Psoriasis during therapy with olanzapine.

The role of several drugs (lithium, betablockers, clonidine, digoxin, nonsteroidal anti-inflammatory agents, interferon and tetracyclines) in inducing or exacerbating psoriasis is not completely understood. We report two cases of psoriasis in patients treated with olanzapine, a new drug used for psychotic disorders. In the first patient worsening of a pre-existing mild psoriasis occurred shortly after starting olanzapine treatment, followed by a relapse of the dermatological disease after a new administration of the anti-psychotic drug. In the second case we observed the onset of psoriasis during olanzapine treatment in an individual without any previous history of psoriasis but with a family history of the disease. Although the mechanism by which psoriasis may be induced or exacerbated by olanzapine remains unknown, these observations underline the need for caution and close follow-up in the pharmacological management of patients with psoriasis or a family history of the disease.

Human papillomavirus type 5 in primary keratinocytes from psoriatic skin.

The role of human papillomaviruses (HPVs) in the pathogenesis of psoriasis is uncertain, and it has been postulated that the virus can act as a putative superantigen or it is activated from a latent status by inflammatory cytokines. To determine the involvement of HPV in the pathogenesis of psoriasis, primary cultures of keratinocytes from psoriatic lesions were analysed for the viral presence and for the production of inflammatory cytokines. Biopsies were taken from psoriatic lesions of 11 patients and from healthy donors undergoing plastic surgery. HPV DNA/RNAs were detected by nested polymerase chain reaction methods. The secretion of interleukin-6 (IL-6), IL-8 and IL-18 was determined in the conditioned medium by commercial enzyme-linked immunosorbent assay kits. Sixty-four per cent of the psoriatic keratinocytes were positive to HPV type 5 (HPV5), whereas no normal samples showed the presence of viral sequences. In the corresponding paraffin-embedded sections, multiple infection by HPV5 and HPV1 was detected. Comparable results in the production of inflammatory cytokines were obtained from HPV-infected vs. non-infected cell cultures. Specific HPV5 mRNAs were detected in the keratinocytes in the absence of cytokine stimulation, indicating that the expression of the viral genome may not be a consequence of the activation of the viral promoter by cytokines. The results are suggestive of an involvement of HPV5 in the psoriasis and reinforce the hypothesis that the replication of this virus in the psoriatic keratinocytes may cause the epidermal hyperproliferation as well as the antigen stimulation, which induces autoimmune phenomena.