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Cobalt-beer cardiomyopathy

A clinical and pathologic study of twenty-eight cases
  • Carl S. Alexander
    Correspondence
    Requests for reprints should be addressed to Dr. Carl S. Alexander, Cardiovascular Section, Veterans Administration Hospital, 54th Street and 48th Avenue South, Minneapolis, Minnesota 55417.
    Footnotes
    Affiliations
    Minneapolis, Minnesota, USA
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  • Author Footnotes
    1 From the Cardiovascular Section, Veterans Administration Hospital, and the Department of Medicine, University of Minnesota, Minneapolis, Minnesota.
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      Abstract

      Cobalt-beer cardiomyopathy is described in twenty-eight patients admitted to the Veterans Administration Hospital in Minneapolis from 1964 to 1967. Clinically, the syndrome differed from alcoholic cardiomyopathy and beriberi by its rather abrupt onset of left ventricular failure, cardiogenic shock and acidosis. Pericardial effusion and polycythemia were present in the majority and suggested cobalt intoxication. It is difficult to explain the cardiotoxic effect of cobalt because the amount ingested in the beer (up to 10 mg/day) is far less than the amount used in the treatment of refractory anemia (up to 50 mg/day). Other factors were therefore considered important in rendering the heart more sensitive to cobalt. These included inadequate protein and vitamin intake, especially thiamine, zinc depletion and prior heart damage from alcohol. Mortality for the acute illness was 18 per cent but late deaths accounted for a total mortality of 43 per cent. These figures are compared with those reported from Belgium, Quebec and Omaha. Some survivors continue to have clinical disability and demonstrate abnormal electrocardiographic changes. The toxicology of cobalt in man is reviewed.
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