a three year history of recurrent vesicular lesions around the mouth.  He has two to three episodes a month.  His mother had a similar problem as a child, but now she takes valcyclovir only on an episodic basis.

 

He was started on acyclovir and treated with suppressive regimen but he still had breakthroughs.  He refuses to take the medication on a regular basis but is willing to take it episodically.  (How does one reason with a four year old?)

 

EXAMINATION:  The examination shows a pleasant, outgoing 4-year-old.  He has a cluster of vesicles on his left lower lip.  A Tzanck smear was positive for multinuclear giant cells.

Clinical Image:

Diagnosis:  Recurrent oro-labial herpes simplex in an apparently immunologically normal child.

 

Questions:

In a normal (stubborn) four year-old, is there any therapeutically suppressive approach that will help?  A suspension of acyclovir is available, but famcyclovir and valcyclovir only come as tablets with no pediatric formulations.

 

Do you know of other instances where frequently recurrent HSV runs in families?  It makes sense that there is some subtle problem with normal immune suppression in this family.

 

Have you had any luck with any of the topical antivirals?  The discounted price of Denavir (penciclovir) is almost $900 for a 5 gram tube?

A Case of Toxic Epidermal Necrolysis treated with Etanercept

Presented by Dr, Henry Foong
Ipoh, Malaysia

A patient in his 50s with a history of non-Hodgkin lymphoma was admitted to our local hospital because of fever and generalised skin eruptions for 5 days.  He had developed conjunctivitis, painful mouth ulcers, and painful genital erosions. He was on cozaar and simvastatin which was started about 3 weeks ago.  He denied taking any new oral medications including OTC supplements. 

On Examination: He had generalised dusky coloured targeted macules on the trunk, extremities including palms and soles.  Some of the lesions appeared to be peeling. Bilateral conjunctival redness were noted in both eyes.  There were superficial erosions on the lips, tongue and inner buccal cavity. superficial erosions were also noted on the glans penis. His body surface area (BSA) is estimated to be 45%. (Fig 1 and 2)

Fig 1

Fig 2

 

A diagnosis of Toxic Epidermal Necrolysis was made. 

A skin biopsy was performed.

Pathology: Section shows prominent spongiosis with focal parakeratosis. The epidermis shows focal necrotic keratinocytes and intra-epidermis lymphocytes. There is zonal epidermal necrosis in the center of the biopsy, associated with hemorrhage and a perivascular lymphocytic cuffing of the superficial dermal vessels. The dermis shows mild perivascular neutrophils infiltration. There is no atypical lymphocyte or malignancy seen. The deeper dermis and subcutaneous fat are normal. Extensive lichenoid dermatosis consistent with erythema multiforme. No atypical lymphocyte seen. (Fig 3)

 

Fig 3

Both the antihypertensive and statin ( and all other non essential medications) was withheld. He was initially treated with IV fluids, IV hydrocortisone 200mg qid, oral toilet with sodium bicarb gargle, dilute KMNO4 wash daily, soft paraffin wax as moisturisers.  His blood counts and biochemistry were unremarkable except for raised urea, creatinine and low bicarbonate.  His SCORTEN* score was calculated to be 5 out of 7. While waiting for s/c etanercept 50mg  to arrive, he was treated with IvIg 25 gm daily and IV hydrocortisone 100mg did as an interim measure for 2 days.  He responded well to treatment and his skin begins to heal on day 2 of s/c etanercept. 

 

The use of TNFa inhibitors was first described in the treatment of SJS/TEN in 2002 using infliximab. (1)  It was believed to be the T cells secreting TNFa induced epithelial cell death through granulysin, nitric oxide FasL pathway, CCL 27 and T reg cells.  In 2014, Paradisi described the successful use of etanercept for TEN in JAAD. (2) A good systemic review of the biologic TNF a inhibitors can be found in JDD in 2019. (3)

 

In this case study, we described the successful use of etanercept in an ill patient with TEN.

1.  Which is preferable? IV IgG vs oral cyclosporin vs s/c etanercept

2.  Is there any role of systemic corticosteroids in SJS or TEN?

3. If s/c etanercept is preferable, what would be the interim treatment while waiting for the medication to arrive?  None of our local Malaysian hospitals keep s/c etanercept in their drug store.

References:

1. Fisher. Anti-TNFa (Infliximab) in the treatment of a patient with TEN. Br J Dermatol 2002:146:707-709

2. Paradisi et al. Etarnercept therapy for TEN. J Am Acad Dermatol 2014: 71: 278-283

3. Zhang S, Tang S, Li S, Pan Y, Ding Y. Biologic TNF-alpha inhibitors in the treatment of Stevens-Johnson syndrome and toxic epidermal necrolysis: a systemic review. J Dermatolog Treat. 2020 Feb;31(1):66-73. doi: 10.1080/09546634.2019.1577548. Epub 2019 Feb 19. PMID: 30702955.

 

SCORTEN Score is  Severity of Illness Score for Toxic Epidermal Necrolysis.  See Wiki and scroll down.

Isotretinoin Failure

This 20-year-old woman has a 6 month history of cystic acne.  Although she has been on isotretinoin for three month her response has been poor and she continues to develop new lesions.  She started on 40 mg of isotretinoin a day but her acne flared and she was dropped to 30 and then 20 mg per day.  Due to her acne flare on isotretinoin, prednisone was started at 40 mg bid (tapered after two weeks).  She is on a combined oral contraceptive but it only has 20 mcg of ethinyl estradiol and spironolactome 100 mg per day.  She was also placed on desloratadine 5 mg a day, but that did not appear to help either. She is feeling discouraged, and sees a therapist for anxiety and that led to a prescription for BuSpar from her therapist.

EXAMINATION:  The examination shows a pleasant, outgoing woman.  She has acne with inflammatory and cystic features on the cheeks and forehead.  Back and chest are clear although she did have some acne on her shoulders that has resolved.  Her weight is 65 kg.  There is no hirsuitism or striae.

Photos 8.5.21(aftr 12 weeks of isotretinoin)

IMPRESSION:  This 20-year-old woman with severe inflammatory cystic continues to have active lesions after 3 months months on isotretinoin.  Her acne worsened significantly after her first month of isotretinoin at 40 mg a day.    

 

Photos Removed for Privacy Issue (for legitimate use please contact djelpernATgmail.com)

PLAN:  For the time being, we will continue prednisone at 20 mg a day for the next week and then drop, isotretinoin 20 mg a day, and continue spironolactone 100 mg a day.  I discussed with her either trimethoprim or Bactrim, but we are going to hold off on that, for the time being.    After a literature review,  an article about adding amoxicillin seemed promising.¹

          Questions:

1. At what point would you initiate a work-up for underlying endocrinopathy, such as Cushings?

2.  Have you treated similar patients who flared with isotretinoin and were difficult to control?

3. Have you had experience with adding amoxicillin in situations like this.

 

Reference:

Safety and effectiveness of amoxicillin in the treatment of inflammatory acne.  Guzman AK, Choi JK, James WD. Int J Womens Dermatol. 2018 Jun 8;4(3):174-175Free Full Text.
Comment from Dr. James:

Amoxicillin is a very good drug for acne. I would start at 500 mg tid, very few get any side effects other than of course possible drug eruption, but most have had penicillin in the past and know if they are allergic or not. At three months I would then go to bid. In the paper it was early in my using it, and I was giving it at lower doses, but I find higher dosing better and well tolerated.

You could also start at a lower dose with isotretinioin, sometimes with prednisone as well for the first three to six weeks, almost always tolerate it in this manner, but hard for those who have flared badly to want to take it again. Avoiding this bad flare is why when I use isotretinoin I start the first month at 20 mg per day, then increase. I have had to start at ten mg per day in some that have flared in the past, along with prednisone.

 

Brown Recluse Spider Bite?

A 50 year-old landscaper presented for evaluation of a lesion on his back that has been present for one day. While working in heavy brush, he felt something go down his shirt and a couple of hours later experienced a sharp pain in the mid-back. When he got home there was the beginning blister and has expanded over the night.

O/E: 24 hours later, there is a 8 cm in diameter bullae with a 4 mm central area that looks like a puncture wound. The fluid is clear and there’s no evidence of necrosis.

Clinical Images:

25.6.21

7.1.21 He was treated with cold compresses and mupirocin ointment and his lesion resolved uneventfully/

7.2.21

Impression: This fits Brown Recluse Spider bite. No arachnid or insect was found.

There is no proven therapy for BRSB. I suggested cold compresses b.i.d. and mupirocin ointment.

The patient will send me daily pictures. We’ll see how this progresses over the next few days. At present, the lesion is not symptomatic.

Most BRSBs resolve uneventfully.  A small number develop significance necrosis.  The spider is rarely found.

Reference

 1. StatPearls [Internet]: Brown Recluse Spider Toxicity

Ifeanyichukwu A. Anoka; Erika L. Robb; Mari B. Baker.
Last Update: August 10, 2020. This is a useful page.

In the United States, Loxosceles reclusa or brown recluse spiders are found mostly in the south, west, and midwest areas. They are usually in dark areas such as under rocks, in the bark of dead trees, attics, basements, cupboards, drawers, boxes, bedsheets, or similar locations. Dermonecrotic arachnidism is the local tissue injury that results from brown recluse spider envenomation, while loxoscelism describes the systemic syndrome caused by envenomation. This activity reviews the pathophysiology and presentation of the brown recluse spider biiteand highlights the role of the interprofessional team in its management.

Squamous Cell Carcinoma of the Lip

56 yo man with 3 month history of a friable tumor mid lower lip. Non smoker.  Works frequently outdoors for years.  He has a history of BCC on his back.

O/E: 1 cm nodule lower lip.  No palpable regional adenopathy

Pathology: Biopsy shows a moderately differentiated SCC with invasion into muscle but no definite perineural invasion or lymphatic invasion on the biopsy.  [3 mm punch biopsy may not be representative of the true picture.]

Diagnosis:  SCC lower lip, moderately differentiated.

Plan: Refer for micrographic surgery.

Questions:

1. Lip SCC < 2 cm diameter are reported to be at little risk for metastasis.  With cases like this should an oncologist be consulted?

2.  Is there a role for imaging preoperative imaging?

3. What cosmetic effects of surgery should the patient expect?

 

References::

1. Squamous Cell Carcinoma of the Lip-A Review of Squamous Cell Carcinogenesis of the Mucosal and Cutaneous Junction. James P Bota. Dermatol Surg. 2017 Apr;43(4):494-506. PMID: 28157733

Abstract: Background: The lip is an anatomic junction for 2 disparate groups of cancer. Cutaneous squamous cell carcinoma (cSCC) is a common malignancy with a favorable prognosis, whereas oral-mucosal squamous cell carcinoma (omSCC) is associated with significantly higher rates of nodal disease and worse outcomes. The squamous cell carcinoma of the lip (lip SCC) is more aggressive than cSCC but less aggressive than omSCC. However, work-up and treatment vary between specialties.

Conclusion: Lip SCC is an overlapping entity that poses many challenges to clinicians. Specialists should be aware of current staging modalities as well as imaging and treatment recommendations to optimize patient outcomes.

 

Comments from two respected Moh’s surgeons:

1. In part it depends on the depth of invasion. But without perineural invasion, PNI, (defined as SCC cells within the perineural sheath, nerve diameter >0.1 mm if intradermal or involving a sub-cutaneous nerve), this is a low risk lesion. With no palpable adenopathy, imaging is not indicated. Neither is an Oncologist. Mohs surgery or an excision with complete peripheral margin exam is the recommended treatment. If Mohs is done, the remaining clinically obvious tumor can be debulked and sent to path for further review for PNI. Cosmetic insult should be low. If not invading muscle, mucosal advancement flaps can usually close it elegantly. If muscle involved we often do a full thickness "v" wedge repair of the lip. You can close a defect involving 40% of the lip without microstomia and this lesion won't remove even 20%. The lip stretches back to its normal size in a few months. I'm on the NCCN nonmelanoma skin cancer Guidelines of Care committee. We just finished our annual review of the guidelines, which of course cover cSCC an hour ago! So you are getting the most up to date info that can possibly be obtained!

 

2. This patient looks to have a pretty straightforward case of a SCC on the lip.  I don't think you need to refer to oncology or do imaging, given size of tumor,  no palpable nodes, no aggressive histology.  He needs Mohs and needs it ASAP, as this has grown to 1 cm size in 3 months. Give the Mohs surgeon a heads up that this is growing relatively rapidly.  The patient wouldn't want it to increase significantly in size while he's waiting for an appt.  This is someone I would have normally given priority to, given the chance for rapid growth.  The lower lip is pretty forgiving and if this SCC doesn't grow significantly, the defect could likely be brought together primarily.  One can remove up to a third of the lower lip and close primarily without causing microstomia.  We know the tumor is into muscle (common on the lip, given thin overlying skin and minimal sc fat), but removing a wedge of muscle will actually help minimize tension on the closure.  Tell him stitching will extend into mouth and below the vermillion (to correct the standing cones created with closure).  I will send in a separate email a few photos of some prior patients I have closed primarily with this type of defect.  Took photo of a scrapbook page, so it may be a little distorted. 

I would follow this fellow for the first year after surgery fairly closely (say, q 3 mo) and feel for any palpable nodes. 

 

 

A Thing of Beauty

 •60 yo woman with few year history LLL lesion

•Full-time care-giver to disabled son

•2-cm liner lesion Left Lower Lid with a central groove

•3 mm punch bx: nodular & infiltrative BCC

Clinical Images:

Pathology (Courtesy of Dr. David Jones, Berkshire Medical Center)

Diagnosis: Linear Basal Cell Carcinoma

Presented for interest and comments.

References:

•Linear basal cell carcinoma occurs most commonly on the lower eyelid  G L Becher, et. al. Clin Exp Dermatol. 2011 Apr;36(3):311-2.

•Linear basal cell carcinoma: a distinct condition?                              Al-Niaimi, C C Lyon. Clin Exp Dermatol. 2011 Apr;36(3):231-4.

•Linear Basal cell carcinoma in an asian patien. Kinoshita Shinsuke  et. al. Open Ophthalmol J. 2007 Dec 17;1:20  Free Full Text PMC

Le MIS

 The patient is a healthy 75 to man with a biopsy proven "evolving melanoma-in-situ" on the glabella.  He has Type I skin.  First seen and biopsied in April 2020.

4.20.2020

4.21.21

Question:
Should this be excised by an oncologic surgeon, by a Mohs surgeon, or is imiquimod acceptable?

Reference: 

1.Topical Imiquimod for Lentigo Maligna: Survival Analysis of 103 Cases With 17 Years Follow-up. Meagan Chambers, et. al.  J Drugs Dermatol 2021 Mar 1;20(3):346-348. PMID

 

2. Low recurrence rates for in situ and invasive melanomas using Mohs micrographic surgery with melanoma antigen recognized by T cells 1 (MART-1) immunostaining: tissue processing methodology to optimize pathologic staging and margin assessment

Jeremy Robert Etzkorn, Christopher J Miller . J Am Acad Dermatol. 2015 May;72(5):840-50. PMID

Follow-up:
The patient underwent micrographic surgery  (with permanent sections).  With one stage the tumor was cleared.  Clinical Image 1 week post-surgery:

70 y.o. man with pre-auricular plaque

Presented by Dr. Henry Foong, Ipoh, Malaysia

The patient is a 70-yr-old man with a 2-month history of mildly pruritic skin eruption on the right preauricular area.  It has gradually increased in size and also felt "thicker" and more "lumpy".  He is otherwise in good health.

O/E shows a well demarcated hyperpigmented patch on the right preauricular area 7.5 cm x 3.0 cm.  on palpation it felt boggy. Regional nodes were not enlarged.  There was no facial nerve palsy.

 

Biopsy:

Microscopic:  Dense superficial and deep infiltrate of lymphocytes and plasma cells.  The deeper dermis shows markedly increases eosinophils. Angiolymphoid proliferation is absent as are granulomas or nerve hypertrophy.

 

Diagnosis:  My thoughts are lymphocytoma cutis versus angiolymphoid hyperplasia with eosinophila (ALHE)' but I have limited experience with these. 

Your suggestions would be appreciated.

 

Reference:

Burhan Engin, et. al. Lymphocytic infiltrations of face. Clin Dermatol. Jan-Feb 2014;32(1):101-8.
Abstract:  The immune system protects our organism and, of course, our skin from harmful factors. One of the key elements of the immune system is lymphocytes. Lymphocytes play a role in the pathogenesis of various skin diseases. Lymphocytic infiltrates are seen in many skin diseases. Some of the skin diseases characterized by lymphocytic infiltration show up in specific anatomic locations, whereas other entities can be placed in all areas of the body. The course of lymphocytic infiltrations of the face is variable and unpredictable, most often lasting from months to years. The most important diseases with lymphocytic infiltration of the face are pseudolymphomas. This review discusses various types of cutaneous pseudolymphomas and other diseases with lymphocytic infiltration mainly involving the face.

 

 

Cystic Acne vs. Filler Reaction

Presented by Dr. Kaare Nordqvist
Grand Forks, North Dakota

The patient is a 35 y.o. television news reporter in a Midwestern state.  For the past two yeas she has had inflammatory facial cysts.  She had acne when younger, but it was not like this.  Recently she’s been treated with intralesional triamcinalone, spironolactone (100 mg/d) and doxycycline 100 mg bid.  She has relocated to her family home in North Dakota due to Covid-19.

History: Anamnesis reveals that she had been receiving Restylane and Juvederm for the past two years for old acne scars.

It’s not clear that this pauci cystic diathesis was typical of her earlier acne.

O.E:  Deep cysts, 1.5 – 3 cm in diameter in cheeks, chin and nasolabial folds.  At any time there are no more than two to three lesions.  No other evidence of acne.

Clinical Images:

Diagnosis:  Are we dealing with pauci cystic acne or a reaction to HA fillers? It is known that injected material can migrate and the literature suggests that HA reactions may be more common after viral infections.

This young woman was on the television news nightly.  She is understandably concerned about these lesions and subsequent scarring once she in back in the public's eye.

References

1.Ofir Artzi  et. al. Delayed Inflammatory Reactions to Hyaluronic Acid Fillers: A Literature Review and Proposed Treatment Algorithm. Clin Cosmet Investig Dermatol. 2020 May 18;13:371-378. PMC

2. Katie Beleznay et al.  Delayed-onset nodules secondary to a smooth cohesive 20 mg/mL hyaluronic acid filler: cause and management. Dermatol Surg. 2015 Aug;41(8):929-39.