October 28, 2013
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Resistin linked to cardiotoxicity in patients undergoing chemotherapy

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Elevated levels of resistin could be a marker of anthracycline-induced cardiotoxicity as seen in patients undergoing chemotherapy for breast cancer, data suggest.

These results also indicate a link between resistin and inflammation, metabolism and heart disease, according to Daniel R. Schwartz, MD, of the Institute for Diabetes, Obesity and Metabolism in the Perelman School of Medicine at the University of Pennsylvania, and colleagues.

“Because resistin continues to be discussed as a biomarker for diagnosis and prognosis in heart failure, these finding suggest a need to more thoroughly and frequently screen for resistin levels to better understand the natural history of resistin change and its relationship to cardiotoxicity,” the researchers wrote.

A humanized mouse model without murine resistin but transgenic for the human RETN gene (Hum-Retn mice) was studied based on similar basal and inflammation-stimulated resistin levels to that of humans. This model caused researchers to extend their study to humans.

“Elevation in serum resistin in a variety of heart failure settings raised the question of whether similar changes would be observed in patients who developed cardiotoxicity from anthracyclines,” researchers wrote.

Therefore, they also assessed the level of resistin in 50 anthracycline-treated adults with breast cancer with and without cardiotoxicity. The patients were examined before chemotherapy and at 3 and 6 months of treatment using questionnaires, echocardiography and blood samples, according to data.

Serum resistin levels in women undergoing anthracycline-containing chemotherapy increased significantly from baseline to 3 months (11.5 ng/mL to 19.6 ng/mL; P<.01). These levels tended to return to baseline by 6 months. However, patients who developed cardiotoxicity displayed consistent elevations (13.5 ng/mL vs. 10.8 ng/mL in no cardiotoxicity; P=.073), researchers added.

“The findings of our pilot study in humans support an important and intriguing relationship between resistin and anthracycline-induced cardiotoxicity. We acknowledge that the molecular etiologies for this injury are multiple and wide ranging. Therefore, some variability in the results presented here is not surprising,” researchers wrote.

Disclosure: One of the researchers reports filing patents related to resistin and consulted for Eli Lilly and Company, Lycera Corp., Madrigal Pharmaceuticals, Merck, Melior Discovery and Novartis.