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Post-transfusion hyperhaemolysis syndrome (PTHS) is a rare life-threatening transfusion complication reported mainly in sickle cell patients. Its pathogenesis is poorly understood. Antibody-mediated haemolysis and bystander effect have been proposed as putative mechanisms, but in half of cases, red cell antibodies are undetectable, and PTHS develops despite transfusion of cross-matched compatible RBC. An alternate hypothesis proposes activated macrophages as the main drivers of red cell destruction through direct phagocytosis. We report the histopathological findings of two patients with PTHS showing extensive macrophage expansion and erythrophagocytosis, supportive of macrophage activation driving PTHS. This supports a possible role for novel therapies that target macrophage activation.

Antithrombin deficiency is identified as one of the most potent risk factors for venous thromboembolism during pregnancy. Therapeutic low molecular weight heparin is recommended, but it can be difficult to attain sufficient anticoagulation since low molecular weight heparin requires antithrombin to exert its anticoagulant effect. We carried out a multicentre case-series assessing the dose of low molecular weight heparin required to achieve therapeutic anti-activated factor X levels in pregnant women with antithrombin deficiency. We assessed 27 pregnancies in 18 women with severe antithrombin deficiency, which we defined as an antithrombin level of

Summary Twenty-six haemophilic patients with advanced HIV infection who had developed resistance or intolerance to zidovudine were treated with didanosine (ddI). 11 patients continue to take ddI at a median time of 14 months from commencement (range 7–18 months). Five of these patients showed an increase in CD4 lymphocyte count, reaching a maximum at a median time of 4 months. Four patients with HIV-related symptoms improved clinically. In general, the CD4 count and clinical improvements were not sustained. 11 patients discontinued ddI after a median of 3 months (range 3 days to 10 months), most commonly due to gastrointestinal side-effects. No case of pancreatitis or peripheral neuropathy was seen. Six patients, all with very advanced HIV disease, died. HIV-infected haemophilic patients who become resistant or intolerant to zidovudine may derive benefit from ddI, although this is usually transient.

The reliability of the international normalized ratios (INR) system in the induction phase of coumarin administration has been studied in 15 serial patients over the first 7-40 days of treatment (mean 13.1). The INR results obtained with a variety of thromboplastin reagents have been compared with those obtained with the WHO second primary IRP, BCT/253. A wide divergence of INR values was observed with the various thromboplastins on each day of testing. INR values cannot therefore be relied upon with some of these reagents in the early days of anticoagulant treatment. This probably arises from the difference in responses of the thromboplastins to depression of vitamin K-dependent clotting factors. Consistent deviations from the IRP suggested that additional error may be due to inaccurate calibration of their products by the manufacturers. When the slopes of the sensitivity of the individual reagents to clotting factors II, VII and X were compared, however, results overall more closely approximated to those of the IRP when the INR were substituted for simple prothrombin ratios.