[Allergic contact dermatitis to nickel: modification of receptor expression on peripheral lymphocytes of women after oral provocation tests (preliminary data)].

Blood lymphocyte subset evaluation was performed before after oral challenge with 10 mg of Ni, in 9 healthy women and in 15 allergic to Ni. Following challenge, 7 allergic showed a flare up of eczema and/or urticaria. In the controls, CD4+ lymphocytes were modified 24 hours after Ni challenge: CD4+/CD44RO- "virgin" cells were reduced while CD4+/CD45RO+ "memory" cells increased.

Intravenous immunoglobulins suppress the recurrences of genital herpes simplex virus: a clinical and immunological study.

Effective treatment is not currently available for suppressing the recurrence of genital herpes simplex virus (HSV) infections. Since intravenous immunoglobulins (IVIG) proved useful against HSV in experimental models, we treated patients with very high frequency of HSV genital recurrences (more than 15 episodes per year) with IVIG (400 mg/Kg every fourth week). The control group was treated with intermittent oral acyclovir (800 mg twice a day for one week every month).

[Immuno-histopathologic changes in the gastrointestinal mucosa in patients with nickel contact allergy].

The study concerns the histological and immunohistochemical findings of the gastrointestinal mucosa of 20 patients (group A) suffering from contact allergic dermatitis (CAD) to Ni, with symptom recrudescence due to food ingested Ni. Results were compared with those observed in 20 patients suffering from CAD to Ni (group B), without sensitivity to food ingested Ni, and in 20 normal subjects (controls). The sensitivity to food ingested Ni, as suggested by history, was demonstrated by placebo-controlled oral-Ni challenge.

Cyclical immunotherapy in patients with psoriasis.

Psoriasis, a chronic and unpredictable dermatosis, is a constant therapeutical challenge to dermatologists. However, new knowledge in immunodermatology has stimulated interest in and encourage the use of new molecules, especially cyclosporin A (CyA). Thanks to certain characteristics, this molecule is capable of modulating and blocking the intense network of cytochine that seems to cause this dermatosis.