The plasma of two patients with heparin-induced thrombocytopenia has been shown to cause platelet aggregation in the presence of heparin. The platelet aggregating factor was isolated in the IgG reaction of the patients' sera suggesting that it was an antibody. This heparin anti-platelet antibody (HAP-Ab) induced platelet aggregation and release but did not cause platelet lysis, although it fixed complement. Platelet aggregation was inhibited by EDTA and by inactivation of complement. There was a significant production of malondialdehyde (MDA) and thromboxane B2 (TXB2) implying a role of the prostaglandin synthesis pathway in HAP-Ab induced aggregation. ADP-release also appeared to be involved as apyrase blocked aggregation while hirudin, a thrombin inhibitor, had no effect. The thrombotic complications that have recently been reported in patients with heparin-induced thrombocytopenia may be explained by some effects of HAP-Ab on platelets, namely: the antibody mediated platelet factor 3 release, prostaglandin endoperoxides and thromboxane A2 (TXA2) production and platelet aggregation in vivo. These HAP-Ab mediated effects could be inhibited by anti-platelet drugs such as aspirin, indomethacin and dipyridamole and thus may have therapeutic implications.

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SUMMARY In eight obese subjects the initially low level of fibrinolytic activity increased after significant weight reduction. Reduction to a normal weight resulted in normal fibrinolytic activity, which was maintained when an isocaloric diet was resumed. Subsequent weight gain in two subjects caused a return of fibrinolytic activity to its initially low level. Overall, the ultimate level of fibrinolysis achieved was closely related to the degree of obesity. The changes in fibrinolysis appeared to be unrelated to changes in plasma levels of fibrinogen, triglyceride, cholesterol, free fatty acids and glucose.

SUMMARY Multiple anthropometric measurements, which included those of weight, height, skinfold thickness, bone diameters and limb circumferences, together with estimations of creatinine excretion, were performed on 52 male and 42 female healthy subjects, both obese and of normal weight. Fat mass was estimated from two equations, which had been derived by previous workers from measurements of body density, and combined total body water content and body density. One was based on weight and skeletal measurements, and the other on the iliac crest circumference and triceps skinfold thickness. It was shown that there was close agreement between these two estimates, even in very obese subjects, thus extending the observations made by the original authors. When the mean of these two values was used as the reference value for fat mass, it was found that the latter could be simply predicted in both sexes from weight/height2 and percentage ideal weight calculations and in males from iliac crest circumference. The error of prediction was less than 6·8 kg. (twice the S.D.). Prediction was better (error less than 5·2 kg.) in both sexes using both weight/height2 and the iliac crest circumference. Skinfold thicknesses were of less value in predicting fat mass. These conclusions only apply to Western populations of this type of body build, in whom fat is almost exclusively responsible for variations in bulk. In interracial studies, skin fold measurements may give a better estimate of relative obesity. With creatinine excretion as our index of muscle mass, we found that no body measurement was of value in estimating muscularity. The best parameter was fat‐free weight, but this was of poor value, especially in obese males. It emphasizes that muscle forms a very variable proportion of fat‐free weight. To obtain a reliable estimate of muscularity in population studies it appears essential to estimate creatinine excretion.

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