Streptomycin-induced hemolytic anemia.

Introduction Two major mechanisms are generally implicated in drug-induced hemolytic anemia. (1) A genetically determined deficiency of erythrocyte glucose-6-phosphate dehydrogenase renders the red cell susceptible to the hemolytic action of certain ordinarily harmless drugs. This was first described in primaquine-induced anemia 1 and subsequently in anemia due to numerous other drugs. 2 (2) A drug-erythrocyte complex stimulates the production of antibodies which are capable of destroying the patient's erythrocytes in the presence of the drug. Stibophen (Fuadin) 3 was the first drug reported to cause hemolysis by this haptenlike action. Other drugs similarly implicated include quindine, 4 methylethylhydantoin ( Mesantoin), 5 phenacetin, 6 and aminosalicylic acid. 6 Other agents such as sodium taurocholate and saponin can cause hemolysis 7 apparently by a direct lytic action on the erythrocytes; this direct mechanism, however, is rarely of clinical significance. The following is the first reported case of streptomycin-induced hemolytic anemia, the mechanism of

[1]  J. Tullis The role of leukocyte and platelet antibody tests in management of diverse clinical disorders. , 1961, Annals of internal medicine.

[2]  Kavelman Da Streptomycin and acute anaphylaxis. , 1961 .

[3]  F. Kissmeyer-Nielsen,et al.  Severe Haemolytic Transfusion Reactions caused by apparently compatible Red Cells , 1961, British journal of haematology.

[4]  H. Horowitz,et al.  An improved technic for the quantitation of serum haptoglobin. , 1960, American journal of clinical pathology.

[5]  A. Tarlov,et al.  Methaemoglobin reduction test: a new, simple, in vitro test for identifying primaquine-sensitivity. , 1960, Bulletin of the World Health Organization.

[6]  J. Stewart,et al.  Rapid Destruction of Apparently Compatible Red Cells , 1959, British medical journal.

[7]  N. Shulman Immunoreactions involving platelets. I. A steric and kinetic model for formation of a complex from a human antibody, quinidine as a haptene, and platelets; and for fixation of complement by the complex. , 1958 .

[8]  A. Lewis Papain, Ficin and Bromelain in the Detection of Incomplete Rhesus Antibodies , 1957, British journal of haematology.

[9]  P. Carson,et al.  Enzymatic deficiency in primaquine-sensitive erythrocytes. , 1956, Science.

[10]  Harris Jw Studies on the Mechanism of a Drug-Induced Hemolytic Anemia. , 1956 .

[11]  E. Brody,et al.  Hemolytic anemia due to quinidine: observations on its mechanism. , 1956, The American journal of medicine.

[12]  I. Snapper,et al.  Hemolytic anemia secondary to mesantoin. , 1953, Annals of internal medicine.

[13]  J. Dausset The agglutination mechanism of trypsin modified red cells. , 1952, Blood.

[14]  S. Boyden THE ADSORPTION OF PROTEINS ON ERYTHROCYTES TREATED WITH TANNIC ACID AND SUBSEQUENT HEMAGGLUTINATION BY ANTIPROTEIN SERA , 1951, The Journal of experimental medicine.

[15]  E. Ponder Hemolysis and related phenomena , 1948 .

[16]  W. Mcdermott Toxicity of streptomycin. , 1947, The American journal of medicine.