Literature DB >> 15962840

Monitoring of cardiac function on the basis of serum troponin I levels in patients with acute leukemia treated with anthracyclines.

Giorgina Specchia1, Caterina Buquicchio, Nicola Pansini, Francesca Di Serio, Vincenzo Liso, Domenico Pastore, Giuseppina Greco, Lucia Ciuffreda, Anna Mestice, Arcangelo Liso.   

Abstract

Anthracyclines are used extensively in the therapy of hematologic malignancies. However, their use has been limited by acute and chronic cardiotoxicity. Cardiac troponins have emerged as sensitive and specific markers of even minor myocardial damage. In this study we prospectively evaluated serial measurements of serum cardiac markers and echocardiography in patients with de novo acute myeloid and lymphoid leukemias (AML and ALL, respectively) treated with anthracyclines. We examined and subdivided 79 patients into 3 groups: group 1 (37 patients with AML, all < 60 years), group 2 (25 with AML, all 260 years), group 3 (17 with ALL). Serum specimens were collected before treatment and during and after therapy and were analyzed for troponin I (Tnl), myoglobin, creatine phosphokinase-muscle myocardium isoenzyme B, and lactate dehydrogenase concentrations. In group 1, 4 of the 37 patients (11%) had increased levels of Tnl on the 14th day of induction therapy, but by the 28th day the Tnl level had returned to normal in 3 of these 4 patients. In group 2, 3 of the 25 patients (12%) demonstrated increased Tnl concentrations on the 7th day of induction therapy, but by the 14th day these levels had normalized in 2 of the 3. In group 3, we detected no increased Tnl concentrations. Echographic study did show a significant correlation with the Tnl levels (P < .001), involving a reversible decrease in left ventricular ejection fraction among patients with increased Tnl levels (> 0.15 ng/mL) on day 14 in group 1 and on day 7 in group 2. These results may aid the clinician in the treatment of patients by identifying high-risk patients who may benefit from closer observation or supportive cardiac therapy.

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Year:  2005        PMID: 15962840     DOI: 10.1016/j.lab.2005.02.003

Source DB:  PubMed          Journal:  J Lab Clin Med        ISSN: 0022-2143


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