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急性心肌梗死早期血清中触珠蛋白浓度的变化

Evolution of haptoglobin concentration in serum during the early phase of acute myocardial infarction.

作者信息

Bernard D R, Langlois M R, Delanghe J R, De Buyzere M L

机构信息

Laboratorium Klinische Scheikunde, Universitair Ziekenhuis Gent, Belgium.

出版信息

Eur J Clin Chem Clin Biochem. 1997 Feb;35(2):85-8. doi: 10.1515/cclm.1997.35.2.85.

DOI:10.1515/cclm.1997.35.2.85
PMID:9056748
Abstract

Haptoglobin (Hp) is a haemoglobin-binding acute phase protein with three genetic types: Hp 1-1, Hp 2-1, Hp 2-2. We investigated 45 patients during the first 48 hours of acute myocardial infarction, and studied determinant factors and clinical correlates. Upon hospital admission, serum haptoglobin concentration was increased (1.95 +/- 0.94 g/l, mean +/- SD, P < 0.001) versus the reference population (0.97 +/- 0.46 g/l, n = 107), independent of haptoglobin type: 1.84 +/- 0.64 g/l (Hp 1-1, n = 11) (P < 0.01), 1.98 +/- 0.79 g/l (Hp 2-1, n = 25) (P < 0.001), 1.98 +/- 1.58 g/l (Hp 2-2, n = 9) (P < 0.001). Moreover, during the first hours of hospitalization, a temporal lowering of haptoglobin was observed suggesting acute haemolysis, independent of the haptoglobin type. Minimal serum haptoglobin was reached 9.6 +/- 5.8 hours after admission. The amplitude of the haptoglobin decrease correlated with initial serum haptoglobin (r = 0.78) and was more pronounced (P < 0.05) in men (0.53 +/- 0.57 g/l) than in women (0.18 +/- 0.17 g/l). Decrease of serum haptoglobin did not correlate with infarct size (based on creatine kinase-MB release). Out of the other acute phase proteins measured upon admission, only C-reactive protein was significantly increased (P < 0.05). During the next 36 hours, haptoglobin increased as a result of the acute phase response to myocardial injury. Our findings suggest that acute myocardial infarction is also preceded by an acute phase response, characterized by an initial high haptoglobin and followed by a temporal haptoglobin decrease due to haemolysis.

摘要

触珠蛋白(Hp)是一种结合血红蛋白的急性期蛋白,有三种基因类型:Hp 1-1、Hp 2-1、Hp 2-2。我们在急性心肌梗死的最初48小时内对45例患者进行了调查,研究了决定因素和临床相关性。入院时,与参考人群(0.97±0.46 g/l,n = 107)相比,血清触珠蛋白浓度升高(1.95±0.94 g/l,均值±标准差,P < 0.001),与触珠蛋白类型无关:1.84±0.64 g/l(Hp 1-1,n = 11)(P < 0.01),1.98±0.79 g/l(Hp 2-1,n = 25)(P < 0.001),1.98±1.58 g/l(Hp 2-2,n = 9)(P < 0.001)。此外,在住院的最初几个小时内,观察到触珠蛋白暂时降低,提示急性溶血,与触珠蛋白类型无关。入院后9.6±5.8小时达到最低血清触珠蛋白水平。触珠蛋白降低的幅度与初始血清触珠蛋白相关(r = 0.78),男性(0.53±0.57 g/l)比女性(0.18±0.17 g/l)更明显(P < 0.05)。血清触珠蛋白降低与梗死面积(基于肌酸激酶-MB释放)无关。入院时检测的其他急性期蛋白中,只有C反应蛋白显著升高(P < 0.05)。在接下来的36小时内,由于对心肌损伤的急性期反应,触珠蛋白升高。我们的研究结果表明,急性心肌梗死之前也有急性期反应,其特征是初始触珠蛋白水平高,随后由于溶血导致触珠蛋白暂时降低。

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