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SummaryApproximately 14% of transfused hemophiliacs develop an anti-factor VIII inhibitory antibody which specifically neutralizes factor VIII procoagulant activity. In this study an association of the major histocompatibility complex (MHC) with inhibitor antibody formation was evaluated by restriction fragment length polymorphism (RFLP) analysis using BamHI, EcoRI, HindII, PstI, PvuII and TaqI digested genomic DNA probed with DP beta, DQ alpha, DQ beta and DR beta class II MHC gene probes. The RFLP patterns for 16 non-inhibitor and 11 inhibitor hemophiliac patients were analyzed. These 24 enzyme:probe combinations generated 231 fragments. Fifteen (15) fragments associated with the inhibitor phenotype; odds ratios ranged from 5.1 to 45 and lower bounds of 95% confidence intervals were > 1.000 for all 15 fragments. Five (5) fragments associated with non-inhibitors, with odds ratios ranging from 6.4 to 51.7. This report establishes a MHC related genetic basis for the inhibitor phenotype. No statistically significant differences in the distribution of serologically defined HLA-DR phenotypes were observed between the inhibitor and non-inhibitor groups.

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High fat diets were given ad libitum or force-fed to rats. The incidence of thrombosis in animals fed a cow butter diet was higher than in those fed a cocoa butter diet. No thrombosis was found in rats fed a diet containing peanut oil. Coagulation studies performed at weekly intervals on blood samples obtained from a tail vein of rats fed the diets ad libitum showed that there was a gradual but marked increase in the levels of Factors II, VII, and X of animals fed a diet containing cow or cocoa butter, but not one containing peanut oil. Several weeks prior to death, however, the level of all coagulation factors, including Factors I and V, fell. A significant prolongation of the values for the partial thromboplastin time was found in animals killed at the time when levels of plasma coagulation factors decreased. The pattern of changes in concentration of plasma coagulation factors was similar in the groups of animals dying with proven thrombosis and in those in which thrombosis was not found. All rats force-fed the above two diets died within two weeks, showing a marked fall in all coagulation factors and no thrombosis. Weight loss was more pronounced in the groups of animals fed the diet containing cow butter and cocoa butter than in animals fed Purina chow. Autopsy findings were: intra-ventricular thrombi with myocardial infarction, lung hemorrhage, pneumonia, and rarely jaundice. No cause of death other than inanition was discernible in some of the animals. Marked fatty infiltration of the liver was a feature of all animals autopsied.

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