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.

We have evaluated the incidence of lupus erythematosus (LE)-specific skin disease in 186 patients with LE, seen retrospectively over a 10-year period at our Dermatology Department and determined the correlation of LE-nonspecific skin disease in patients with systemic involvement. Chronic cutaneous LE (CCLE) with classical discoid lesions (localized, 70%; generalized, 30%) was the most common cutaneous manifestation (72.5%). Subacute cutaneous LE (SCLE) represented only 8% of LE skin disease (annular-polycyclic type, 73%; papulo-squamous type, 27%). Acute cutaneous LE (ACLE) was detected in 15% of our patients: the butterfly erythema was the most frequent skin lesion (96%) while only one case of bullous LE and one case of widespread maculo-papular eruption in association with malar erythema were demonstrated. In 8 patients no LE-specific skin lesions (lupus sine lupo) were found. LE-nonspecific skin lesions were found in 31% of our patients with systemic LE (SLE): Raynaud's phenomenon was found in 23/58 (39.6%), cutaneous small vessel leukocytoclastic vasculitis in 8/58 (13.7%), nonscarring alopecia in 18/58 (31%), lupus pernio in 6/58 (10.3%), hemorrhagic lesions in 4/58 (6.8%), livedo reticularis in 5/58 (8.6%), mucosal ulcers in 3/58 (5.1%) and periungual telangiectasia in 12/58 (20.6%) SLE patients. LE-nonspecific skin lesions are detected only in patients with SLE and usually in the active phases of the disease.

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.

Scarring alopecia is a very frequent feature of chronic discoid lupus erythematosus (DLE). So far in the literature, only clinic-pathologic features or histopathologic-immunopathologic traits of DLE scarring alopecia (DLESA) have been reported. We describe the most significant features of clinical morphology, histopathology, serum and tissue immunopathology of 36 DLESA patients (41.9% of all our scarring alopecia patients). Clinically, 33.3% presented a single lesion and 52.7% presented multiple lesions of scarring alopecia, while 13.8% exhibited a picture resembling Pseudopelade of Brocq, with the classic 'footprints in the snow' appearance. The most frequent morphologic features were sclero-atrophy (80.5%) and erythema (63.8%). The main histopathologic aspects appeared to be fibrosis (100%), follicular hyperkeratosis (91.4%), epidermal atrophy (88.5%), lymphocytic infiltrate (88.5%), thickened basement membrane (77.1%) and basal vacuolar degeneration (74.2%). Antinuclear antibodies were present in 42.8% of patients and antigastric mucosa, antithyroid and anticardiolipin antibodies in 17-21% of patients. A positive lupus band test was demonstrated in 81.8% of cases and perivascular deposit in 30.3% of patients. Histopathology alone allowed a correct diagnosis only in 68.5% of cases; in the other cases, the diagnosis was assessed also taking into account immunopathologic findings. Our study defines the clinic, histopathologic and immunopathologic features of DLESA patients and points out that a multiparametric approach is mandatory to assess the diagnosis of DLESA.

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These data suggest that an inflammatory infiltrate is involved in the production of PG bullous lesions. In particular, we assume that the Th2 cells might be implicated in the very early stages of autoimmune response and may exercise a broad influence in blister formation in this disease.