Abstract
Transforming growth factor beta‐1 (TGF‐β1) is expressed in normal epidermis. TGF‐β1 potently inhibits keratinocyte proliferation and immunomodulatory properties, mainly by suppressing immune responses to self‐antigens. Lichen planus (LP) is a form of dermatitis caused by cell‐mediated immune dysfunction, but the exact pathogenic pathways are unknown, which poses therapeutic challenges. We report on a 68‐year‐old man who developed multiple pruritic, discrete, and well‐demarcated flat‐topped red‐purple papules and macules on the back and upper arms following 4 cycles of treatment with TGF‐β receptor I (TGFBR‐I) inhibitor; ly3200882; for metastatic chondrosarcoma. The biopsy showed hyperkeratosis, wedge‐shaped hypergranulosis, elongation of the rete ridges, and a dense band‐like lymphohistiocytic infiltrate admixed with colloid bodies and pigment incontinence, consistent with LP. Temporal correlation suggested that the TGFBR‐I inhibitor might be a trigger. Treatment with topical clobetasol and oral metronidazole led to partial resolution of the lesions with postinflammatory hyperpigmentation. We believe this is the first reported case of LP related to TGFBR‐I inhibitor therapy. This report expands the list of cutaneous adverse events associated with this novel class of targeted therapy. More importantly, this report supports emerging evidence that failure of TGF‐β1 activation/signal transduction is an important mechanism in the pathogenesis of LP and suggests the TGF‐β1 pathway as a potential therapeutic target in this disease.This article is protected by copyright. All rights reserved.
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