Verrucous porokeratosis of the gluteal cleft (porokeratosis ptychotropica): a rare disorder easily misdiagnosed.

Porokeratosis represents a heterogeneous group of disorders characterized clinically by a distinctive ridge-like border and histologically by cornoid lamellae. A verrucous variant of porokeratosis involving the gluteal cleft has been recently described. We present 5 new cases and review the current literature to highlight the clinical and histopathologic features of this disorder. Descriptive terms including hyperkeratotic porokeratosis, genitogluteal porokeratosis, porokeratoma, follicular porokeratosis, and porokeratosis ptychotropica have all been used to describe this verrucous variant of porokeratosis involving the gluteal cleft. To avoid further confusion, we propose a consolidation of terminologies and suggest verrucous porokeratosis be added to the commonly described variants of porokeratosis.

Efalizumab therapy for atopic dermatitis causes marked increases in circulating effector memory CD4+ T cells that express cutaneous lymphocyte antigen.

Efalizumab is an mAb directed against CD11a, a molecule involved in T-cell activation and extravasation from blood into tissue. Ten patients with severe atopic dermatitis were treated with efalizumab for 84 days, and peripheral blood mononuclear cells were analyzed for expression of activation and adhesion markers. Efalizumab treatment led to decreases in CD11a mean fluorescence intensity (MFI) on naive, central memory, and effector memory CD4+ and CD8+ T cell subsets. MFI for CD18 was decreased in both CD4+ and CD8+ T cells. Percentages of cells positive for cutaneous lymphocyte antigen (CLA) were increased fourfold in all CD4+ and CD8+ T cell subsets. Increases in the percentages of CD4+ and CD8+ T cells expressing beta7 and CD49d were also observed. No significant changes were observed in the percentages of CD4+ and CD8+ T cells that produced either IFN-gamma or IL-4. In summary, efalizumab treatment resulted in (i) decreases in CD11a and CD18 expression in all circulating T-cell subsets and (ii) increases in the percentages of blood T cells expressing tissue homing markers (CLA, beta7, CD49d). These data suggest that blockade of T-cell extravasation into tissue is the major pathway by which efalizumab leads to improvement in cutaneous inflammation.