Jerusalem in the Arab Israeli conflict 1967-1998.

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Drug-induced red cell dyscrasias

Major advances have been made in recent years in our understanding of the pathogenetic mechanisms of drug-induced blood dyscrasias, particularly those involving the red cell. Among the latter, hemolytic anemia is the most common. Drug-induced red cell destruction may occur on an immune basis or through disruption by the drug of red cell metabolism. The immunological basis of drug-induced hemolysis is reviewed with emphasis on the clinical and laboratory manifestations, differential diagnosis and the major mechanisms involved. Drug-induced oxidative hemolysis both in normal individuals and in those with certain enzymopathies, notably glucose-6-phosphate dehydrogenase deficiency, is summarized. Drugs may also produce red cell dyscrasias by acting on the immature erythroid compartment. Some of these inhibit erythroid growth by as yet poorly understood mechanisms. Others exert more specific metabolic effects in erythroid precursors. These include drugs which interfere with DNA synthesis causing megaloblastic erythropoiesis and those which disrupt mitochondrial function and the synthesis of heme manifested by sideroblastic erythropoiesis. A brief consideration of heme biosynthesis and the action of drugs which are associated with sideroblastic anemia, including the antituberculous agents, lead, alcohol and chloramphenicol is presented. Finally, where pertinent, an updated listing of drugs involved in red cell dyscrasias is included

Case Report Glanzmann's Thrombasthenia Diagnosed following Knee Arthroscopy

A 41-year-old man with an unremarkable medical history presented with a painful knee after a sports injury. He was diagnosed with a medial meniscal tear. Symptoms did not abate after 6 months of physical therapy, and he underwent arthroscopic partial medial meniscectomy. A week after beginning physical therapy he experienced a knee effusion, decreased ROM, and inability to flex his quadriceps. His knee was aspirated. Blood tests were ordered and his complete blood count, liver functions tests, and INR/PTT were normal. The patient had recurrent effusions requiring three additional joint aspirations. Ten weeks after the initial surgery, the patient underwent a second arthroscopy, during which a hematoma was removed and a synovectomy performed. The patient continued bleeding from the incisions after portals were sutured, and he was admitted to the hospital. A hematologist was consulted and comprehensive platelet aggregation testing revealed previously undiagnosed Glanzmann's thrombasthenia. The patient began treatment with platelet infusions and desmopressin and progressed to a full recovery. Clinical suspicion for surgical patients with unusual repetitive postoperative bleeding should include previously undetected rare bleeding disorders even in adults