Eruptive SKs may be appreciated in 2 clinical circumstances: associated with an internal malignancy (Leser-Trélat sign), or secondary to an erythrodermic eruption. Flugman et al5 reported 2 cases of eruptive SKs in association with erythroderma. Their first patient developed erythroderma after initiating UVB therapy for psoriasis. The second patient developed an erythrodermic drug hypersensitivity reaction after switching to generic forms of quinidine gluconate and ranitidine. The SKs spontaneously resolved within 6 months and 10 weeks of the resolution of erythroderma, respectively.5 Most of our patient’s eruptive SKs resolved within a few months of their presentation, consistent with the time frame reported in the literature.
Telaprevir-related dermatitis presumably served as the inciting factor for the development of SKs in our patient, as the lesions improved after discontinuation of telaprevir despite continued therapy with ribavirin. As noted by Flugman et al,5 SKs may be seen in erythroderma due to diverse etiologies such as psoriasis, pityriasis rubra pilaris, or allergic contact dermatitis. We hypothesize that the eruption immunologically releases cytokines and/or growth factors that stimulate the production of the SKs. Fibroblast growth factor receptor 3 mutations have been associated with SKs.6 An erythrodermic milieu may incite such mutations in genetically predisposed patients.
We present a case of eruptive SKs related to telaprevir therapy. Our report expands the clinical scenarios in which the clinician can observe eruptive SKs. Although further research is necessary to ascertain the pathogenesis of these lesions, patients may be reassured that most lesions will spontaneously resolve.