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To print: Select File and then Print from your browser's menu Title: Growth Hormone Benefits Cardiomyopathy Patients |
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American Heart Journal 2002;144(2):359-364 "Growth hormone administration reduces circulating proinflammatory cytokines and soluble Fas/soluble Fas ligand system in patients with chronic heart failure secondary to idiopathic dilated cardiomyopathy" 09/02/2002 03:18:49 PM By David Loshak Growth hormone reduces serum levels of proinflammatory cytokines in patients with chronic heart failure secondary to idiopathic dilated cardiomyopathy. It also reduces soluble Fas and soluble Fas ligand system in these patients. These immunomodulatory effects may be associated with patients' improved clinical performance and exercise capacity, according to investigators in Athens, Greece. They noted that abnormal proinflammatory cytokine expression and apoptotic process had been shown to contribute to adverse left ventricular remodeling and progress of chronic heart failure. This led them to study the effects of growth hormone on serum levels of representative proinflammatory cytokines and soluble apoptosis mediators in chronic heart failure secondary to idiopathic dilated cardiomyopathy. Serum levels of tumour necrosis factor-alpha and its two soluble receptors, interleukin-6 (IL-6) and soluble IL-6 receptor, and soluble Fas and soluble Fas ligand were determined by enzyme-linked immunosorbent assay in 10 patients (New York Heart Association class III, ejection fraction 24 ± 2.0 percent). These determinations were made before and after a three-month subcutaneous administration of growth hormone 4.0 IU every other day. The investigators also used peak oxygen consumption to evaluate functional status. Growth hormone treatment produced significant reductions in serum levels of TNF-[a, its soluble receptors, IL-6, soluble IL-6 receptor, soluble Fas and soluble Fas ligand. The investigators also observed significant improvements in peak oxygen consumption. These correlated well with reductions induced by growth hormone in both TNF-a and soluble FAS ligand. |
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