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血清淀粉样蛋白A和高密度脂蛋白参与川崎病的急性期反应。

Serum amyloid A and high density lipoprotein participate in the acute phase response of Kawasaki disease.

作者信息

Cabana V G, Gidding S S, Getz G S, Chapman J, Shulman S T

机构信息

Department of Pathology, Pritzker School of Medicine, The University of Chicago, Illinois 60637, USA.

出版信息

Pediatr Res. 1997 Nov;42(5):651-5. doi: 10.1203/00006450-199711000-00017.

Abstract

In this study we report changes in HDL concentration and composition in acute and convalescent Kawasaki disease. Notable reductions in plasma HDL-cholesterol (0.54 +/- 0.2 mmol/L, normal level 0.7-1.81 mmol/L) and apolipoprotein A-I (apoA-I) (56 +/- 28 mg/dL, normal level 141 +/- 22 mg/dL) were observed in all 24 patients studied during the acute phase of Kawasaki disease. These changes were accompanied by the marked appearance of serum amyloid A (SAA) protein in the plasma, associated with HDL3-like lipoprotein particles. The distribution of apoA-I was analyzed in five patients and showed a significant increase in lipid-free apoA-I in the bottom fraction (28.8 +/- 4.1%, normal range 10-15%), suggesting displacement of apoA-I from the HDL particles by SAA. Within 2 wk after acute Kawasaki disease, levels of HDL-cholesterol and apoA-I returned to the normal range, and SAA disappeared from the plasma. The HDL of patients with Kawasaki disease was markedly enriched in triglyceride even in the absence of changes in total plasma triglyceride. The core composition of HDL returned to the normal range more slowly than the plasma HDL-cholesterol and apoA-I levels. This suggests that Kawasaki disease has a profound effect on the lipoprotein profile acutely and a more subtle sustained effect on the HDL composition. We interpret these changes as manifestations of the acute phase response in Kawasaki disease.

摘要

在本研究中,我们报告了急性和恢复期川崎病患者高密度脂蛋白(HDL)浓度及组成的变化。在24例川崎病急性期患者中,均观察到血浆高密度脂蛋白胆固醇(0.54±0.2 mmol/L,正常水平0.7 - 1.81 mmol/L)和载脂蛋白A-I(apoA-I)(56±28 mg/dL,正常水平141±22 mg/dL)显著降低。这些变化伴随着血浆中血清淀粉样蛋白A(SAA)蛋白的显著出现,其与HDL3样脂蛋白颗粒相关。对5例患者的apoA-I分布进行分析,结果显示底部组分中无脂apoA-I显著增加(28.8±4.1%,正常范围10 - 15%),提示SAA将apoA-I从HDL颗粒中置换出来。急性川崎病发病后2周内,HDL胆固醇和apoA-I水平恢复至正常范围,且SAA从血浆中消失。即使血浆总甘油三酯无变化,川崎病患者的HDL中甘油三酯也显著富集。HDL的核心组成恢复至正常范围的速度比血浆HDL胆固醇和apoA-I水平更慢。这表明川崎病对脂蛋白谱有急性的深远影响,对HDL组成有更细微的持续影响。我们将这些变化解释为川崎病急性期反应的表现。

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