The American Journal of Hematology provides broad coverage of experimental and clinical features of blood diseases in humans and in animal models of human disease. The journal publishes original contributions in non-malignant and malignant hematological diseases including clinical and basic studies in hemostasis and thrombosis, immunology, blood banking, and stem cell biology. Clinical translational reports describing novel therapeutic approaches to diagnosis and treatment of hematological diseases are welcomed and encouraged. The journal includes regular original laboratory and clinical research articles, brief research reports, critical reviews, images in hematology, letters and correspondence.
Michael H. Rosove, P M Brewer, Alice Runge, Karim F. Hirji
AbstractLupus anticoagulants and/or anticardiolipin antibodies were detected in 100 patients with autoimmune disorders, thrombosis, or pregnancy loss. Significant agreement between tests for these two antipnospholipid activities was lacking. Performing both assays is thus important in maximizing the likelihood of detecting antiphospnolipids that may have clinical relevance.
Philip L. Cimo, Joel L. Moake, Ronald S. Weinger, Yoram Ben‐Menachem, Kamal Khalil
AbstractEleven 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 thrombocytopenic. 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.
Margaret V. Ragni, Jessica H. Lewis, Joel A. Spero, Ute Hasiba
AbstractThis report describes three patients with factor (F) VII deficiency: two adult siblings and an unrelated 5½‐month‐old child who succumbed after several central nervous system (CNS) hemorrhages. This event prompted a review of the literature concerning the incidence and characteristics of intracranial hemorrhage in congenital F VII deficiency.Of 138 patients reported to have F VII deficiency, only 75 were considered to have a true deficiency. There was a 1:1 sex distribution with a 19% incidence of consanguinity in the 63 families which these 75 patients represented.CNS hemorrhage occurred in 12 of the 75 proven factor‐deficient patients – an incidence of 16.0%. There was a 1.4:1 female predominance in this group, with a 44.4% incidence of consanguinity in their nine families. Except for one patient with hypertension, there was no history of preceding trauma or previous underlying CNS abnormality, though head trauma with a difficult vaginal delivery may have occurred in five infants. Diagnostic lumbar puncture or ventricular tap revealed bloody, xanthochromic cerebrospinal fluid in five.Five patients with F VII deficiency developed a CNS hemorrhage prior to 1 week of age, and none survived. Seven patients older than 1 week of age suffered such an event, and four of these survived. It is concluded that the greatest risk factor for development of CNS hemorrhage is trauma related to the birth process.
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