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[慢性心力衰竭与恶病质:内分泌系统的作用]

[Chronic heart failure and cachexia: role of endocrine system].

作者信息

Dei Cas A, Muoio A, Zavaroni I

机构信息

Dipartimento di Medicina Interna e Scienze Biomediche, Università degli Studi di Parma, Parma, Italia.

出版信息

Minerva Cardioangiol. 2011 Dec;59(6):601-12. Epub 2009 Nov 30.

PMID:19946251
Abstract

Chronic heart failure (CHF) is a major health problem that carries a devastating prognosis. The prognosis worsens considerably once cardiac cachexia has been diagnosed. Neurohormonal, metabolic, hemodynamic and immunological alterations are involved in the initiation and progression of cardiac cachexia. Cachexia is characterized by a hypothalamic inappropriate response to the mechanisms controlling energy homeostasis. Levels of the anorexigenic hormone leptin are decreased whereas the orexigenic gherlin hormone levels are normal or elevated. Nevertheless, energy intake is not increased as expected due to a persistent activation of the proopiomelanocortin (POMC) system (anorexigenic) paralleled by a decreased activity of the neuropeptide Y (NPY, orexigenic) neurons. Cachexia is also characterized by an imbalance in anabolic (impairment in the growth hormone/insulin-like growth factor-I axis, insulin resistance) and catabolic (increased levels of catecholamines, increased cortisol/dehydroepiandrosterone ratio and activation of proinflammatory cytokines such as tumor necrosis factor-alpha, interleuchin-6, interleuchin-1') at the basis of the wasting process. This review discusses the complex role of the endocrine system in modulating energy balance, appetite and metabolism in patients with chronic heart failure. A joint multidisciplinary effort of the cardiologists, immunologists and endocrinologists might be useful to identify the precise mechanisms involved in the neuroendocrine alteration and to develop therapeutic strategies able to improve the prognosis of CHF patients.

摘要

慢性心力衰竭(CHF)是一个严重的健康问题,预后不佳。一旦诊断出心脏恶病质,预后会显著恶化。神经激素、代谢、血流动力学和免疫改变参与了心脏恶病质的发生和发展。恶病质的特征是下丘脑对控制能量稳态的机制反应异常。厌食激素瘦素水平降低,而食欲素胃饥饿素水平正常或升高。然而,由于促肾上腺皮质激素原(POMC,厌食性)系统持续激活,同时神经肽Y(NPY,食欲性)神经元活性降低,能量摄入并未如预期增加。恶病质的另一个特征是在消瘦过程中,合成代谢(生长激素/胰岛素样生长因子-I轴受损、胰岛素抵抗)和分解代谢(儿茶酚胺水平升高、皮质醇/脱氢表雄酮比值增加以及促炎细胞因子如肿瘤坏死因子-α、白细胞介素-6、白细胞介素-1'激活)失衡。本综述讨论了内分泌系统在调节慢性心力衰竭患者能量平衡、食欲和代谢方面的复杂作用。心脏病专家、免疫学家和内分泌学家的多学科联合努力可能有助于确定神经内分泌改变所涉及的精确机制,并制定能够改善CHF患者预后的治疗策略。

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