Summary. Venous thromboembolism (VTE) is a wellrecognized complication of autoimmune haemolytic anaemia (AIHA), and is a major cause of morbidity and mortality in this disorder. However, the incidence, pathogenesis and risk-factors for VTE in AIHA remain poorly defined. Lupus anticoagulants (LA) and anticardiolipin (ACA) antibodies are autoantibodies directed against epitopes on prothrombin or b2 glycoprotein I (b2-GPI). Both LA and ACA (together called antiphospholipid antibodies, APLA) are associated with VTE. We have prospectively studied the occurrence of VTE and APLA in 30 patients with AIHA. VTE was objectively documented in eight (27%) patients. APLA were detected in 19 (63%) patients with AIHA, of whom nine (30%) had a LA and 17 (57%) ACA. Seven patients had both LA and ACA. Among the eight patients with VTE, LA was detected in five (63%) and ACA in four (50%). There was a statistically significant association between presence of LA and occurrence of VTE (RR: 7AE50, 95% CI: 1AE25-45AE2, P ¼ 0AE03). VTE is a frequent and life-threatening complication of AIHA. Detection of the lupus anticoagulant in patients with AIHA identifies individuals at significantly increased risk for VTE. Future studies should address the role of prophylactic anticoagulation in patients with AIHA.

Objective We evaluated the effects of the B-cell activating factor (BAFF)-targeting antibody Belimumab on human nonmemory B-cell pools. Human B-cell pools were identified using surface markers adapted from mouse studies that specifically assessed reductions in immature B cells due to BAFF depletion. Patients with systemic lupus erythematosus (SLE) have high levels of both BAFF and immature B cells. Mechanistic mouse studies provide a framework for understanding human responses to therapies that target B cells. Methods Peripheral blood mononuclear cells were isolated from healthy donors and SLE patients on Belimumab or standard-of-care therapy (SCT). Cells were stained for flow cytometry to identify B-cell subsets based on CD21/CD24. Differences in subset proportions were determined by one-way ANOVA and Tukey’s post hoc test. Results Patients treated with Belimumab show alterations in the nonmemory B-cell pool characterized by a decrease in the Transitional 2 (T2) subset ( p = 0.002), and an increase in the proportion of Transitional 1 (T1) cells ( p = 0.005) as compared with healthy donors and SCT patients. The naïve B-cell compartment showed no significant differences between the groups ( p = 0.293). Conclusion Using a translational approach, we show that Belimumab-mediated BAFF depletion reduces the T2 subset in patients, similar to observations in mouse models with BAFF depletion.