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.
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Wednesday, December 24, 2008
Monday, December 15, 2008
Retroauricular Dermatitis
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.
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.
Tuesday, December 02, 2008
Scalp Folliculitis in a Patient on Chemotherapy
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.
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.
Saturday, November 15, 2008
Pyoderma Gangrenosum
Abstract: 46 yo man with 1.5 year history of leg ulcers
History: The patient, a disabled 46 yo Cambodian man, has a four year history of poorly controlled ulcerative colitis. He has had painful leg ulcers for the past two years. These begin with pustules or vesicles by history. At present he is taking 1200 mg of Asacol t.i.d. and prednisone 30 mg. per day. In addition to the prednisone he has used potent topical steroids for his ulcers and has been treated at a wound care clinic.
Social History: The patient emigrated from Cambodia 25 years ago. He is married with three children and was employed until he became disabled 2 years ago from colitis and leg ulcers. His English is limited and I had no Cambodian translator.
O/E: There are two ulcers with raised overhanging borders on the left medial malleolus. In addition, there is post-inflammatory hyperpigmentation and proximal scarring secondary to previous ulcerations. The patient has Cushingoid facies.
Clinical Photos:
Lab: N/A
Histopath: N/A
Diagnosis: Pyoderma gangrenosum (P.g.)
Discussion: There is no effective therapeutic protocol for P.g. He has been treated with high dose prednisone for months and his P.g. is only poorly controlled. Super-potent topical steroids have been used without improvement. It seems to us that tacrolimus ointment should be tried because there are many reports of its efficacy with P.g. and it is a more benign therapy than oral cysclsporin or mycophenolate mofetil. Colectomy may be a more permanent solution, but the patient and his gastroenterologists are not ready for that.
Questions: Your suggestions are welcome.
References:
1. eMedicine.com: P.G.
2. Reichrath J, Bens G, Bonowitz A, Tilgen W. Treatment recommendations for pyoderma gangrenosum: an evidence-based review of the literature based on more than 350 patients. J Am Acad Dermatol. 2005 Aug;53(2):273-83.
Dermatology Clinic, The Saarland University Hospital, Homburg/Saar, Germany. hajrei@uniklinik-saarland.de
Because the incidence of pyoderma gangrenosum (PG) is low, no prospective randomized controlled trials and only a few studies with case numbers of more than 15 patients have been published. To date no guidelines for treatment of PG have been established far. The aim of the study was to provide an evidence-based review of the literature and an evaluation of recommendations for PG treatment. We performed an electronic search using the PubMed database and the term "pyoderma- gangrenosum." Literature published in the English language during the past two decades was reviewed. All relevant studies that could be obtained regardless of the study design were evaluated for grades of recommendation and levels of evidence. Data on patient characteristics including severity of the disease, localization of lesions, associated diseases, and treatment procedures were abstracted and evaluated for therapeutic outcome. We conclude that therapeutic efficacy of systemic treatment with corticosteroids and cyclosporine is best documented in the literature for disseminated as well as for localized disease and should be considered first-line therapy. In cases that do not respond to this treatment, we recommend alternative therapeutic procedures (eg, systemic treatment with corticosteroids and mycophenolate mofetil; mycophenolate mofetil and cyclosporine; tacrolimus; infliximab; or plasmapheresis), considering additional factors including associated diseases.
History: The patient, a disabled 46 yo Cambodian man, has a four year history of poorly controlled ulcerative colitis. He has had painful leg ulcers for the past two years. These begin with pustules or vesicles by history. At present he is taking 1200 mg of Asacol t.i.d. and prednisone 30 mg. per day. In addition to the prednisone he has used potent topical steroids for his ulcers and has been treated at a wound care clinic.
Social History: The patient emigrated from Cambodia 25 years ago. He is married with three children and was employed until he became disabled 2 years ago from colitis and leg ulcers. His English is limited and I had no Cambodian translator.
O/E: There are two ulcers with raised overhanging borders on the left medial malleolus. In addition, there is post-inflammatory hyperpigmentation and proximal scarring secondary to previous ulcerations. The patient has Cushingoid facies.
Clinical Photos:
Lab: N/A
Histopath: N/A
Diagnosis: Pyoderma gangrenosum (P.g.)
Discussion: There is no effective therapeutic protocol for P.g. He has been treated with high dose prednisone for months and his P.g. is only poorly controlled. Super-potent topical steroids have been used without improvement. It seems to us that tacrolimus ointment should be tried because there are many reports of its efficacy with P.g. and it is a more benign therapy than oral cysclsporin or mycophenolate mofetil. Colectomy may be a more permanent solution, but the patient and his gastroenterologists are not ready for that.
Questions: Your suggestions are welcome.
References:
1. eMedicine.com: P.G.
2. Reichrath J, Bens G, Bonowitz A, Tilgen W. Treatment recommendations for pyoderma gangrenosum: an evidence-based review of the literature based on more than 350 patients. J Am Acad Dermatol. 2005 Aug;53(2):273-83.
Dermatology Clinic, The Saarland University Hospital, Homburg/Saar, Germany. hajrei@uniklinik-saarland.de
Because the incidence of pyoderma gangrenosum (PG) is low, no prospective randomized controlled trials and only a few studies with case numbers of more than 15 patients have been published. To date no guidelines for treatment of PG have been established far. The aim of the study was to provide an evidence-based review of the literature and an evaluation of recommendations for PG treatment. We performed an electronic search using the PubMed database and the term "pyoderma- gangrenosum." Literature published in the English language during the past two decades was reviewed. All relevant studies that could be obtained regardless of the study design were evaluated for grades of recommendation and levels of evidence. Data on patient characteristics including severity of the disease, localization of lesions, associated diseases, and treatment procedures were abstracted and evaluated for therapeutic outcome. We conclude that therapeutic efficacy of systemic treatment with corticosteroids and cyclosporine is best documented in the literature for disseminated as well as for localized disease and should be considered first-line therapy. In cases that do not respond to this treatment, we recommend alternative therapeutic procedures (eg, systemic treatment with corticosteroids and mycophenolate mofetil; mycophenolate mofetil and cyclosporine; tacrolimus; infliximab; or plasmapheresis), considering additional factors including associated diseases.
Alopecia in a Child
This 11 yo boy has had this alopecic area since infancy. He has been with adoptive parents since he was a baby and his mother says this has been here since coming to live with her. At first, I thought this was a nevus sebaceous, but the scalp looks normal here with none of the raised "pebbly" surface seen in this disorders in older children.
My working diagnosis here is "Congenital Triangular Alopecia."
References: (supplied by Brian Maurer)
1. Elmer KB, George RM. Congenital triangular alopecia: a case report and review. Cutis. 2002 Apr;69(4):255-6.
Congenital triangular alopecia is a nonscarring loss of hair mass on the scalp's temporal regions. The area of hair diminution commonly is described as triangular or lancet shaped. Although previously considered congenital, this condition usually is noticed after 2 years of age and, more recently, is thought to be acquired. We propose that this entity be renamed triangular alopecia. Because this condition involves normal rather than inflamed skin, it does not respond to topical or intralesional steroids. It is important to make the correct diagnosis to avoid unnecessary and potentially harmful interventions. We present the case of a 10-year-old boy with triangular alopecia.
2. Congenital Triangular Alopecia occurring in sisters. Full Text. Original in Portugese
3. García-Hernández MJ, Rodríguez-Pichardo A, Camacho F. Congenital triangular alopecia (Brauer nevus). Pediatr Dermatol. 1995 Dec;12(4):301-3.Department of Medical-Surgical Dermatology and Venereology, Virgen Macarena University Hospital, Seville, Spain.
Abstract: Congenital triangular alopecia is manifested at 3 to 5 years of age by unilateral or, less frequently, bilateral patches of alopecia in the frontotemporal region. At this age the differential diagnosis is important, particularly as regards alopecia areata. Only about 47 cases have been reported, probably because the lesion is benign and nonprogressive. In 6200 patients seen in index visits, we found 7 with triangular alopecia, a frequency of 0.11%. We believe that males do not require treatment because of the later development of androgenic alopecia, but in women, surgical treatment is successful.2. Tosti A. Congenital triangular alopecia. Report of fourteen cases.
4. Tosti A. Congenital triangular alopecia. Report of fourteen cases. J Am Acad Dermatol. 1987 May;16(5 Pt 1):991-3.
Abstract: Fourteen patients affected by congenital triangular alopecia are presented. The clinical and histologic features of this condition are discussed. I suggest that the condition is considerably more common than hitherto has been thought.
My working diagnosis here is "Congenital Triangular Alopecia."
References: (supplied by Brian Maurer)
1. Elmer KB, George RM. Congenital triangular alopecia: a case report and review. Cutis. 2002 Apr;69(4):255-6.
Congenital triangular alopecia is a nonscarring loss of hair mass on the scalp's temporal regions. The area of hair diminution commonly is described as triangular or lancet shaped. Although previously considered congenital, this condition usually is noticed after 2 years of age and, more recently, is thought to be acquired. We propose that this entity be renamed triangular alopecia. Because this condition involves normal rather than inflamed skin, it does not respond to topical or intralesional steroids. It is important to make the correct diagnosis to avoid unnecessary and potentially harmful interventions. We present the case of a 10-year-old boy with triangular alopecia.
2. Congenital Triangular Alopecia occurring in sisters. Full Text. Original in Portugese
3. García-Hernández MJ, Rodríguez-Pichardo A, Camacho F. Congenital triangular alopecia (Brauer nevus). Pediatr Dermatol. 1995 Dec;12(4):301-3.Department of Medical-Surgical Dermatology and Venereology, Virgen Macarena University Hospital, Seville, Spain.
Abstract: Congenital triangular alopecia is manifested at 3 to 5 years of age by unilateral or, less frequently, bilateral patches of alopecia in the frontotemporal region. At this age the differential diagnosis is important, particularly as regards alopecia areata. Only about 47 cases have been reported, probably because the lesion is benign and nonprogressive. In 6200 patients seen in index visits, we found 7 with triangular alopecia, a frequency of 0.11%. We believe that males do not require treatment because of the later development of androgenic alopecia, but in women, surgical treatment is successful.2. Tosti A. Congenital triangular alopecia. Report of fourteen cases.
4. Tosti A. Congenital triangular alopecia. Report of fourteen cases. J Am Acad Dermatol. 1987 May;16(5 Pt 1):991-3.
Abstract: Fourteen patients affected by congenital triangular alopecia are presented. The clinical and histologic features of this condition are discussed. I suggest that the condition is considerably more common than hitherto has been thought.
Tuesday, November 11, 2008
Acanthosis Nigricans in a Child
Abstract: 11 yo girl with three year history of acanthosis nigricans
History: This is a healthy 11 y.o. girl. Her mother noticed gradual darkening of skin in neck folds, axillae and groin around three years ago. The child is Chinese. Has not had her first menstrual cycle yet, although has some breast development. She is mildly overweight (not obese). Fitzpatrick Skin Type IV - V. No hirsuitism.
O/E: Velvety hyperpigmentation of skin folds. There are a few skin tags in axillae. Some perioral darkening
Clinical Photo:
Lab: Insulin Level 43 (nl 3 - 28)
Hgb A1C normal, Serum Testosterone Level 75 (normal < style="font-weight: bold;">Histopathology: N/A
Diagnosis or DDx: Acanthosis Nigricans
This child may have AN associated with obesity or a syndromic AN associated with insulin resistance. Too early to say if PCOS is related. We do not have any pediatric endocrinologists in our area, but I feel that she should travel to see one. Dr. Susan Ratzan has kindly given us some guidelines (see below)
Questions: How would you approach this patient and initiate an appropriate work-up? (See Dr. Ratzan's comments below) Is this high insulin level significant?
Reason(s) Presented: To Discuss implications of this diagnosis and work-up.
References:
1. eMedicine.com
2. Hermanns-Lê T, Scheen A, Piérard GE. Acanthosis nigricans associated with insulin resistance : pathophysiology and management. Am J Clin Dermatol. 2004;5(3):199-203.
Departments of Dermatopathology, University of Liège, Liège, Belgium.
The association of acanthosis nigricans, skin tags, diabetes mellitus due to insulin resistance, and obesity in adolescents and young adults represents a well defined syndrome. Hyperandrogenism may also be present. The endocrine origin of this condition is beyond doubt. Insulin and insulin-like growth factor-1, and their receptors on keratinocytes are obviously involved in the complex regulations leading to the peculiar epidermal hyperplasia. This condition is unrelated to other types of acanthosis nigricans, including the congenital and the paraneoplastic types.Control of obesity contributes largely to reverse the whole process, essentially by reducing both insulin resistance and compensatory hyperinsulinemia. Several drugs including metformin, octreotide, retinoids and topical colecalciferol (vitamin D(3)) analogs are also beneficial in clearing acanthosis nigricans.
Comments by Susan Ratzan, M.D. (pediatric endocrinologist):
As far as I am concerned AN is the cutaneous manifestation of hyperinsulinism or insulin resistance. For starters I would get a very good family history for type 2 diabetes, PCOS, hirsutism, infertility, irregular menses, and obesity. You described her very politely as "chunky" but what is her BMI? The way I would document her degree of insulin resistance/carbohydrate tolerance is by doing a 2 hr oral glucose tolerance test with samples at 0, 30, 60, 90 and 120 minutes for BOTH insulin and glucose. At the 0 sample, since she will be fasting, I would also get cholesterol, LDLdirect, triglycerides and HDL(many of these children have the dyslipidemia associated with metabolic syndrome which is elevated TG and low HDL). The best treatment for insulin resistance, but the most difficult to achieve, is a healthier lifestyle, lots of fresh fruits and veggies, healthy oils, fat free milk, no fast food, no soda or other sugar sweetened beverages and juice limited to 4-6 oz/day. We also recommend limiting carbs to 5-6 servings(and they need to be taught what a serving is)/day. If only I could live like this!! Exercise needs to be worked up to an hour a day by turning off the TV and the video games/internet. If the child has glucose intolerance or severe insulin resistance, we use metformin even in children as young as 11, but nothing works as well as lifestyle change.
History: This is a healthy 11 y.o. girl. Her mother noticed gradual darkening of skin in neck folds, axillae and groin around three years ago. The child is Chinese. Has not had her first menstrual cycle yet, although has some breast development. She is mildly overweight (not obese). Fitzpatrick Skin Type IV - V. No hirsuitism.
O/E: Velvety hyperpigmentation of skin folds. There are a few skin tags in axillae. Some perioral darkening
Clinical Photo:
Lab: Insulin Level 43 (nl 3 - 28)
Hgb A1C normal, Serum Testosterone Level 75 (normal < style="font-weight: bold;">Histopathology: N/A
Diagnosis or DDx: Acanthosis Nigricans
This child may have AN associated with obesity or a syndromic AN associated with insulin resistance. Too early to say if PCOS is related. We do not have any pediatric endocrinologists in our area, but I feel that she should travel to see one. Dr. Susan Ratzan has kindly given us some guidelines (see below)
Questions: How would you approach this patient and initiate an appropriate work-up? (See Dr. Ratzan's comments below) Is this high insulin level significant?
Reason(s) Presented: To Discuss implications of this diagnosis and work-up.
References:
1. eMedicine.com
2. Hermanns-Lê T, Scheen A, Piérard GE. Acanthosis nigricans associated with insulin resistance : pathophysiology and management. Am J Clin Dermatol. 2004;5(3):199-203.
Departments of Dermatopathology, University of Liège, Liège, Belgium.
The association of acanthosis nigricans, skin tags, diabetes mellitus due to insulin resistance, and obesity in adolescents and young adults represents a well defined syndrome. Hyperandrogenism may also be present. The endocrine origin of this condition is beyond doubt. Insulin and insulin-like growth factor-1, and their receptors on keratinocytes are obviously involved in the complex regulations leading to the peculiar epidermal hyperplasia. This condition is unrelated to other types of acanthosis nigricans, including the congenital and the paraneoplastic types.Control of obesity contributes largely to reverse the whole process, essentially by reducing both insulin resistance and compensatory hyperinsulinemia. Several drugs including metformin, octreotide, retinoids and topical colecalciferol (vitamin D(3)) analogs are also beneficial in clearing acanthosis nigricans.
Comments by Susan Ratzan, M.D. (pediatric endocrinologist):
As far as I am concerned AN is the cutaneous manifestation of hyperinsulinism or insulin resistance. For starters I would get a very good family history for type 2 diabetes, PCOS, hirsutism, infertility, irregular menses, and obesity. You described her very politely as "chunky" but what is her BMI? The way I would document her degree of insulin resistance/carbohydrate tolerance is by doing a 2 hr oral glucose tolerance test with samples at 0, 30, 60, 90 and 120 minutes for BOTH insulin and glucose. At the 0 sample, since she will be fasting, I would also get cholesterol, LDLdirect, triglycerides and HDL(many of these children have the dyslipidemia associated with metabolic syndrome which is elevated TG and low HDL). The best treatment for insulin resistance, but the most difficult to achieve, is a healthier lifestyle, lots of fresh fruits and veggies, healthy oils, fat free milk, no fast food, no soda or other sugar sweetened beverages and juice limited to 4-6 oz/day. We also recommend limiting carbs to 5-6 servings(and they need to be taught what a serving is)/day. If only I could live like this!! Exercise needs to be worked up to an hour a day by turning off the TV and the video games/internet. If the child has glucose intolerance or severe insulin resistance, we use metformin even in children as young as 11, but nothing works as well as lifestyle change.
Tuesday, October 21, 2008
Hypopigmentation in a Young Child
Presented by Dr. Henry Foong
Ipoh, Malaysia
History: A 6 year old boy presented with patches of hypopigmentation on the trunk and extremities since one year's of age. It was occasionally pruritic. He is otherwise well and has no history of fever or other constitutional symptoms. There was no family history of similar problem and no personal or family history of atopy.
Examination showed the skin was quite dry. Multiple irregular patches of hypopigmentation 2-4 cm diameter were distributed over the back of trunk involving both the lower back extending to the gluteal areas, the arms and anterior chest wall. Sensation was normal in the affected areas.
Photos:
Ipoh, Malaysia
History: A 6 year old boy presented with patches of hypopigmentation on the trunk and extremities since one year's of age. It was occasionally pruritic. He is otherwise well and has no history of fever or other constitutional symptoms. There was no family history of similar problem and no personal or family history of atopy.
Examination showed the skin was quite dry. Multiple irregular patches of hypopigmentation 2-4 cm diameter were distributed over the back of trunk involving both the lower back extending to the gluteal areas, the arms and anterior chest wall. Sensation was normal in the affected areas.
Photos:
Lab: KOH examination did not reveal hyphae or spores.
Pathology: Biopsy not performed as yet.
Diagnosis: ? Progressive Macular Hypopigmentation ? Pityriasis Alba
Questions: Have you seen this in a young child?? What is your diagnosis and therapeutic recommendations.
Reference:
Pathology: Biopsy not performed as yet.
Diagnosis: ? Progressive Macular Hypopigmentation ? Pityriasis Alba
Questions: Have you seen this in a young child?? What is your diagnosis and therapeutic recommendations.
Reference:
Progressive macular hypomelanosis: an overview.
Relyveld GN, Menke HE, Westerhof W.
Am J Clin Dermatol. 2007;8(1):13-9.
The Netherlands Institute for Pigment Disorders, Academic Medical Center,
University of Amsterdam, Amsterdam, The Netherlands.
Wednesday, October 15, 2008
Distinctive Disorder
The patient is a seven-year old girl with a one year history of a linear band of confluent hypopigmented scaly papules. She has Fitzpatrick Skin Type IV.
The clinical diagnosis is Lichen Striatus.
Reference: You can read a good chapter about L.S. on: Emedicine.com
Questions: This does not particularly bother the child or her parents. Would you treat this? And if so with what? A topical corticosteroid? Pimecrolimus? Tacrolimus? Other?
The clinical diagnosis is Lichen Striatus.
Reference: You can read a good chapter about L.S. on: Emedicine.com
Questions: This does not particularly bother the child or her parents. Would you treat this? And if so with what? A topical corticosteroid? Pimecrolimus? Tacrolimus? Other?
Sunday, October 05, 2008
Clam Digger's Legs
Mike LaCombe, a cardiologist from Maine, has a question for our panel.
"G.M. is a 48 y.o. clam digger from Maine. These individuals are exposed to avian schistosomiasis, and on a web search, the consequent clam-digger’s itch has been rarely associated with lymphedema.
Sorry, I have no pictures. This man has well-documented lymphedema of the lower extremities for six months.
All studies negative: CT scans of pelvis, abdomen, chest, ultrasound of leg veins, cardiac echo ruling out any cor pulmonale, and labs showing no evidence of liver disease, hypoalbuminemia.
My questions are:
1. Does anyone have any experience with this?
2. Any specific tests to confirm the diagnosis?
3. Therapy suggestions? "
There are more things in heaven and earth, Horatio, than are dreamt of in your philosophy." Always something new.
"G.M. is a 48 y.o. clam digger from Maine. These individuals are exposed to avian schistosomiasis, and on a web search, the consequent clam-digger’s itch has been rarely associated with lymphedema.
Sorry, I have no pictures. This man has well-documented lymphedema of the lower extremities for six months.
All studies negative: CT scans of pelvis, abdomen, chest, ultrasound of leg veins, cardiac echo ruling out any cor pulmonale, and labs showing no evidence of liver disease, hypoalbuminemia.
My questions are:
1. Does anyone have any experience with this?
2. Any specific tests to confirm the diagnosis?
3. Therapy suggestions? "
There are more things in heaven and earth, Horatio, than are dreamt of in your philosophy." Always something new.
Sunday, September 21, 2008
Hypopigmentation in an African Child
Katie Ratzan, a third year Dartmouth Medical School student serving as a Schweitzer Fellow at the Schweitzer Hospital in Gabon, Africa, would like help and advice.
" I would like to ask your help with a six year old girl who presented to our clinic at the Hopital Schweitzer, with her father & aunt. The child has a recent onset of hypopigmentation of the left side of her face & neck. As of six to seven weeks ago, her skin was entirely normal. This change in skin color progressed over the past six weeks. It is asymptomatic. She has had no constitutional symptoms. She was not sick during the months/weeks prior to the color change, did not take any medications prior to the skin change, did not travel, did not have an accident with any sort of chemical, does not use anything on her face (i.e. cremes, etc.). No one else around her has anything like this. No one else around her is sick. She's never had this before. She now puts some sort of indigenous healing/darkening creme on the spots on the back of her neck, which is why that is darker than the areas of her face.
By history, this started on her cheek and moved toward her nose. It stops abruptly at midline. It has since spread to her neck and scalp. It's macular/patch-like depending on the confluence of abutting lesions. There is no involvement of mucous membrance (mouth & vagina are normal). She has no trouble with vision, taste, hearing, and her neuro exam (my brief version of it which essentially only tested sensation and gross motor) was normal.
Questions from Katie:
1. Does anyone think this is anything other than vitiligo?
2. Is this segmental vitiligo, and if so what special significance does this have?
3. What therapy would be appropriate for a child like this in this setting?
4. What is known of the psychological and social implications of such hypopigmentation in a girl in this setting?
Thank you,
Katie
" I would like to ask your help with a six year old girl who presented to our clinic at the Hopital Schweitzer, with her father & aunt. The child has a recent onset of hypopigmentation of the left side of her face & neck. As of six to seven weeks ago, her skin was entirely normal. This change in skin color progressed over the past six weeks. It is asymptomatic. She has had no constitutional symptoms. She was not sick during the months/weeks prior to the color change, did not take any medications prior to the skin change, did not travel, did not have an accident with any sort of chemical, does not use anything on her face (i.e. cremes, etc.). No one else around her has anything like this. No one else around her is sick. She's never had this before. She now puts some sort of indigenous healing/darkening creme on the spots on the back of her neck, which is why that is darker than the areas of her face.
By history, this started on her cheek and moved toward her nose. It stops abruptly at midline. It has since spread to her neck and scalp. It's macular/patch-like depending on the confluence of abutting lesions. There is no involvement of mucous membrance (mouth & vagina are normal). She has no trouble with vision, taste, hearing, and her neuro exam (my brief version of it which essentially only tested sensation and gross motor) was normal.
Questions from Katie:
1. Does anyone think this is anything other than vitiligo?
2. Is this segmental vitiligo, and if so what special significance does this have?
3. What therapy would be appropriate for a child like this in this setting?
4. What is known of the psychological and social implications of such hypopigmentation in a girl in this setting?
Thank you,
Katie
Wednesday, August 27, 2008
One More Unfortunate...
Gina Kaulukukui is a grief counselor on the island of Kauai, Hawaii. She sent me the following text along with these photographs. Your impressions may help to solve this tragic mystery.
“I would like you to review the attached photos and give me your impressions. This 21 y.o woman was found in the water at Tunnels Beach on the north shore of Kauai following a night of partying. She was reportedly in the water about 7-15 minutes when she was pulled out unresponsive. When she was brought to the ER (at least a ½ drive) it was believed that she nearly drowned. She was unresponsive and not expected to survive.
While in the ER she presented on her thighs with unusual markings. The first appeared red jagged rings starting from her bikini line to just above the knee on one side and more toward the inner thigh on the other leg. Both were oval and completely blanched in the middle. There was a slight bruised color line in the center of one of the blanched areas. There were no others marks, lesions, etc.
The next day, the blanching went away and the red ring doubled in size from about 1 inch to about 2 inches. It was very red, raised and angry looking.
Later in the day when I went to check the young lady and convinced the ICU to photograph the area as it was again changing. Where the bruising was, small water blisters began to appear on the one leg, while the markings on the other leg was beginning to disappear. When the doctor was called to look at the blistering, she diagnosed it as a thermal burns.
The attached pictures were taken few hours following her death and as you can see on one side there is no marking left (the red mark on the upper thigh is from her blood pooling and not the original location of the blanching). The other side speaks for it self.
There were never any marks or puncture wounds that would indicate a jelly fish sting. The water was calm that day. She had high levels of cocaine and alcohol in her system. I would love to know what you think. We have yet to receive the biopsy results. I appreciate your time...love and aloha Gina
“I would like you to review the attached photos and give me your impressions. This 21 y.o woman was found in the water at Tunnels Beach on the north shore of Kauai following a night of partying. She was reportedly in the water about 7-15 minutes when she was pulled out unresponsive. When she was brought to the ER (at least a ½ drive) it was believed that she nearly drowned. She was unresponsive and not expected to survive.
While in the ER she presented on her thighs with unusual markings. The first appeared red jagged rings starting from her bikini line to just above the knee on one side and more toward the inner thigh on the other leg. Both were oval and completely blanched in the middle. There was a slight bruised color line in the center of one of the blanched areas. There were no others marks, lesions, etc.
The next day, the blanching went away and the red ring doubled in size from about 1 inch to about 2 inches. It was very red, raised and angry looking.
Later in the day when I went to check the young lady and convinced the ICU to photograph the area as it was again changing. Where the bruising was, small water blisters began to appear on the one leg, while the markings on the other leg was beginning to disappear. When the doctor was called to look at the blistering, she diagnosed it as a thermal burns.
The attached pictures were taken few hours following her death and as you can see on one side there is no marking left (the red mark on the upper thigh is from her blood pooling and not the original location of the blanching). The other side speaks for it self.
There were never any marks or puncture wounds that would indicate a jelly fish sting. The water was calm that day. She had high levels of cocaine and alcohol in her system. I would love to know what you think. We have yet to receive the biopsy results. I appreciate your time...love and aloha Gina
Wednesday, July 30, 2008
Distal Onycholysis
Abstract: 76 yo retired nurse with a 1 year history of nail dystrophy.
History: This 76 yo retired registered nurse had distal onycholysis of her right thumb nail a little over a year ago. It eventually "spread" to involve all finger nails. Her medications include lorazepam, citalopram, Premarin and thyroid. All have been taken for many years. She has not used acrylic nails for more than five years. No unusual trauma, but she does use a nail file now. She was seen for around a year by a provider who was treating her with ciclopirox. The patient admits to being very anxious and plays with her nails.
O/E.: The patient is a pleasant, well-groomed woman who appears anxious and concerned. She has distal onycholysis of all finger nails. Toe nails are normal. Scant subungual debris.
Clinical Photos:
Lab: Three KOH preps negative. Fungal cultures were obtained 30 July, 2008.
Pathology: A "few" fungal elements were reported on PASD stained clipping of an affected nail
Diagnosis: Distal onycholysis. I am leaning away from onychomycosis. This would be an unusual presentation. I think this will likely be traumatic onycholysis.
Therapy: Pending culture report, I initiated therapy with 15% sulfactamide in ethanol twice daily. She was asked not to use a nail file and to clip separated portions of nails every day or so. Also, keep hands out of water as much as possible.
Questions: What are your thoughts? Any further work-up?
References:
1. eMedicine.com
History: This 76 yo retired registered nurse had distal onycholysis of her right thumb nail a little over a year ago. It eventually "spread" to involve all finger nails. Her medications include lorazepam, citalopram, Premarin and thyroid. All have been taken for many years. She has not used acrylic nails for more than five years. No unusual trauma, but she does use a nail file now. She was seen for around a year by a provider who was treating her with ciclopirox. The patient admits to being very anxious and plays with her nails.
O/E.: The patient is a pleasant, well-groomed woman who appears anxious and concerned. She has distal onycholysis of all finger nails. Toe nails are normal. Scant subungual debris.
Clinical Photos:
Lab: Three KOH preps negative. Fungal cultures were obtained 30 July, 2008.
Pathology: A "few" fungal elements were reported on PASD stained clipping of an affected nail
Diagnosis: Distal onycholysis. I am leaning away from onychomycosis. This would be an unusual presentation. I think this will likely be traumatic onycholysis.
Therapy: Pending culture report, I initiated therapy with 15% sulfactamide in ethanol twice daily. She was asked not to use a nail file and to clip separated portions of nails every day or so. Also, keep hands out of water as much as possible.
Questions: What are your thoughts? Any further work-up?
References:
1. eMedicine.com
Sunday, July 27, 2008
Skin Cancer Observation from Baghdad
Case presentation by:
Professor Khalifa Sharquie,
Baghdad, Iraq
Professor Khalifa Sharquie,
Baghdad, Iraq
I have had the opportunity to see many cases of skin grafting on the face after excision of multiple skin solar keratosis and skin malignancy. Some of these have been in patients with xeroderma pigmentosa (XP). The grafts remained free of actinic disease and have stayed clear for many years, in some cases for more than 20 years. I have never observed them to develop solar damage, solar keratosis or malignancy.
Today, I am presenting one of these cases. A 65 yo man with history of marked sun damage since early life. During the course of his illness, he has developed frequent and multiple solar keratosis and squamous cell carcinoma. Positive family history was seen in his son. Excisions and graftings have been carried out for big cancers since 1982 but he has never developed any solar damage or skin malignancy in the grafts.
Questions:
1. Is it justifiable to excise the skin of such patients with multiple keratosis and malignancies, especially in patients with XP early in life as a part of preventive measures against skin malignancy especially malignant melanoma.
2. What is the mechanism behind this odd observation. Could fibroblasts of the graft share in prevention?
3. Is there any role in the use of imiquimod in these patients? (last question from DJ Elpern)
Wednesday, June 25, 2008
Erythema Migrans with Pustules
This 27 yo woman was sent from the E.R. with a 5 day history of a solitary 20 cm annular plaque on the right hip. It looks classical for erythema migrans (EM) of Lyme disease. Her three year-old daughter had a tick on her skin 2 weeks ago, but she has no history of tick bite. The patient is well otherwise.
Photos taken June 24, 2008
Clinically, this is Lyme disease, but no reports in literature of pustules. There is one from China with vesicles (which these may have been initially).
Lyme titers are pending (but this is a clinical dx at this point) and a culture of a pustule was taken.
E.R. doc put her on cefuroxime because she can't tolerate doxycycline (bad GI upset). She has a f/u appointment in a week.
Photos taken June 24, 2008
Clinically, this is Lyme disease, but no reports in literature of pustules. There is one from China with vesicles (which these may have been initially).
Lyme titers are pending (but this is a clinical dx at this point) and a culture of a pustule was taken.
E.R. doc put her on cefuroxime because she can't tolerate doxycycline (bad GI upset). She has a f/u appointment in a week.
Monday, June 23, 2008
Ranula
Abstract: 16 mo girl with mucous cyst of lower lip.
HPI: This 16 mo Chinese girl presented for evaluation of a lip lesion that has been present for two months. It waxes and wanes in size. The lesion does not appear to bother her. Her mother speaks little English and is very worried about this lesion.
O/E: 6 mm translucent cyst lower lip
Clincal Photo:
Lab/Path: N/A
Diagnosis: Mucous Cyst (Ranula)
Questions: How would you approach this patient? I need to find a translator so that I can have a meaningful discussion with the child's mother. In the past, I have treated a few of these with liquid nitrogen and they did well, but that might be very traumatic for this child (and the mother). Might have to find a pediatric ENT (the closest would be ~ 75 miles from here)
Reference: There are two good chapters on eMedicine.com
and eMedicine2.com The latter is more detailed.
This is the largest study I found, and I'll write to the authors.
Clinical review.com2 of 580 ranulas.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 Sep;98(3):281-7.
Zhao YF, Jia Y, Chen XM, Zhang WF.
CONCLUSION: Three patterns of ranula have similar clinical and histopathologic findings, although plunging ranula has some different clinical features. Removal of the sublingual gland via an intraoral approach is necessary in the management of various clinical patterns of the ranula. Recurrence rates of ranulas of any type are excessive unless the involved sublingual gland is removed.
HPI: This 16 mo Chinese girl presented for evaluation of a lip lesion that has been present for two months. It waxes and wanes in size. The lesion does not appear to bother her. Her mother speaks little English and is very worried about this lesion.
O/E: 6 mm translucent cyst lower lip
Clincal Photo:
Lab/Path: N/A
Diagnosis: Mucous Cyst (Ranula)
Questions: How would you approach this patient? I need to find a translator so that I can have a meaningful discussion with the child's mother. In the past, I have treated a few of these with liquid nitrogen and they did well, but that might be very traumatic for this child (and the mother). Might have to find a pediatric ENT (the closest would be ~ 75 miles from here)
Reference: There are two good chapters on eMedicine.com
and eMedicine2.com The latter is more detailed.
This is the largest study I found, and I'll write to the authors.
Clinical review.com2 of 580 ranulas.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 Sep;98(3):281-7.
Zhao YF, Jia Y, Chen XM, Zhang WF.
CONCLUSION: Three patterns of ranula have similar clinical and histopathologic findings, although plunging ranula has some different clinical features. Removal of the sublingual gland via an intraoral approach is necessary in the management of various clinical patterns of the ranula. Recurrence rates of ranulas of any type are excessive unless the involved sublingual gland is removed.
Sunday, June 15, 2008
Man from Mauritius
Presented by Dr. Philip Li Loong, Quatre Bornes, Mauritius
Abstract: 27 year old man with four year history of a papular eruption.
HPI: This man's lesions began on the face four years ago and later developed in the groins and axillae. Initially macules, they became papular and much more numerous. At onest, they were felt to be verruca plana. Cryotherapy was tried without success.
O/E: The lesions are 2 - 3 mm in diameter brown to yellowish papules. Distribution: Face, crural folds, axillae.
Clinical Photos:
Lab: Full blood count normal, cholesterol 5.2 upper limit, triglycerides normal, LDL HDL also normal, Immumoglobulins normal, plasma electrophoresis normal, thyroid function tests normal.
Pathology: Two biopsies were done.
The first showed a mild chronic inflammatory infiltrate in the upper dermis made up of small lymphocytes and histiocytes with occasional macrophages.
Repeat biopsy from the right axilla was reported as aggregates of foam cells admixed with other histiocytes, lymphocytes and some fibroblasts: "appearance consistent with eruptive xanthomas"
Diagnosis: Do you think this man has xanthoma disseminatum?
Questions: This entity may be associated with paraproteinemia and mucous membrane involvement. Comments for diagnosis and management will be most welcome. What are your thoughts? What further would you do?
Abstract: 27 year old man with four year history of a papular eruption.
HPI: This man's lesions began on the face four years ago and later developed in the groins and axillae. Initially macules, they became papular and much more numerous. At onest, they were felt to be verruca plana. Cryotherapy was tried without success.
O/E: The lesions are 2 - 3 mm in diameter brown to yellowish papules. Distribution: Face, crural folds, axillae.
Clinical Photos:
Lab: Full blood count normal, cholesterol 5.2 upper limit, triglycerides normal, LDL HDL also normal, Immumoglobulins normal, plasma electrophoresis normal, thyroid function tests normal.
Pathology: Two biopsies were done.
The first showed a mild chronic inflammatory infiltrate in the upper dermis made up of small lymphocytes and histiocytes with occasional macrophages.
Repeat biopsy from the right axilla was reported as aggregates of foam cells admixed with other histiocytes, lymphocytes and some fibroblasts: "appearance consistent with eruptive xanthomas"
Diagnosis: Do you think this man has xanthoma disseminatum?
Questions: This entity may be associated with paraproteinemia and mucous membrane involvement. Comments for diagnosis and management will be most welcome. What are your thoughts? What further would you do?
Saturday, May 31, 2008
Know When to Cut, Know when to Punt
The patient is an 87 yo man with a mild dementia. He lives in an assisted care facility. Has an attentive and caring daughter. In October of 2007 he had a wide-local excision of s large SCC on the left forehead by a general surgeon. Path report showed "clear margins." When seen on May 30, 2008 a 4 x 3 cm recurrence was noted. The picture of the right TMJ area shows a scar from micrographic surgery from a similar lesion the patient had ~ 10 years ago. His daughter said it took 6 months to heal.
Questions:
1. What contributes to the aggressive behavior of this small subset of SCCs?
2. Would you refer to Mohs, XRT, or just watch?
3. Are you comfortable playing God with patients like these?
Comment: There is a subset of SCCs that metastasize and kill patients. MA Weinstock and his collaborators have written on this subject.
Questions:
1. What contributes to the aggressive behavior of this small subset of SCCs?
2. Would you refer to Mohs, XRT, or just watch?
3. Are you comfortable playing God with patients like these?
Comment: There is a subset of SCCs that metastasize and kill patients. MA Weinstock and his collaborators have written on this subject.
Weinstock MA, et. al.
Nonmelanoma skin cancer mortality. A population-based study.
Arch Dermatol. 1991 Aug;127(8):1194-7.
Department of Medicine, Veterans Affairs Medical Center
Providence, RI 02908.
To estimate the magnitude of nonmelanoma skin cancer mortality
and describe itsparameters, we reviewed the medical records of
all deaths certified as due to this cause among Rhode Island
residents from 1979 through 1987. After excluding acquired
immunodeficiency syndrome-associated Kaposi's sarcoma, we
confirmed that nonmelanoma skin cancer was the cause of death
for 51 individuals, a quarter of the number of melanoma deaths
reported. The age-adjusted nonmelanoma skin cancer mortality rate
was 0.44/10(5) per year. Fifty-nine percent were due to squamous
cell carcinoma, and 20% were due to basal cell carcinoma. Most
appeared actinically induced. Among deaths from SCCs, the mean age
was 73 years. At least 80% of the squamous cell carcinomas metas-
tasized, and 47% arose on the ear. None appeared due to refusal of
treatment. Among deaths frombasal cell carcinoma, the mean age was
85 years, and refusal of surgical intervention was documented in
40%. Study of nonmelanoma skin cancer mortality provides for estimation
of the magnitude of this problem, complements otherstudies of
prognosis, and helps guide prevention, early detection, and treatment.
Monday, May 26, 2008
Two Foot and One Hand Disease
These are the hands of a 35 year-old plumber I saw recently. He was not aware of a dermatitis of his feet, but inspection showed mild moccasin-type T. pedis on both feet and subtle onychomycosis. KOH prep from the right hand was positive for septate hyaline hyphae. We all see two foot and one hand disease regularly. Do you have any theories as to why only one hand is involved? This is a peculiar dermatologic vignette.
Right Hand
Left Hand
Right Hand
Left Hand
Monday, May 19, 2008
Penile Pain
The patient is 40 yo heterosexual male in a monogamous relationship for the last 6 years. Neither he nor his partner has a history of having had sex with anyone else ever before.
Three months ago he had the onset of pain at the tip of his glans during coitus and experienced pain also on pulling at the tip of his foreskin. A month later he noticed a few grouped "vesicles" at the ventral tip of his glans. These lesions have persisted unchanged. The pain in these lesions persists since being first noticed.
Clinical Photo:
The wife is asymptomatic although she had symptoms suggestive of vaginitis 3-4 months back which improved on clotrimazole pessaries (this was almost the same time when the patient developed pain during coitus which has never subsided).
What is the diagnosis?
What would you do at this point?
Note: Two respondents have suggested "Pearly Penile Papules." This does not look like a typical case of PPP. For comparison a picture is below. PPP is usually around the corona and is rarely this symptomatic.
Three months ago he had the onset of pain at the tip of his glans during coitus and experienced pain also on pulling at the tip of his foreskin. A month later he noticed a few grouped "vesicles" at the ventral tip of his glans. These lesions have persisted unchanged. The pain in these lesions persists since being first noticed.
Clinical Photo:
The wife is asymptomatic although she had symptoms suggestive of vaginitis 3-4 months back which improved on clotrimazole pessaries (this was almost the same time when the patient developed pain during coitus which has never subsided).
What is the diagnosis?
What would you do at this point?
Note: Two respondents have suggested "Pearly Penile Papules." This does not look like a typical case of PPP. For comparison a picture is below. PPP is usually around the corona and is rarely this symptomatic.
Monday, May 12, 2008
21 yo man with warty plaque on foot
Presented by Henry Foong, Ipoh, Malaysia
A 21 yr old student presented with 5-year history of warty growth on the
right foot. It started as a small lesion which gradually got bigger.
Pertinent findings on examination were raised hyperkeratotic plaque 5 x 3 cm
on the medial border of the dorsum of the right foot. It has a verrucous
surface with blackish dots. Regional nodes were not palpable.
Clinically he has chromoblastomycosis of the right foot.
A biopsy was done and the epithelium shows marked acanthosis with elongation
of rete ridges and intraepithelial collections of neutrophils. The dermis is
densely infiltrated by lymphocytes, plasma cells and few neutrophils.
Culture of organism was not done.
I may repeat the biopsy and perform fungal culture.
I plan to treat him with liquid nitrogen together with some combination
therapy with antifungals: itraconazole 100mg bd ( 200mg bd??) for several
months together with another antifungals. 5FU or IV amphotericin.
Would appreciate your comments on this patient.
A 21 yr old student presented with 5-year history of warty growth on the
right foot. It started as a small lesion which gradually got bigger.
Pertinent findings on examination were raised hyperkeratotic plaque 5 x 3 cm
on the medial border of the dorsum of the right foot. It has a verrucous
surface with blackish dots. Regional nodes were not palpable.
Clinically he has chromoblastomycosis of the right foot.
A biopsy was done and the epithelium shows marked acanthosis with elongation
of rete ridges and intraepithelial collections of neutrophils. The dermis is
densely infiltrated by lymphocytes, plasma cells and few neutrophils.
Culture of organism was not done.
I may repeat the biopsy and perform fungal culture.
I plan to treat him with liquid nitrogen together with some combination
therapy with antifungals: itraconazole 100mg bd ( 200mg bd??) for several
months together with another antifungals. 5FU or IV amphotericin.
Would appreciate your comments on this patient.
Saturday, April 26, 2008
No Man is an Island
Thallium poisoning with skin manifestations
Presented by Professor Khalifa Sharquie
Baghdad, Iraq
History: A few weeks ago, an outbreak of thallium poisoning occurred in Baghdad and all of the patients had positive tests for thallium. We had the opportunity to see cases with skin manifestations. All patients gave a history of eating cakes and presented to hospital with nausea, vomiting followed by mental and peripheral neurological complaints. The case I am presenting was that of a 30 yo adult male referred to me two weeks after poisoning. He had severe hair loss, both diffuse and patchy, affecting mainly scalp and body hair. Also he had a non-pruritic rash affecting the face, limbs and groins.
O/E: The striking findings were severe anagen hair loss, diffuse and in patches. The hairs were easily plucked and microscopically were typical anagen phase. The next important finding was dermatitis-like picture that covered the face especially around the mouth and the limbs mainly on the dorsae of both hands. The groins had intertrigo simulating tinea cruris. The rash was dusky red and ecchymotic in appearance.
Photographs:
This picture was strange enough to make one think about the following Differential Diagnosis:
Acquired zinc deficiency
Pellagra
Erythema multiforme
But only suspicion can lead you into right diagnosis. Accordingly, before the definite diagnosis was established, we gave oral zinc sulfate 100mg 3 times a day for some patients. Surprisingly they recovered and resolved.
Reason Presented: Thallium is nice rat poison since it is colorless, tasteless and odourless. It can be used as massive lethal chemical weapon and is practiced this way in Iraq as a way to kill people. It is my opinion that thallium should be prohibited and considered as a chemical weapon like nitrogen mustard. It is better to let rats run free than to kill human beings.
Reference: A good article on this subject appeared in the Archives of Dermatology in January, 2007. Short-term thallium intoxication: dermatological findings correlated with thallium concentration.
Arch Dermatol. 2007 Jan;143(1):93-8.
Lu CI, Huang CC, Chang YC, Tsai YT, Kuo HC, Chuang YH, Shih TS.
Department of Dermatology, Chang Gung Memorial Hospital, Taipei, Taiwan.
One can view this free online: Arch Dermatol article
Comment: John Donne wrote: "All mankind is of one author, and is one volume; when one man dies, one chapter is not torn out of the book, but translated into a better language; and every chapter must be so translated....No man is an island, entire of itself...any man's death diminishes me, because I am involved in mankind; and therefore never send to know for whom the bell tolls; it tolls for thee."
Our Western civilization began in the Fertile Crescent. Iraq was at the epicenter. The strory told here diminishes all of us. Professor Sharquie bravely bears witness as he helps and serves his people.
Presented by Professor Khalifa Sharquie
Baghdad, Iraq
History: A few weeks ago, an outbreak of thallium poisoning occurred in Baghdad and all of the patients had positive tests for thallium. We had the opportunity to see cases with skin manifestations. All patients gave a history of eating cakes and presented to hospital with nausea, vomiting followed by mental and peripheral neurological complaints. The case I am presenting was that of a 30 yo adult male referred to me two weeks after poisoning. He had severe hair loss, both diffuse and patchy, affecting mainly scalp and body hair. Also he had a non-pruritic rash affecting the face, limbs and groins.
O/E: The striking findings were severe anagen hair loss, diffuse and in patches. The hairs were easily plucked and microscopically were typical anagen phase. The next important finding was dermatitis-like picture that covered the face especially around the mouth and the limbs mainly on the dorsae of both hands. The groins had intertrigo simulating tinea cruris. The rash was dusky red and ecchymotic in appearance.
Photographs:
This picture was strange enough to make one think about the following Differential Diagnosis:
Acquired zinc deficiency
Pellagra
Erythema multiforme
But only suspicion can lead you into right diagnosis. Accordingly, before the definite diagnosis was established, we gave oral zinc sulfate 100mg 3 times a day for some patients. Surprisingly they recovered and resolved.
Reason Presented: Thallium is nice rat poison since it is colorless, tasteless and odourless. It can be used as massive lethal chemical weapon and is practiced this way in Iraq as a way to kill people. It is my opinion that thallium should be prohibited and considered as a chemical weapon like nitrogen mustard. It is better to let rats run free than to kill human beings.
Reference: A good article on this subject appeared in the Archives of Dermatology in January, 2007. Short-term thallium intoxication: dermatological findings correlated with thallium concentration.
Arch Dermatol. 2007 Jan;143(1):93-8.
Lu CI, Huang CC, Chang YC, Tsai YT, Kuo HC, Chuang YH, Shih TS.
Department of Dermatology, Chang Gung Memorial Hospital, Taipei, Taiwan.
One can view this free online: Arch Dermatol article
Comment: John Donne wrote: "All mankind is of one author, and is one volume; when one man dies, one chapter is not torn out of the book, but translated into a better language; and every chapter must be so translated....No man is an island, entire of itself...any man's death diminishes me, because I am involved in mankind; and therefore never send to know for whom the bell tolls; it tolls for thee."
Our Western civilization began in the Fertile Crescent. Iraq was at the epicenter. The strory told here diminishes all of us. Professor Sharquie bravely bears witness as he helps and serves his people.