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Stroger Cook County Hospital, March 2009 Chicago Dermatological Society______________________________________ Craig A. Elmets, MD Dr. Sidney Barsky Lecture John H. Stroger Jr. Hospital of Cook County Dr Elmets’ lecture is funded by the Chicago Dermatological Society ______________________________________________________________________________ 1 Chicago Dermatological Society______________________________________ ______________________________________________________________________________ 2 Chicago Dermatological Society______________________________________ TABLE OF CONTENTS Case Number Page 1. Harlequin ichthyosis 6 2. Erythema nodosum leprosum 8 3. Congenital cutaneous candidiasis 10 4. Prostatic adenocarcinoma with metastasis to the skin 12 5. Unknown # 1 14 6. Benign cutaneous polyarteritis nodosa 15 7. Disseminated discoid lupus erythematosus 19 8. Post-transfusion urticarial vascultis secondary to serum sickness 21 9. Borderline lepromatous leprosy 23 10. Unknown # 2 25 11. Unknown # 3 (video to be presented) 26 12. Exogenous ochronosis 27 13. Kaposi sarcoma 29 14. Primary systemic (AL type) amyloidosis 31 15. Atypical generalized herpes zoster without primary dermatomal involvement 34 16. Secondary syphilis with HIV co-infection 37 17. Epidermolytic hyperkeratosis 39 18. Chronic actinic dermatitis 41 19. Lymphocytic Sweet syndrome with associated acute myelogenous leukemia 43 20. Cutaneous cryptococcus infection 46 ______________________________________________________________________________ 3 Chicago Dermatological Society______________________________________ ______________________________________________________________________________ 4 Chicago Dermatological Society______________________________________ We extend our sincere thanks to Dr. Darryl Bronson and Dr. Jesse Jiang for their review of the histopathology from these cases. ______________________________________________________________________________ 5 Chicago Dermatological Society______________________________________ Key Locations: eyes, face, trunk, hands Case # 1 Presented by Victoria Negrete, MD and Warren Piette, MD History of Present Illness: This one day old neonate male was transferred to Stroger Hospital NICU after being delivered at an outside hospital to a 29 year old G2P1 mother at 38 weeks gestational age. The mother received prenatal care throughout her entire pregnancy, which was complicated by preeclampsia, gestational diabetes, and premature rupture of membranes. He was stable at the time of transfer. Past Medical History: None Medications/Allergies: Ampicillin, gentamycin, and acetaminophen. No known drug allergies. Family History: No family history of skin disorders. Parents are non-consanguineous. Physical Exam: General: neonate appropriate for gestational age, with reactive normal cry. Skin: scalp and body with firm platelike skin interrupted by deep fissures. HEENT: severe ectropion, severe eclabium, and hypoplastic malformed pinna with hyperkeratotic skin filling the external auditory canals. GU: rudimentary penis and scrotum, epispadias, and undescended testicles. Extremities: hypoplastic fingers and toes with mitten-like casing and distal cyanosis, hemorrhage, and erosion. Laboratory Data: The following were abnormal or positive: Hemoglobin 7.9 g/dL [13.5-22.0 g/dL] MCV 160.1 fL [88-120 fL] Platelets 108 k/uL [200-400 k/uL] Calcium 7.1 mg/dL [8.5-10.5 mg/dL] Potassium 3.1 mEq/L [3.5-5.0 mEq/dL] The following were normal or negative: Blood cultures, white blood cell count, BUN, and creatinine. Diagnosis: Harlequin ichthyosis Treatment and Course: The patient was placed in a high humidity chamber (90-95%) in reverse isolation. Petrolatum ointment was applied to his skin every two hours under loosely applied plastic wrap. He was closely followed for fluid and electrolyte imbalances by the primary NICU team. The prophylactic antibiotics were discontinued on day 5 of life. The ophthalmology service recommended lubricating ophthalmic drops and erythromycin ophthalmic ointment for management of his ectropion, but on day 10 of life he developed mucopurulent discharge with conjunctival injection. A conjunctival culture revealed multi- resistant Staphylococcus epidermidis and Escherichia coli. The erythromycin ointment was discontinued, and a triple antibiotic ointment and gatifloxicin drops were initiated with resolution of the discharge. ______________________________________________________________________________ 6 Chicago Dermatological Society______________________________________ Case # 1 continued By day 10 of life, much of the encasement on his trunk had sloughed and transitioned to diffuse erythema with clinical improvement in his ectropion and eclabium. The mitten like casing of his fingers and toes slowly sloughed with improvement in perfusion to the digits. He failed to gain weight, and his formula feeds were increased four-fold with supplemental nasogastric tube feeds. Given the natural sloughing of the plaques, systemic retinoids were not initiated. On day 29 of life, he developed few pustules on the right cheek, which were positive for hyphae and budding yeast on KOH examination. Nystatin cream was initiated with improvement of the lesions. Discussion: Harlequin ichthyosis (HI) is a rare, severe congenital ichthyosis presenting with ectropion, eclabium, flattened ears, and large plate-like scales with deep fissures affecting the entire body. The prognosis is very poor, with few neonates surviving beyond the first few weeks of life. HI is an autosomal recessive disease due to a deletion mutation in the ABCA12 gene, which encodes an ATP binding cassette protein that transports glucosylceramides from the Golgi apparatus into lamellar bodies. A missence mutation in the ABCA12 gene results in type 2 lamellar ichthyosis. Because few to no lipids are delivered to the stratum corneum, the epidermis compensates with an intense, hyperplastic response leading to thick plate-like encasement. This defect also results in a defective skin barrier, placing the neonates at increased risk of fluid loss, electrolyte imbalances, hypothermia, and sepsis. Of the few neonates who survive, they most commonly progress to a severe congenital ichthyosiform erythroderma. The ATP binding cassettes (ABCs) are a large group of proteins that transport different substrates across cellular membranes and are divided into seven subfamilies, A-G. The ABCA transporters function as cellular lipid-transporting organelles. ABCA transporter gene mutations are associated with disorders of lipid metabolism, including Tangier disease (ABCA1) and Stargardt disease (ABCA4), as well as neonatal surfactant deficiency, which has been associated with ABCA3 deficiency. Prior to 2001, only seven reported children with HI survived beyond one year of life. All had been on a systemic retinoid (isotretinoin in one, etretinate in five, and acitretin in one) for short or intermittent periods. Systemic retinoids have been shown to help slough the thick adherent plaques within weeks, as well as improve ectropion and eclabium. Anecdotal experience suggests that systemic retinoids may help prevent ischemia and autoamputation of the digits. Peroxisome proliferators-activated receptors (PPARs) are a potential therapy on the horizon for HI. PPARs have been shown to stimulate corneocyte envelope formation, stimulate epidermal lipid synthesis, accelerate LB secretion, and improve epidermal permeability barrier homeostasis. Recently, it has been shown that PPAR-γ induces ABCA12 mRNA expression in normal cultured keratinocytes, and may improve epidermal permeability barrier homeostasis in HI patients with residual ABCA12 expression. References: 1. Akiyama M. The pathogenesis of severe congenital ichthyosis of the neonate. J Derm Science 1999;21:96-104. 2. Elias PM, Williams ML, Holleran WM, et al. Pathogenesis of permeability barrier abnormalities in the ichthyoses: inherited disorders of lipid metabolism. J Lipid Res 2008;49:697-714. 3. Franco RC. Successful treatment of harlequin ichthyosis with acitretin. Int J Derm 2001;40:472- 3. 4. Jiang YJ, Lu B, Kim P, et al. PPAR and LXR activators regulate ABCA12 expression in human keratinocytes. J Invest Derm 2008;128:104-109. ______________________________________________________________________________ 7 Chicago Dermatological Society______________________________________ Key Locations: ears & extremities Case #2 Presented by Morayo Adisa, MD, Sidney Barsky, MD and Warren Piette, MD History of present Illness: A 23 year-old Mexican man with a 2-year history of borderline lepromatous leprosy presented to our clinic in 2004 with complaints of new recurrent cutaneous lesions despite treatment. He had completed 20 months of a two-year regimen of multidrug therapy including dapsone, rifampin and clofazamine prior to his visit. He denied any neurological symptoms. The new tender lesions were intermittent and were mainly on his legs, flanks and earlobes. Past Medical History: Borderline lepromatous leprosy Medications/Allergies: As above Family History: None Review of Systems: Intermittent fever, cough, and occasional wrist and ankle pain associated with the lesional flares Physical Exam: 07/04 Calves, left earlobe and abdomen: erythematous nodules Flanks: erythematous to violaceous reticulated patches 10/06 Trunk and extremities: slate-gray to brown patches 01/08 Earlobes: erythematous papules Thighs and legs: erythematous plaques Laboratory Data: The following were normal or negative (throughout 4 years): Complete blood count with differential, basic metabolic panel, liver enzymes
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