Comparison of circulating levels of interleukin-6 and tumor necrosis factor-alpha in hypertrophic cardiomyopathy and in idiopathic dilated cardiomyopathy

Comparison of circulating levels of interleukin-6 and tumor necrosis factor-alpha in hypertrophic cardiomyopathy and in idiopathic dilated cardiomyopathy
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DOI:
10.1016/j.amjcard.2004.03.078
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发表时间:
2004-07-15
影响因子:
2.8
通讯作者:
Buzás, K
Buzás, K
中科院分区:
医学3区
文献类型:
--
作者:
Högye, M;Mándi, Y;Buzás, K

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从文献中已知,肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的循环水平在心力衰竭和特发性扩张型心肌病(IDC)中升高。关于肥厚型心肌病(HQ)细胞因子的产生,几乎没有令人信服的数据。检测了19例HC患者、31例IDC患者和20例健康受试者(对照组)的循环IL-6、可溶性IL-6受体(sIL-6 R)和TNF-α水平,并与其临床参数进行比较。IDC患者血清中TNF-α和循环IL-6水平升高。HC患者血清TNF-α水平无明显升高,但IL-6和sIL-6 R水平明显高于IDC患者。虽然IL-6水平升高可能与IDC的左心室功能障碍的程度相关,但显著升高的IL-6水平与HC的左心室功能无关。IDC中显著升高的TNF-α水平与升高的IL-6水平相关,可能是由于炎症过程和/或心力衰竭。相反,在纽约心脏协会功能分级实际上良好的HC中,甚至更高的IL-6和sIL-6 R水平与TNF-α升高无关。在HC中,IL-6和sIL-6 R升高是由于另一种机制,可能是通过心脏营养素相关的gp 130受体。HC产生IL-6的来源尚不清楚。(C)2004年,Excerpta Medica,Inc.
It is known from the literature that the circulating levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) are elevated in heart failure and idiopathic dilated cardiomyopathy (IDC). Few convincing data are available on the production of cytokines in hypertrophic cardiomyopathy (HQ. The levels of circulating IL-6, the soluble form of the IL-6 receptor (sIL-6R), and TNF-alpha in 19 patients with HC, 31 patients with IDC, and 20 healthy subjects (control group) were examined and compared with their clinical parameters. The levels of TNF-alpha and circulating IL-6 proved to be elevated in the sera of patients with IDC. In contrast, the level of TNF-alpha was not elevated in HC, although the levels of IL-6 and sIL-6R were significantly higher than those in the sera of patients with IDC. Although elevated levels of IL-6 may correlate with the extent of left ventricular dysfunction in IDC, the markedly elevated IL-6 levels did not correlate with left ventricular function in HC. The markedly elevated TNF-alpha levels in IDC were associated with the elevated IL-6 levels, probably because of an inflammatory process and/or heart failure. In contrast, in HC, in which the New York Heart Assocation functional class was actually good, the even higher IL-6 and sIL-6R levels were not associated with a TNF-alpha elevation. In HC, the IL-6 and sIL-6R elevations were due to another mechanism, probably by way of the cardiotrophin-associated gp130 receptor. The sources of IL-6 production in HC are not clear yet. (C) 2004 by Excerpta Medica, Inc.