[Anthracyclin-cardiomyopathy (author's transl)].
Doxorubicin is one of the most effective antineoplastic drugs in clinical practice. Its clinical usefulness extends from acute leucemia and lymphoma to a wide range of solid tumors. However, the use of this drug is limited by its cardiac toxicity, that is often life-threatening. A number of clinical approaches discussed in this paper have been used to circumvent the problem of doxorubicin-induced congestive heart failure. A summarizing survey of the literature has led to establish two principles for prevention of doxorubicin-induced congestive heart failure with clinical meaning in the moment: --the way of administration --the clinical use of Ca-antagonist. The two principles provide an objective basis for preventation of congestive heart failure. The pathobiochemical background, analysed in this paper in detail, demonstrates that the same metabolic condition exist in the myocardial cell as in red blood cell. These interactions are the basis for a further analysis of metabolism in the cell, especially the redox metabolism of glutathione.
D000818:Animals; D006332:Cardiomegaly / Q000139:chemically induced / Q000201:enzymology; D009202:Cardiomyopathies / Q000139:chemically induced* / Q000201:enzymology; D002374:Catalase / Q000378:metabolism; D004317:Doxorubicin / Q000009:adverse effects*; D004562:Electrocardiography; D005979:Glutathione Peroxidase / Q000378:metabolism; D006333:Heart Failure / Q000139:chemically induced* / Q000201:enzymology; D006801:Humans; D009206:Myocardium / Q000201:enzymology; D013482:Superoxide Dismutase / Q000378:metabolism
D004317:Doxorubicin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase
Anthrazyklin-Kardiomopathie.