A randomized, open-label, multicenter trial of topical tacrolimus for the treatment of pruritis in patients with atopic dermatitis.

Background: Pruritis caused by atopic dermatitis (AD) is not always well controlled by topical corticosteroid therapy, but use of tacrolimus often helps to soothe such intractable pruritis in clinical settings.

Objective: To determine the anti-pruritic efficacy of topical tacrolimus in treating AD in induction and maintenance therapy.

Methods: Prior to the study, patients were randomly allocated into two groups, induction therapy followed by tacrolimus monotherapy maintenance, and induction therapy followed by emollient-only maintenance.

[A fatal case of drug-induced hypersensitivity syndrome due to allopurinol].

A 83-years-old Japanese woman visited our hospital, complaining of fever, erythema over the entire body and erosion on the lips after taking allopurinol for a month. Laboratory examinations showed liver dysfunction and renal failure. The histological study showed dense lymphocytic and eosinophilic perivascular infiltrations in the upper dermis at the erythematous lesion.

The IL-6 family cytokines, interleukin-6, interleukin-11, oncostatin M, and leukemia inhibitory factor, enhance mast cell growth through fibroblast-dependent pathway in mice.

Mast cell hyperplasia is observed in various inflammatory skin diseases. Although the mechanisms involved in the pathogenesis of these conditions remains largely uninvestigated, it is speculated that mediators produced in the lesional skin provide a favorable microenvironment for mast cell growth. Among the proinflammatory mediators, leukemia inhibitory factor (LIF), which shares a receptor component (gp130 subunit) with interleukin-6 (IL-6), has been identified as a mast cell growth-enhancing factor produced by cells of the keratinocyte-derived cell line (KCMH-1).

Leukemia inhibitory factor enhances mast cell growth in a mast cell/fibroblast co-culture system through stat3 signaling pathway of fibroblasts.

Leukemia inhibitory factor (LIF) enhanced mast cell growth in a mast cell/3T3 fibroblast co-culture system, however the precise mechanisms have not been defined. Western blot analysis showed that bone marrow-derived mast cells failed to express both LIF receptor (LIFR) and gp130, whereas 3T3 fibroblasts expressed both LIFR and gp130. This result indicates that the activity of LIF for mast cell growth is mediated by 3T3 fibroblasts.