Thrombocytopenia drugs associated with

Isolated thrombocytopenia after the use of quinine for malaria or leg cramps has been described in isolated cases. The FDA s Center for Drug Evaluation and Research received 141 reports of isolated thrombocytopenia in association with quinine from 1974 to December 2000 (18). After elimination of cases that were confounded by acute or chronic disease or concomitant drug therapy, 64 reports of quinine-associated thrombocytopenia were analysed. Thrombocytopenia occurred soon after the start of therapy (median 7 days) and was often severe (hospitalization reported in 55 of the 64 cases). 

Kelton JG, Meltzer D, Moore J, Giles AR, Wilson WE, Barr R, Hirsh J, Neame PB, Powers PJ, Walker I, Bianchi F, Carter CJ. Drug-induced thrombocytopenia is associated with increased binding of IgG to platelets both in vivo and in vitro. Blood 1981 58(3) 524-9. 

A case of antazoline-induced thrombocytopenia has been described. The thrombocytopenia was associated with haemolytic anaemia, haemoglobinurea and acute renal failure (23 ). The symptom occurred on three occasions when the drug was given to control allergic manifestations. In the patient s serum antibodies to antazoline were... 

Many drugs, especially quinidine and heparin, induce antibodies leading to thrombocytopenia. In most cases the antibodies are drug-dependent however, there are many examples in which the antibodies are autoimmune in nature [42], even for drugs, such as quinidine that are classically associated with drug-dependent antibodies [43], Gold therapy, in particular, is associated with autoimmune-thrombocytopenia [44],... 

Hypersensitivity or idiosyncrasy to quinidine or other cinchona derivatives manifested by thrombocytopenia, skin eruption or febrile reactions myasthenia gravis history of thrombocytopenic purpura associated with quinidine administration digitalis intoxication manifested by arrhythmias or AV conduction disorders complete heart block left bundle branch block or other severe intraventricular conduction defects exhibiting marked QRS widening or bizarre complexes complete AV block with an AV nodal or idioventricular pacemaker aberrant ectopic impulses and abnormal rhythms due to escape mechanisms history of drug-induced torsade de pointes history of long QT syndrome. 

Autoimmune reactions associated with a-methyldopa treatment include thrombocytopenia and leukopenia. Since a few cases of an a-methyldopa-induced hepatitis have occurred, the drug is contraindicated in patients with active hepatic disease. FluUke symptoms also are known to occur. 

The major toxicity associated with mitomycin therapy is unpredictably long and cumulative myelosup-pression that affects both white blood cells and platelets. A syndrome of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure also has been described. Renal, hepatic, and pulmonary toxicity may occur. The drug is teratogenic and carcinogenic, and it can cause local bhstering. 

Among the more severe adverse reactions, Stevens-Johnson epidermal necrolysis syndrome, thrombocytopenia, agranulocytosis, and nephrotic syndrome have all been observed. Like diclofenac, sulindac may have some propensity to cause elevation of serum aminotransferases it is also sometimes associated with cholestatic liver damage, which disappears when the drug is stopped. 

The most common adverse effects are indirect hyperbilirubinemia and nephrolithiasis due to crystallization of the drug. Nephrolithiasis can occur within days after initiating therapy, with an estimated incidence of 3-15%, and may be associated with renal failure. Consumption of at least 48 oz of water daily is important to maintain adequate hydration and prevent nephrolithiasis. Thrombocytopenia, elevations of serum aminotransferase levels, nausea, diarrhea, and irritability have also been reported. There have also been rare cases of acute hemolytic anemia. In rats, high doses of indinavir are associated with development of thyroid adenomas. 

Blood dyscrasias, mostly dose independent, are among the most important allergic-type adverse reactions to drugs. Aplastic anemia is a serious but rare (presumably) idiosyncratic reaction. It has been reported in association with chloramphenicol, quinacrine, phenylbutazone, mephenytoin, gold compounds, and potassium chlorate. Hemolytic anemia, thrombocytopenia, and agranulocytosis may result from an unusual, acquired sensitivity to a variety of widely used drugs including aminopyrine, phenylbutazone, phenothiazines, propylthiouracil, diphenylhydantoin, penicillins, chloramphenicol, sulfisoxazole, and tolbutamide. 

The most serious side effects associated with acetazolamide are blood dyscrasias.Thrombocytopenia, agranulocytosis, and aplastic anemia have all occurred in patients taking acetazolamide however, drug-induced blood dyscrasias are extremely rare. 

Thrombocytopenia has rarely been reported, always associated with cefalotin (83-85). In one case there were drug-dependent antibodies. In two other cases the role of drug-dependent antibodies was further evaluated. In one case the antibodies only reacted with platelets in the presence of exogenons cefotetan, but not with cefotetan-coated platelets (86). In another case associated with cefamandole, antibodies cross-reacted with two cephalosporins that had a thiomethyltetrazole gronp at position 3 but not with other cephalosporins (87). In an additional case, cefuroxime has been implicated (88). In abont one-third of cases with cephalosporin-indnced nentropenia, slight concomitant thrombocjdopenia has been found (73). 

Rodriguez SU, Leikin SL, Hiller MC. Neonatal thrombocytopenia associated with ante-partum administration of thiazide drugs. N Engl J Med 1964 270 881. ... 

Rodriguez J. Thrombocytopenia associated with meclofena-mate. Drug Intell Clin Pharm 1981 5(12) 999. 

HIV-infected patients (SEDA-20, 337), and a reduced platelet count, sometimes associated with coagulation abnormalities, was retrospectively identified in nine of 28 patients who received prolonged G-CSF with antiretroviral drugs (42). Emperipolesis of neutrophils within megakaryocytes, an unusual feature of thrombocytopenia, was also reported in one patient receiving high-dose G-CSF (43). 

From the therapeutic point of view, prophylaxis of thrombosis must be continued after withdrawal of heparin, since even when there is no evidence of thrombosis in association with heparin-induced thrombocytopenia, thrombosis can follow after some days (52). Because of cross-reactivity, low molecular weight heparin should not be used when heparin has been withdrawn because of heparin-induced thrombocytopenia nor should warfarin be used, because of the risk of venous gangrene, at least until the thrombocytopenia has resolved. Patients with life-threatening or limb-threatening thrombosis can be treated with thrombolytic drugs. Current views are that two antithrombotic drugs should be used, for example danaparoid plus lepirudin (58). 

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