Publications by authors named "Conleth A Egan"

Background: Wells syndrome is an uncommon inflammatory dermatosis first described in 1971 by Wells. The clinical eruption is characterized by varying morphology and severity and usually follows a relapsing remitting course. The majority of the reported cases are of unknown etiology, drug induced Wells syndrome has rarely been reported.

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A 27-year-old woman presented with linear, flesh-colored papules along her vermillion borders, 4 years after a cosmetic lip tattoo was applied. A biopsy of the lesion was performed and histology showed it to be a granulomatous reaction surrounding the tattoo pigment. Following the biopsy, the lesions began to resolve spontaneously within 4 weeks and were not noticeable at a follow-up review.

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A 65-year-old man presented with a history of multiple skin coloured papules on his face that were asymptomatic. He had an adenocarcinoma resected from his proximal colon 12 years prior to presentation as well as a family history of colon cancer on the maternal side. Diagnostic biopsies showed the lesions to be sebaceous adenomas and epitheliomas and the diagnosis of Muir-Torre syndrome was made.

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A 59-year-old woman undergoing narrowband UVB phototherapy for treatment of psoriasis presented suddenly with tense blisters on both hips. The blisters were asymptomatic and disappeared within 24 hours. Histopathology together with a negative porphyrin screen made the diagnosis of pseudoporphyria.

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A 67-year-old man presented with a history of lymphadenopathy, fevers and separate skin eruptions of erythrodermic spongiotic dermatitis initially and subsequent toxic epidermal necrolysis. Initial lymph node biopsies showed non-specific granulomatous changes, and skin biopsies and bone marrow aspirate were not diagnostic. His toxic epidermal necrolysis responded well to 3 days of intravenous immunoglobulin.

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A 23-year-old man presented with an atrophic lesion on his left anterior shoulder that had been present for at least 10 years. A previous biopsy had suggested a fibrohistiocytic origin; however, clinically it resembled morphoea or atrophoderma, and the lesion was observed. Fifteen months later, the lesion was noted to have grown slightly.

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We report the clinical and immunopathologic findings in a cohort of 35 patients with anti-epiligrin cicatricial pemphigoid (AECP). These patients have a mucosal predominant subepithelial blistering disease that is clinically indistinguishable from other forms of cicatricial pemphigoid. The mucosal surfaces of the mouth and eye are most commonly involved.

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Anti-p200 pemphigoid is a recently defined subepidermal immunobullous disease. It is characterized by the binding of circulating IgG autoantibodies to the dermal side of 1 M NaCl split skin and by reactivity of these autoantibodies to a unique 200-kd antigen on immunoblot of dermal extract. On immunoelectron microscopic examination, these autoantibodies deposit at the lamina lucida-lamina densa interface.

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