Patients with SLE and LA are at approximately six times greater risk for VT than patients without LA, whereas patients with SLE and aCL are approximately two times greater risk for VT than patients without aCL. We have identified important methodologic limitations and differences in study characteristics. Other risk factors for VT have not been thoroughly evaluated in these studies. Further studies are needed that provide an accurate estimate of the absolute risk for aPL related VT.

Patients with systemic lupus erythematosus (SLE) and antiphospholipid antibodies (aPL) are at a greater risk for venous thromboembolism (VTE) than SLE patients without these antibodies. For patients without SLE there is a controversy about the risk associated with these antibodies and about their prognostic significance. We reviewed the degree of evidence and describe the odds ratio for VTE associated with aPL, namely the lupus anticoagulant (LA) and anticardiolipin antibodies (aCL), in patients without SLE. The study was a meta-analysis of seven observational studies of risk for antiphospholipid associated venous thromboembolism (VTE), excluding SLE patients. The strategies to identify published research included a computerized literature search and the review of citations in primarily relevant articles for the period 1983 to 1997. A summary of study characteristics and a critical appraisal of study quality were done. Summary odds ratios were obtained conducted using a random and a fixed effects-model. The overall odds ratio for aCL associated VTE obtained by fixed-effects model was 1.56 (95% CI, 1.10-2.24) and 1.64 (95% CI, 0.93-2.89) by random-effects model. The heterogeneity of these results appeared to be due in part to the detection limit of the aCL assay: the odds ratio was 3.21 (95% CI, 1.11-9.28) with both models when high titres only were considered. The overall odds ratio for LA associated VTE was 11.1 (95% CI, 3.81-32.3). In conclusion meta-analysis of the risk for antiphospholipid associated thrombosis demonstrated a higher risk in patients with the LA than in other patients. This risk was also higher than in patients with aCL even when high titres only were considered.

Several haematological and immunological parameters were studied before and after a 4-week trial of oral levamisole (300 mg/week) in 15 patients with chronic lymphocytic leukaemia. We found no statistically significant difference in the mean peripheral blood counts of total lymphocytes, E-rosette-forming lymphocytes, monocytes, polymorphonuclear neutrophils, eosinophils and platelets. Mean serum levels of IgG, IgA, IgM, IgD, C3 and C4 were not statistically affected by levamisole nor was the mean lymphocyte stimulation modified by various mitogens (phytohaemagglutinin, concanavalin A, pokeweed mitogen, tuberculin, candidin). The mean IgE level was statistically increased (p < 0.05) after levamisole administration but remained below the normal upper limit. A high rate (46%) of clinical and haematological adverse reactions (1 patient developed thrombocytopenia) was associated with levamisole administration. These results suggest that levamisole, as given in this trial, has no obvious beneficial effect and cannot be recommended in patients with chronic lymphocytic leukaemia.

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