Eleven patients with heparin-induced thrombocytopenia were studied. Thrombocytopenia appeared 3-16 days following the initiation of prophylactic or therapeutic doses of heparin. The mean lowest platelet count recorded was 48,000/mm3. When heparin was stopped, recovery from thrombocytopenia began within 24 hours and was complete by ten days. Two patients developed fatal thromboses, and two others had myocardial infarctions while thrombo-cytopenic. In the serum of seven patients, including three of the four with arterial thrombosis, a heparin-dependent platelet aggregating factor was present. The factor caused release of platelet 14C serotonin but did not lyse platelets. It was present in the globulin fraction of all positive sera, and in one serum studied it was isolated in the IgG/IgA immunoglobulin fraction. The factor was not present in 16 normal sera or in the sera of 15 nonthrombocytopenic patients receiving heparin. Our observations suggest that heparin-induced thrombocytopenia is common and that, in some patients it may be accompanied by severe arterial thrombosis. In vivo platelet aggregation is a possible explanation for the thrombocytopenia and the thrombosis in this disorder.

Two families are described with members who have both von Willebrand's disease and telangiectasias. Family A has four members in three consecutive generations that have both von Willebrand's disease and telangiectasias. von Willebrand's disease in this family is characterized by decreased ristocetin cofactor (FVIII-vWF), variably depressed factor VIII coagulant (FVIII-AHG), and factor VIII-related antigen (FVIII-AGN) levels. FVIII-AGN mobility on two-dimensional crossed immunoelectrophoresis was found to be normal. Four generations in Family B have von Willebrand's disease characterized by decreased FVIIII-AHG, FVIII-vWF, FVIII-AGN, and prolonged template bleeding times. Two members of this family also have telangiectasias and recurrent gastrointestinal bleeding. Results in these two families suggest an association between von Willebrand's disease and telangiectasia--perhaps a defect in vascular endothelial cell function.

A young male patient is described with acute leukaemia whose bone marrow and peripheral blood contained abundant cells of the eosinophilic series in all stages of maturation. These cells, proven histochemically to be true eosinophils, were abnormal in both maturation and proliferation. Upon electron microscopic study of bone marrow and peripheral blood, abnormalities in the eosinophilic series were identified as early as the promyelocytic stage as well as in the most mature eosinophil seen. The clinical and morphologic picture of this patient's disease raises the possibility of this being an acute eosinophilic leukaemia.

Eleven days after administration of multiple penicillin analogs, a 55-year-old female developed a Coombs-positive hemolytic anemia. The patient's erythrocytes were coated with IgG, complement components (C4/C3) and her serum contained elevated 125I-Clq binding activity (a measure of the presence of immune complexes). Her serum, in the presence of fresh complement and penicillin, induced complement sensitization of normal erythrocytes. Immune complex-mediated complement activation and the haptene type of erythrocyte sensitization accounted for accelerated red blood cell destruction in this patient.