ELEVATED CIRCULATING LEVELS OF TUMOR-NECROSIS-FACTOR IN SEVERE CHRONIC HEART-FAILURE
ELEVATED CIRCULATING LEVELS OF TUMOR-NECROSIS-FACTOR IN SEVERE CHRONIC HEART-FAILURE
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DOI：
10.1056/nejm199007263230405
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发表时间：
1990-07-26
影响因子：
158.5
通讯作者：
PACKER, M
中科院分区：
文献类型：
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作者：
LEVINE, B;KALMAN, J;PACKER, M
背景和方法：虽然恶病质常伴有晚期心力衰竭，但对恶病质状态的原因知之甚少。为了评估肿瘤坏死因子在心脏恶病质发病机制中的潜在作用，我们检测了33名慢性心力衰竭患者、33名年龄匹配的健康对照组和9名慢性肾功能衰竭患者的血清肿瘤坏死因子水平。结果：平均值(.+-.扫描电子显微镜)心力衰竭患者血清肿瘤坏死因子水平较高(115。+-)。25U/毫升)高于健康对照组(9.0+-)。每毫升3U；宝洁0.001)。19例慢性心力衰竭患者血清肿瘤坏死因子水平明显升高。每毫升39U(高于对照组平均值2 SD)，而其余14名患者的血清肿瘤坏死因子水平低于这一水平。肿瘤坏死因子水平高的患者比低水平的患者更容易出现恶病质(82.+-)。3比95。+-。分别为理想体重的6%；P<；0.05)，并有更晚期的心力衰竭，这从他们血浆肾素活性的较高值(2.92.+-)中得到了证明。0.53比1.06+-每升每秒0.53 ng[10.5+-.1.9比3.8。+-。每毫升每小时1.9 ng]；P<；0.01)和较低的血清钠浓度(135.+-)。1比138。+-每升1摩尔；P<；0.05)。肿瘤坏死因子水平高的组也有较低的血红蛋白水平(7.82.+-.0.2比8.69+-每升0.4 mmol[12.6+-.0.4比14.0。+-。每分升0.6克])和较高的血尿素氮数值(19.5+-)。2.2比12.5。+-。1.8 mmol/L)高于肿瘤坏死因子低水平组(P<；0.05)。然而，肿瘤坏死因子水平的升高并不完全是由于肾清除功能降低，因为心力衰竭患者的肿瘤坏死因子水平显著高于9例慢性肾功能衰竭患者(115。+-)。25对45。+-。每毫升25U，P<；0.05)。结论：这些发现表明慢性心力衰竭恶病质患者循环中肿瘤坏死因子水平升高，这种升高与终末期心脏病患者肾素-血管紧张素系统的显著激活有关。
Background and Methods: Although cachexia often accompanies advanced heart failure, little is known about the causes of the cachectic state. To assess the potential role of tumor necrosis factor in the pathogenesis of cardiac cachexia, we measured serum levels of the factor in 33 patients with chronic heart failure, 33 age-matched healthy controls, and 9 patients with chronic renal failure. Results: Mean (.+-. SEM) serum levels of tumor necrosis factor were higher in the patients with heart failure (115 .+-. 25 U per milliliter) than in the healthy controls (9 .+-. 3 U per milliliter; P < 0.001). Nineteen of the patients with chronic heart failure had serum levels of tumor necrosis factor .gtoreq. 39 U per milliliter (> 2 SD above the mean value for the control group), whereas the remaining 14 patients had serum levels of tumor necrosis factor below this level. The patients with high levels of tumor necrosis factor were more cachectic than those with low levels (82 .+-. 3 vs. 95 .+-. 6 percent of ideal body weight, respectively; P < 0.05) and had more advanced heart failure, as evidenced by their higher values for plasma renin activity (2.92 .+-. 0.53 vs. 1.06 .+-. 0.53 ng per liter per second [10.5 .+-. 1.9 vs. 3.8 .+-. 1.9 ng per milliliter per hour]; P < 0.01) and lower serum sodium concentration (135 .+-. 1 vs. 138 .+-. 1 mmol per per liter; P < 0.05). The group with high levels of tumor necrosis factor also had lower hemoglobin levels (7.82 .+-. 0.2 vs. 8.69 .+-. 0.4 mmol per liter [12.6 .+-. 0.4 vs. 14.0 .+-. 0.6 g per deciliter]) and higher values for blood urea nitrogen (19.5 .+-. 2.2 vs. 12.5 .+-. 1.8 mmol per liter) than the group with low levels of tumor necrosis factor (P < 0.05 for both). The high levels of tumor necrosis factor were not due solely to decreased renal clearance, however, since the levels in the patients with heart failure were considerably higher than those in the nine patients with chronic renal failure (115 .+-. 25 vs. 45 .+-. 25 U per milliliter, P < 0.05). Conclusions: These findings indicate that circulating levels of tumor necrosis factor are increased in cachectic patients with chronic heart failure and that this elevation is associated with the marked activation of the renin-angiotensin system seen in patients with end-stage cardiac disease.