A 67-year-old woman with rheumatoid arthritis (RA) treated with systemic prednisolone and methotrexate over 20 years developed eruptive molluscum contagiosums on the trunk and extremities. Investigation revealed lung cancer 2 years later. Newly development of molluscum contagiosums ceased after the surgical operation of lung cancer. Immunologic dysfunctions have been shown in RA, and especially patients under long-term methotrexate therapy are susceptible to miscellaneous skin conditions. Eruptive molluscum contagiosums are induced in association with hematologic malignancies such as lymphoma, leukemia, and HIV infection; however, it is important to investigate internal malignancies, not only hematologic malignancies but also solid cancers, when patients with RA under immunosuppressive therapies presented eruptive or disseminated molluscum contagiosums.

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Transforming growth factor-β1 (TGF-β1) has been thought to play a key role in the pathogenesis of scleroderma; however, therapeutic approaches targeting TGF-β1 and/or related molecules have provided inconsistent results. In this study, we demonstrate the antifibrotic effects of local administration of latency-associated peptide (LAP), a linker propeptide that specifically converts the active form of TGF-β1 to the inactive from, in the bleomycin (BLM)-induced scleroderma mouse model. Histologically, co-injection of BLM and LAP into the dorsal skin prevented proinflammatory and later sclerotic responses, features seen in mice injected with BLM alone or together with PBS as control. In addition, the skin sites co-injected with BLM and LAP showed a marked decrease in mast cell infiltration. Isoform-specific ELISA and real-time RT-PCR revealed transient decreases in connective tissue growth factor and collagen α1(I) mRNA expression 2 weeks after the co-injection, preceded by a decrease in active TGF-β1 protein production. In contrast, the baseline expression of TGF-β1 mRNA remained unchanged. By contrast, after induction of scleroderma by BLM, the inhibitory effects of LAP did not occur, suggesting time course-dependent TGF-β1 regulation. Our data may have novel therapeutic implications regarding in vivo TGF-β1 inactivation in human scleroderma, and the post-transcriptional interrelationship between major fibrogenic cytokines in the autoimmune aspects of the disease.

4 Su arez-Amor O, P erez-Bustillo A, Ruiz-Gonz alez I, Rodr ıguez-Prieto MA. Necrobiosis lipoidica therapy with biologicals: an ulcerated case responding to etanercept and a review of the literature. Dermatology 2010; 221: 117-121. 5 Wakusawa C, Fujimura T, Kambayashi Y, Furudate S, Hashimoto A, Aiba S. Pigmented necrobiosis lipoidica accompanied by insulin-dependent diabetes mellitus induces CD163 proinflammatory macrophages and interleukin-17-producing cells. Acta Derm Venereol 2013; 93: 475-476. the rare co-occurrence of NL and psoriasis/PPP suggest that mechanisms other than Th17 may play an important role in the pathogenesis of NL, and further studies are necessary.

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