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Human heart-type fatty acid-binding protein as an early diagnostic marker of doxorubicin cardiac toxicity

Hematology Reports

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Title Statement Human heart-type fatty acid-binding protein as an early diagnostic marker of doxorubicin cardiac toxicity
Added Entry - Uncontrolled Name Ashraf H. ElGhandour; Faculty of Medicine, Alexandria UNI Hematology Unit
Manal El Sorady; Faculty of Medicine, Alexandria UNI Hematology Unit
Sahar Azab; Faculty of Medicine, Alexandria UNI, Cardiology Department
Mohammed ElRahman; Military Medical Academy, Egypt
Summary, etc. Progressive cardiotoxicity following treatment with doxorubicin-based chemotherapy in patients with non-Hodgkin’s lymphoma (NHL) may lead to late onset cardiomyopathy. So, early prediction of toxicity can lead to prevention of heart failure in these patients. The aim of this work was to investigate the role of H-FABP as an early diagnostic marker of anthracycline-induced cardiac toxicity together with brain natriuretic peptide (BNP) as an indication of ventricular dysfunction in such patients. Our study was conducted on 40 NHL patients who received 6 cycles of a doxorubicin containing chemotherapy protocol (CHOP), not exceeding the total allowed dose of doxorubicin (500 mg/m2). Ten healthy controls were included in our study. Human heart-type fatty acid binding protein (H-FABP) was assessed 24 hours after the first cycle of CHOP. Plasma levels of BNP were estimated both before starting chemotherapy and after the last cycle of CHOP. Resting echocardiography was also performed before and at the end of chemotherapy cycles. The ejection fraction (EF) of 8 of our patients decreased below 50% at the end of the sixth cycle. Elevated levels of both H-FABP and BNP were found in all patients wth EF below 50% and both markers showed a positive correlation with each other. We concluded that H-FABP may serve as a reliable early marker for prediction of cardiomyopathy induced by doxorubicin. Thus, in patients with elevated H-FABP, alternative treatment modalities with no cardiac toxicity may be considered in order to prevent subsequent heart failure in these patients.
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Data Source Entry Hematology Reports; Vol 1, No 1 (2009); e6
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