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Objective A number of open-label studies have suggested the potential benefit of rituximab (RTX) in systemic lupus erythematosus (SLE). However, in 2 recent randomized controlled trials (RCTs) of RTX, the primary end points were not met. We undertook this study to evaluate the safety and efficacy of RTX in off-trial patients with SLE seen in regular clinical practice. Methods We analyzed prospective data from the French AutoImmunity and Rituximab (AIR) registry, which includes data on patients with autoimmune disorders treated with RTX. Results One hundred thirty-six patients received treatment for SLE. The mean ± SD score on the Safety of Estrogens in Lupus Erythematosus: National Assessment (SELENA) version of the SLE Disease Activity Index (SLEDAI) was 11.3 ± 8.9 at baseline. Severe infections were noted in 12 patients (9%), corresponding to a rate of 6.6/100 patient-years. Most severe infections occurred within the first 3 months after the last RTX infusion. Five patients died, due to severe infection (n = 3) or refractory autoimmune disease (n = 2). Overall response was observed in 80 of 113 patients (71%) by the SELENA–SLEDAI assessment. Efficacy did not differ significantly between patients receiving RTX monotherapy and those receiving concomitant immunosuppressive agents (who had higher baseline disease activity). Articular, cutaneous, renal, and hematologic improvements were noted in 72%, 70%, 74%, and 88% of patients, respectively. Among responders, 41% experienced a relapse of disease, with a response in 91% after retreatment with RTX. Conclusion Data from the AIR registry show a satisfactory tolerance profile and clinical efficacy of RTX in patients with SLE. The contrasting results with those from recent RCTs leave open the question of the therapeutic use of RTX in SLE. Additional controlled studies with new designs are needed to define the place of RTX in the therapeutic arsenal for SLE.

Objective Recent studies have shown that in vitro endothelial cells are activated by antiphospholipid antibodies and may support leukocyte adhesion. We studied levels of soluble intercellular adhesion molecule 1 (sICAM-1, sCD54), soluble vascular cell adhesion molecule 1 (sVCAM-1, sCD106), and soluble E-selectin (soluble endothelial leukocyte adhesion molecule 1 [sELAM-1, sCD62E]) in sera from patients with primary antiphospholipid syndrome (primary APS), and compared them with those from patients with systemic lupus erythematosus–associated APS (SLE-APS) or pure SLE, as well as with those from 2 control groups composed of healthy volunteers and patients with thrombosis unrelated to autoimmune diseases. Methods Serum samples from 24 patients with primary APS, 15 patients with SLE-APS, 22 patients with pure SLE, 48 control patients with thrombosis, and 18 healthy volunteers were examined using enzyme-linked immunosorbent assays specific for sICAM-1, sVCAM-1, and sELAM-1. Results Serum levels of sVCAM-1, but not sICAM-1 or sELAM-1, were significantly increased in all patient study groups compared with thrombosis control patients and healthy volunteers, but did not differ between the groups of patients with primary APS, SLE-APS, or pure SLE. Concentrations of sVCAM-1 were significantly higher in primary APS or SLE-APS patients with severe, recurrent thrombosis and were negatively correlated with platelet counts in primary APS patients. In patients with primary APS, sVCAM-1 levels were higher if there was thrombotic kidney involvement and correlated with creatinemia. Conclusion Serum sVCAM-1 concentrations are increased in patients with primary APS, especially those with repeated thrombotic events or kidney involvement. These findings suggest that endothelial/monocyte interaction may be important in the pathogenesis of primary APS.

Objective. To characterize muscle metabolic anomalies associated with polymyalgia rheumatica (PMR) using P-31 magnetic resonance spectroscopy (MRS). Methods. Seventeen patients with PMR and 9 age-matched control subjects were investigated. The forearm flexor muscles were examined by P-31 MRS in a 4.7 T superconducting horizontal magnet (Biospec Bruker 47/30) during a rest-exercise-recovery protocol. The intracellular pH and the relative concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), ATP, and phosphomonoesters were measured every minute during the protocol. Based on the PCr and pH timedependent changes during exercise and recovery, the rates of ATP production from PCr hydrolysis, glycogenolysis, and aerobic metabolism were calculated for each minute of exercise. Results. At rest, the metabolic parameters [PCr]: [Pi], pH, and [PCr]:[ATP] were not significantly different between the PMR patients and the control subjects. During exercise, the energetic cost and the contribution of anaerobic and oxidative pathways to energy supply were similar in the 2 groups, as were the recovery kinetics of the phosphorylated compounds and pH. Conclusion. Muscle MRS does not confirm the findings of histologic and biochemical studies that suggest an alteration of mitochondrial function in PMR. No other modifications in glycolytic or glycogenolytic pathways or in proton handling were found that could indicate an alteration of muscle energetics in patients with PMR.

We report a case of fibromyalgia occurring after hypophysectomy for Cushing's disease. Clinical examination revealed tender points at 12 of the 18 tender point sites described in the American College of Rheumatology 1990 criteria for the classification of fibromyalgia. The cause of fibromyalgia remains unknown. In our patient, hypophysectomy may have played a role by disturbing endorphin secretion and pain modulation.