Penicillamine-associated cutis laxa and milia en plaque - case report and review of cutaneous changes associated with penicillamine.

Penicillamine-induced skin changes are rare and include: hypersensitivity reactions, autoimmune reactions, and cutaneous elastoses. We report a case of a 73-year-old man with cystinuria taking penicillamine for over 50 years who presented with penicillamine-induced cutis laxa and milia en plaque. A brief review of penicillamine induced skin changes, specifically cutis laxa and milia en plaque, is presented.

Latanoprost-induced prostaglandin-associated periorbitopathy.

PURPOSE: To report, with supporting photo-documentation, cases of latanoprost-induced prostaglandin-associated periorbitopathy (PAP). CASE SERIES: Retrospective small case series with three cases. Chart review with photo-documentation of clinical features of prostaglandin-associated periorbitopathy resulting from latanoprost use. Patients developed involution of dermatochalasia, blepharoptosis, deepening of orbital sulci, and flattening of lower eyelid bags after a mean usage period of 6 years (3 to 8 years). CONCLUSIONS: Latanoprost can cause PAP, although it has a lower risk and longer latency of onset than those with bimatoprost and travoprost. Clinicians should be aware of this side effect and monitor for signs periodically. Chronic unilateral prostaglandin use may cause unfavorable asymmetry in the appearance of the periorbital area.

Toxic dermatolysis, tissue necrosis and impaired wound healing due to sunitinib treatment leading to forefoot amputation.

Innovative treatment strategies in urologic oncology confront the treating physician with a new spectrum of adverse events. With growing understanding of underlying pathomechanisms, we need to identify contraindications against the use of certain antiproliferative drugs. The management of toxicities involves a multidisciplinary approach and thus, the exchange of experience across medical specialties is mandatory. We report a case of fulminant toxic dermatolysis, tissue necrosis and impaired wound healing resulting in the amputation of one forefoot after 6 days of treatment with sunitinib.

Periorbital changes associated with topical bimatoprost.

PURPOSE: To describe periorbital changes induced by chronic topical therapy with daily bimatoprost 0.03% (Lumigan, Allergan Inc., Irvine, CA, U.S.A.). METHODS: A clinical investigation of 5 nonconsecutive patients with unilateral glaucoma treated daily with topical bimatoprost 0.03% for up to 4 years prior to presentation. RESULTS: In eyes treated with bimatoprost 0.03% the authors noted periorbital fat atrophy, deepening of the upper eyelid sulcus, relative enophthalmos, loss of the lower eyelid fullness, and involution of dermatochalasis compared with the fellow untreated eye. By inspecting old photographs the authors confirmed that these unilateral changes were not present prior to starting bimatoprost. In addition, these changes were partially reversible after discontinuation of the medication, whenever that was possible. In 2 cases imaging studies confirmed the clinical impression that these findings were not related to primary orbital pathology. CONCLUSIONS: Physicians and patients should be aware of the potential of bimatoprost 0.03% to produce periorbital changes.

Clinical and histological spectrum of elastotic changes induced by penicillamine.

A 79-year-old-man with cystinuria requiring long-term penicillamine therapy presented with a 6-month history of itchy annular lesions in both axillae. Clinical examination revealed lesions consisting of crusted keratotic papules coalescing in an annular distribution. Associated findings included generalized skin laxity accentuated on the upper trunk and arms, as well as small yellowish papules on the neck. Histological evaluation revealed short, thick, eosinophilic elastic fibres with nodular protrusions. Transepidermal elimination of abnormal elastic fibres was also evident. We discuss the histological and clinical spectrum of penicillamine-induced elastotic changes and compare these changes to those seen in primary elastotic disorders.

Acquired cutis laxa: case report and review of disorders of elastolysis.

A 10-year-old boy developed cutis laxa while receiving isoniazid therapy; no systemic manifestations occurred. There are several well-documented cases of acquired cutis laxa. We propose a classification of the elastolysis syndromes, including inherited, neonatal, and acquired forms of cutis laxa.

Fatal, penicillin-induced, generalized, postinflammatory elastolysis (cutis laxa).

A 13-year-old boy received penicillin for influenza and otitis media. Within days of taking this medication, he developed recurrent edema of the face and a generalized urticarial eruption which waxed and waned. The salient and unusual features of this person's disease were: 1) A senile appearance of his face with flaccid folds and sagging of the skin. Histopathologic findings were dense dermal inflammatory-cell infiltrates with numerous eosinophils and destruction of elastic fibers. Findings by electron microscopy were fragmentation and clumping of elastic fibers and accumulation of granular material in the dermis. 2) Dermatitis herpetiformis-like cutaneous lesions and gluten-sensitive enteropathy. 3) Elastolysis increased in time and led to further deterioration of the patient's physical appearance. Six years later, the patient developed severe internal manifestations and died. We assume that the inflammatory-cell infiltrates and prolonged edema following therapy with penicillin caused the dissolution of elastic tissue and resultant systemic elastolysis.

Studies of the mechanism of epidermal injury by a Staphylococcal epidermolytic toxin.

Experimental animal models of the two forms of toxic epidermal necrolysis have been reviewed: a murine model of staphylococcal-induced epidermolysis and a hamster model of graft-versus-host disease. In the former, a protein exotoxin, epidermolysin, has been purified and characterized. The exotoxin has a molecular weight of approximately 30,000 and causes a split beneath the granular layer. It is effective at 3 times 10(-12) moles. Epidermolysin does not require an intact complement system for its action since B10D2 mice deficient in C5 or mice injected with the decomplementing agent in cobra venom factor were susceptible to its epidermolytic effects. Neither are immunocompetent thymocytes required for the action of the toxin since hairless, athymic adult (nu/nu) mice are susceptible. A few reports of epidermolysis due to an exotoxin of group I Staphylococcus aureus have appeared. This toxin is antigenically different from the exotoxin of group II organisms. A model of drug-induced toxic epidermal necrolysis has been described in hamsters, but the toxic principle released from sensitized lymphoid cells has not yet been characterized.