Human leukocyte antigen (HLA)-G is a non-classical HLA class I molecule that exerts a generalized immunosuppressive action. A deficit in membrane bound and soluble HLA-G levels seems to cause a defective control on immune responses and trigger off several autoimmune diseases. As psoriasis is considered an autoimmune disease, lower levels of soluble HLA-G (sHLA-G) might be expected in psoriatic patients than in healthy controls. The aims of this descriptive study were: (1) to evaluate whether sHLA-G levels are different in psoriatic patients compared to controls; (2) to compare sHLA-G levels between groups of patients treated with different therapies; (3) to evaluate whether any differences found in HLA-G expression could be related to a genetic control. Peripheral blood samples were investigated for sHLA-G and IL-10 levels and for HLA-G 14 bp polymorphism in 65 patients with moderate-to-severe plaque psoriasis treated with systemic drugs or with topical or physical treatments and in controls. Significantly lower plasma levels of both sHLA-G and IL-10 were found in psoriatic group compared to controls and in local treated patients in comparison with systemic treated patients. These findings could indicate that low sHLA-G levels may contribute to susceptibility to psoriasis. Absence of differences in HLA-G 14 bp allele and genotype frequencies between psoriatic patients and controls and between patients following different treatments seems to exclude genetic bases of sHLA-G levels. It could be speculated that therapeutics antagonizing systemic T helper 1 activation may induce sHLA-G secretion via an IL-10-dependent pathway.

We report the case of a 61-year-old woman who developed an anaplastic CD30+ cutaneous T-cell lymphoma during oral cyclosporine (CsA) therapy for recalcitrant psoriasis. Two months after CsA discontinuation, clinical and histological resolution of the lymphoma was observed. However, 3 years later extracutaneous involvement of the lymphoma could be detected. The association between CsA administration and the occurrence of the lymphoma may be casual, but a relationship with immunosuppression may also be hypothesized. We have reviewed all relevant data in the literature. To our knowledge, this is the first case of primary cutaneous CD30+ anaplastic large T-cell lymphoma in a patient treated with CsA for psoriasis.

The trunk and the limbs of an 82-year-old man were covered with large sheets of flat-topped erythematous papules arranged in a reticulate pattern which suddenly coalesced assuming erythroderma-like aspects. Body and positional folds were characteristically spared (deck chair sign). Mild eosinophilia was present. The histological and immunohistochemical examinations revealed an unspecific eczematous pattern. After systemic steroids and PUVA treatment the patient recovered from the dermatosis. Papuloerythroderma is a distinctive clinical entity, but it is not clear whether the dermatosis is the skin marker of systemic pathological conditions or a precursor of cutaneous lymphomas.

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