Anker S D, Chua T P, Ponikowski P, Harrington D, Swan J W, Kox W J, Poole-Wilson P A, Coats A J
Cardiac Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, UK.
Circulation. 1997 Jul 15;96(2):526-34. doi: 10.1161/01.cir.96.2.526.
The role of hormonal and cytokine abnormalities in the development of cardiac cachexia remains obscure.
Healthy control subjects (n=16) and patients with chronic heart failure (CHF), classified clinically as cachectic (8% to 35% weight loss over > or = 6 months before study, n=16) or noncachectic (n=37), were assessed for markers of disease severity (maximal oxygen consumption, left ventricular ejection fraction, NYHA functional class). These markers were compared with plasma concentrations of potentially important anabolic and catabolic factors. The degree of neurohormonal activation and catabolic/anabolic imbalance was closely related to wasting but not to conventional measures of the severity of heart failure. Compared with control subjects and noncachectic patients, cachectic patients had reduced plasma sodium and increased norepinephrine, epinephrine (all P<.0001), cortisol, tumor necrosis factor (TNF)-alpha (both P<.002), and human growth hormone (P<.05). Insulin-like growth factor-1, testosterone, and estrogen were similar in all groups. Insulin was increased only in the noncachectic patients (P<.005 versus control subjects). Dehydroepiandrosterone was reduced in the cachectic patients (P<.02 versus control subjects). Insulin, cortisol, TNF-alpha, and norepinephrine correlated independently with wasting in CHF (P<.05; multiple regression of these four factors versus percent ideal weight, R2=.50, P<.0001).
Cachexia is more closely associated with hormonal changes in CHF than conventional measures of the severity of CHF. This study suggests that the syndrome of heart failure progresses to cardiac cachexia if the normal metabolic balance between catabolism and anabolism is altered.
激素和细胞因子异常在心脏恶病质发生中的作用仍不清楚。
对健康对照者（n = 16）以及临床分类为恶病质（研究前≥6个月体重减轻8%至35%，n = 16）或非恶病质（n = 37）的慢性心力衰竭（CHF）患者进行疾病严重程度指标（最大摄氧量、左心室射血分数、纽约心脏协会功能分级）评估。将这些指标与可能重要的合成代谢和分解代谢因子的血浆浓度进行比较。神经激素激活程度和分解代谢/合成代谢失衡与消瘦密切相关，但与心力衰竭严重程度的传统指标无关。与对照者和非恶病质患者相比，恶病质患者血浆钠降低，去甲肾上腺素、肾上腺素（均P<0.0001）、皮质醇、肿瘤坏死因子（TNF）-α（均P<0.002）和人生长激素升高（P<0.05）。胰岛素样生长因子-1、睾酮和雌激素在所有组中相似。胰岛素仅在非恶病质患者中升高（与对照者相比P<0.005）。恶病质患者脱氢表雄酮降低（与对照者相比P<0.02）。胰岛素、皮质醇、TNF-α和去甲肾上腺素与CHF患者的消瘦独立相关（P<0.05；这四个因子与理想体重百分比的多元回归，R2 = 0.50，P<0.0001）。
与心力衰竭严重程度的传统指标相比，恶病质与CHF中的激素变化关系更为密切。本研究提示，如果分解代谢和合成代谢之间的正常代谢平衡发生改变，心力衰竭综合征会进展为心脏恶病质。
