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Hemolytic anaemia

Although manifest hemolytic anaemia is rare a positive Coomb s test may develop in about 3% of patients. As with the penicillins neurotoxicity manifested by hallucinations, confusion and convulsions may occur with high doses or in patients with renal impairment. [Pg.409]

Hematologic disorders Agranulocytosis, eoisnophilia, leukopenia, hemolytic anaemia, pancytopenia, thrombocytopenic purpura. [Pg.149]

Bolchoz LJC, Morrow JD, JoIIow DJ, et al. Primaquine induced hemolytic anaemia effect of 6-methoxy-8-hydroxylaminoquinoline on rat erythrocyte sulphydryl status, membrane lipids, cytoskeletal proteins and morphology. J Pharmacol Exp Ther 2002 303 141-148. [Pg.405]

Hormones has the ability to suppress mitosis in lymphocytes and this effect is duly utilized in the treatment of neoplastic diseases. Adrenocorticosteroids specifically are effective in the treatment of leukemia in children and in the management of hemolytic anaemia and hemorrhagic complications of thrombocytopenia that mostly occur in malignant lymphomas and chronic lymphocitic leukemia. Acute lymphoblastic leukemias in children are better treated with corticosteroids rather than antimetabolities and remission take place more rapidly. The hormones have been beneficial in breast cancer and other carcinomas although palliative effects are of short duration. [Pg.830]

In a few cases there was intravasal hemolysis after administration of isoniazid. Freedman and Linn (1978) describe a positive direct antiglobulin test in such a case of hemolytic anaemia after isoniazid. The antibody was bound to IgG-com-plement-fixing antibodies and reacted best at 37 °C with the antiglobulin technique and only with cells previously sensitized with isoniazid. Sometimes antinuclear antibodies develop during treatment with isoniazid (Alarc6n-Segovia 1973 Roth-FIELD et al. 1978). [Pg.541]

Adams, W. S., 1974, Hereditary hemolytic anaemia with human erythrocyte pyrimidine 5 -nucleotidase deficiency, J. Clin. Invest., 54 866. [Pg.108]

Previous reports had suggested that erythrocytes of these patients have decreased metabolic activity in the pentose phosphate shunt leading to cell fragility and therefore to hemolytic anaemia. The calorimetric investigations did not support this hypothesis when the erythrocyte pentose pathway activity was stimulated with MB [11,12,13]. [Pg.661]

Clinical manifestation. It includes several syndromes a) pulmotoxic and irritative syndrome - expressed by catarrhal changes on the contact mucosa and respiratory tract, toxic pulmonary oedema b) hemotoxic syndrome - expressed by severe hemolysis of different degrees, in the severe forms - hemolytic shock and anaemia c) hepatal syndrome - characterised by subicterus or icterus, increased liver and bilirubinaemia d) renal syndrome - by oliguria or anuria, pathological deviations in the urine and acute kidney insufficiency. In the extremely severe forms consciousness is disordered. Laboratory blood and urine chemical tests show evidence of phenol metabolites, data for blood damage (increased values of free hemoglobin, reduced number of erythrocytes), positive liver tests etc. [Pg.49]


See other pages where Hemolytic anaemia is mentioned: [Pg.49]    [Pg.577]    [Pg.10]    [Pg.420]    [Pg.47]    [Pg.49]    [Pg.577]    [Pg.10]    [Pg.420]    [Pg.47]    [Pg.413]   
See also in sourсe #XX -- [ Pg.47 ]




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