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Objective: To verify the possible relationship between the presence of antiphospholipid antibodies (APLA) and the presence of epileptic seizures in patients with systemic lupus erythematosus (SLE)., Methods: A total of 168 patients with SLE were studied. Fifteen patients had antecedents of epilepsy which were non attributable to a cause other than SLE. Epilepsy was diagnosed on clinical and electroencephalographic grounds. Antibodies to cardiolipin (CLa) and lupus anticoagulant (LA) were measured., Results: Epileptic seizures were generalized in 13 and partial in two patients. The lupus anticoagulant was positive in 40% of patients with epilepsy compared to 32% in the control group; CLa IgG in 53.5% compared to 65.6%, and CLa IgM in 40% compared to 35.2%. Differences were never statistically significant. Neither when patients with moderate/high CLa levels were studied. Seven patients (40%) had some of the classical manifestations of antiphospholipid syndrome., Conclusions: No association was found between positive APLA and epilepsy in patients with SLE.

The prevalence of infection with VZV in 145 patients with SLE was investigated, with a mean follow-up of 7.6 years; its relationship with different variables, particularly with therapy of the underlying disease, was analyzed. Twenty episodes of VZV infection in 19 patients were diagnosed (13.1%). In no case was the therapeutic regime changed nor was worsening of SLE observed. There was neither dissemination of herpes nor superinfection. An increase in the number of VZV infections was observed in patients with SLE under corticosteroid therapy (p = 0.04) and particularly when drug administration was on a daily basis (p = 0.00006). Cytotoxic agents also favored the infection (p = 0.0014). VZV infection is of a benign nature in SLE and its emergence is favored by immunosuppressive agents. The risk is lower if corticosteroid administration is on alternate days. There is no need to decrease therapy for SLE.

Because doctors are reluctant to diagnose systemic lupus erythematosus (SLE) in elderly patients, the initial diagnosis in this age group is usually tardy. Furthermore, the presenting manifestations in these patients are commonly atypical. We describe a 72-year-old woman in whom chronic ascites with antiphospholipid antibodies was the initial predominant manifestation of subsequently fatal SLE. Only 13 cases of chronic lupus ascites have been reported in the English and French literature. Our patient represents the first case reported in an elderly person.

We analyzed the effects of interleukin 2 (IL 2) and IL 4 isolated and in association on the specific response of human B cells triggered by trinitrophenylated polyacrylamide beads (TNP-PAA). IL 2 induced an increase (more than 10 times) in the number of hapten-binding cells [detected by a rosette-forming cell (RFC) assay] as well as the generation of antibody-producing cells [detected by a plaque-forming cell (PFC) assay]. IL 4 induced an isolated RFC response without PFC response. We verified that the IL 4 (as well as 12)-induced RFC were hapten specific and mediated through membrane IgM. Density fractionation experiments showed that IL 4-induced RFC were equally distributed between high-density and intermediate-density B cells. IL 2 appeared to drive more B cells into the intermediate density fraction. IL 2-induced PFC belonged to the RFC population and were intermediate-size B cells. IL 2 drove more RFC into an activated stage and it induced the differentiation of a number of them into antibody-producing cells. The evaluation of the proportion of RFC able to incorporate thymidine showed that both IL induced a substantial proliferation of antigen-activated B cells. However, IL 4 inhibited the IL 2-dependent PFC without affecting the number of RFC nor the proportion of proliferating RFC induced by this IL. These results directly demonstrate that human IL 4 triggers the expansion of antigen-activated B cells and selectively inhibits the IL 2-induced differentiation.