Caforio A L, Goldman J H, Baig M K, Mahon N J, Haven A J, Souberbielle B E, Holt D W, Dalgleish A G, McKenna W J
Division of Cardiology, Department of Clinical and Experimental Medicine, University of Padua, Padua, Italy.
Eur J Heart Fail. 2001 Mar;3(2):155-63. doi: 10.1016/s1388-9842(00)00148-3.
It has not been assessed whether high levels of soluble interleukin 2 receptor (sIL-2R), neopterin and beta-2 microglobulin in idiopathic dilated cardiomyopathy reflect heart failure severity and/or an active autoimmune process. The aim of this study was to relate serum levels of these markers to clinical and autoimmune features.
We studied 60 patients with idiopathic dilated cardiomyopathy, 67 controls with ischemic heart failure and 34 normals.
Abnormal levels of sIL-2R, but not of neopterin and beta-2 microglobulin, were more frequent in idiopathic dilated cardiomyopathy than in ischemic patients (35% vs. 16%; P=0.02) or in normals (35% vs. 12%, P=0.01); mean sIL-2R levels were, however, similar in idiopathic dilated cardiomyopathy and ischemic heart failure (842+/-75 vs. 762+/-93 U/ml, P=NS). In idiopathic dilated cardiomyopathy abnormal levels of sIL-2R were associated with lower peak oxygen consumption (P=0.008), higher neopterin and HLA class II expression in the myocardium (P=0.02), but were unrelated to cardiac autoantibody status or titer. In addition, abnormal levels of neopterin were associated with adverse prognosis and higher beta-2 microglobulin; abnormal levels of beta-2 microglobulin with lower echocardiographic percent fractional shortening, higher sIL-2R and higher neopterin.
There is no convincing evidence that abnormal sIL-2R, neopterin and/or beta-2 microglobulin are disease-specific markers of idiopathic dilated cardiomyopathy. The lack of association with cardiac autoantibodies suggests that these abnormalities are mainly related to heart failure severity rather than autoimmune pathogenesis. In keeping with this view, high levels of sIL-2R, neopterin and/or beta-2 microglobulin identified a subset of idiopathic dilated cardiomyopathy patients with advanced disease and poor prognosis.
特发性扩张型心肌病中高水平的可溶性白细胞介素2受体(sIL-2R)、新蝶呤和β2微球蛋白是否反映心力衰竭的严重程度和/或活跃的自身免疫过程尚未得到评估。本研究的目的是将这些标志物的血清水平与临床和自身免疫特征联系起来。
我们研究了60例特发性扩张型心肌病患者、67例缺血性心力衰竭对照者和34例正常人。
特发性扩张型心肌病患者中sIL-2R水平异常(而非新蝶呤和β2微球蛋白水平异常)比缺血性患者(35%对16%;P=0.02)或正常人(35%对12%,P=0.01)更常见;然而,特发性扩张型心肌病和缺血性心力衰竭患者的平均sIL-2R水平相似(842±75对762±93 U/ml,P=无显著差异)。在特发性扩张型心肌病中,sIL-2R水平异常与较低的峰值耗氧量(P=0.008)、心肌中较高的新蝶呤和HLA-II类表达(P=0.02)相关,但与心脏自身抗体状态或滴度无关。此外,新蝶呤水平异常与不良预后和较高的β2微球蛋白相关;β2微球蛋白水平异常与较低的超声心动图缩短分数百分比、较高的sIL-2R和较高的新蝶呤相关。
没有令人信服的证据表明sIL-2R、新蝶呤和/或β2微球蛋白异常是特发性扩张型心肌病的疾病特异性标志物。与心脏自身抗体缺乏关联表明这些异常主要与心力衰竭严重程度有关,而非自身免疫发病机制。与此观点一致的是,高水平的sIL-2R、新蝶呤和/或β2微球蛋白确定了一组疾病进展且预后不良的特发性扩张型心肌病患者。