Patients with erythroderma often experience severe and highly debilitating pruritus. Despite numerous treatment options, control of pruritus is difficult. Recent studies of pruritus hypothesize a local origin caused by several proinflammatory cytokines and neuroinflammatory mediators.1 Although the precise nature of tumor necrosis factor α (TNF-α) in pruritus remains unclear, it may underlie many of the key steps of inflammatory pathways that lead to induction and maintenance of the condition. Tumor necrosis factor α is produced by the activation of transcription factor nuclear factor κB through numerous extracellular stimuli mediated via antigen-specific T- and B-cell receptors or immunomodulatory receptors such as CD40.2 Because etanercept is a TNF-α–antagonist fusion protein that neutralizes TNF-α by direct binding, it is regarded as a potent anti-inflammatory agent. Most recently, a study of 12 patients reported positive responses with etanercept use in the early stage of relapsed cutaneous T-cell lymphoma.3 Using this agent, we observed a rapid and marked improvement of severe pruritus in 2 patients with idiopathic erythroderma suggestive (but nondiagnostic) of cutaneous T-cell lymphoma.
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Effect of treatment with etanercept on erythroderma, lichenification, and excoriation in patient 2. A, Before treatment; B, during treatment.
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