Vitiligo is a skin disease that is caused by selective destruction of melanocytes and is characterized by white spots. Melanocytes and keratinocytes seem to exhibit a functional close relationship, mediated at least in part by keratinocyte-derived cytokines, which seem important for survival and activity of melanocytic cells. We wanted to investigate the hypothesis that in vitiligo the expression of epidermal cytokines may be modified compared with normal skin. In 15 patients with active, non-segmental vitiligo, biopsies were obtained from lesional, perilesional and non-lesional skin; normal skin from five healthy donors was also tested. Tissue sections were tested using immunohistochemistry for the expression of keratinocyte-derived cytokines with stimulating activity, such as granulocyte-monocyte colony stimulating factor (GM-CSF), basic fibroblastic growth factor (bFGF), and stem cell factor (SCF) or with inhibiting activity, such as interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-alpha) on melanocytes. Cytokine receptors and specific melanocytic markers were also investigated. No melanocyte was identified in lesional skin by means of specific markers or c-kit receptor, whereas in perilesional, non-lesional and healthy skin, melanocytes were found in similar number. In vitiligo skin a significantly lower expression of GM-CSF, bFGF and SCF was found, and a significantly higher expression of IL-6 and TNF-alpha was detected, compared with perilesional, non-lesional and healthy skin. In conclusion, we provided evidence that a significant change of epidermal cytokines exists in vitiligo skin compared with perilesional, non-lesional and healthy skin, suggesting that the cytokine production of epidermal microenvironment may be involved in vitiligo.

In conclusion, PB is a type of scarring alopecia of the scalp associated with a peculiar clinical presentation and evolution, which cannot be considered an autonomous nosologic entity because in 66.6% of patients it is the end stage of other inflammatory chronic diseases such as LPP and DLE. It is conceivable that even in those cases in which the histopathological and immunopathological findings did not allow for a specific diagnosis, LPP and DLE were also involved. It is noteworthy that in our study the histopathological and the immunopathological examinations did not conflict and often the results were even coincidental, thus confirming the compatibility of the combined histo-immunopathological approach in the diagnostic evaluation of PB.

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We describe a 5-year-old boy with red-pink, firm, nodular lesions, with central resolution and prominent borders, localized to the face, backs of the hands, extensor surfaces of the arms and legs, and the buttocks. He also had recurrent bacterial respiratory infections. Quantitative immunoglobulin levels revealed hypogammaglobulinemia and increased IgM levels. Histopathologic examination of a nodular lesion revealed perivascular and periadnexal granulomas composed of epithelioid cells surrounded by a mantle of lymphocytes; three cultures for fungi and acid-fast bacilli were negative. Clinical, histopathologic, and immunologic studies supported a diagnosis of hyper-IgM (HIM) syndrome. The boy was treated with pulsed-dose antibiotics and intravenous gamma globulin every 3 weeks, with improvement of clinical symptoms. Skin lesions were treated with topical corticosteroids, with immediate recurrence upon cessation of therapy. To the best of our knowledge, this is the first description of cutaneous granulomas in HIM syndrome.