目的：通过测定川崎病（KD）患儿血清心型脂肪酸结合蛋白(h-FABP)水平变化，以探讨h-FABP在反映KD患儿心肌损害中的临床价值。方法：选择40例KD患儿为研究对象，以30例正常儿童为对照组。对KD组及对照组采用酶联免疫吸附法检测血清h-FABP、肌钙蛋白I（cTnI），同时利用杜邦全自动生化分析仪检测肌酸磷酸激酶同功酶（CK-MB）。并行心脏彩色多普勒(UCG)检测冠状动脉内径，将KD组分为冠状动脉病变（CAL）组和非冠状动脉病变（NCAL）组。结果：KD组血清h-FABP浓度、阳性率与对照组比较差异有显著性（P<0.01），cTnI浓度及阳性率明显高于对照组(P<0.05)，而CK-MB浓度和阳性率与对照组比较差异无显著性（P>0.05）；h-FABP与cTnI阳性率比较差异有显著性（P<0.01）；CAL组和NCAL组血清hFABP浓度对比差异有显著性（P<0.01）。结论：血浆h-FABP、cTnI浓度可作为KD患儿早期心肌损害的生化标志物，而h-FABP具有更高的灵敏度和特异性；血浆h-FABP浓度对川崎病以及川崎病合并冠状动脉病变的早期诊断、指导治疗具有重要的临床意义。

OBJECTIVE: This study examined serum level of heart-type fatty acid-binding protein (h-FABP) in children with Kawasaki disease (KD) in order to assess its value in KD. METHODS: Forty children with KD and 30 healthy children were enrolled. Serum levels of h-FABP and cardiac troponin I (cTnI) were measured using ELISA. Serum creatine kinase-MB (CK-MB) level was detected using an autoanalyer. The KD group was classified into two subgroups, with or without coronary artery lesions, based on the findings of the echocardiography. RESULTS: Mean serum levels of h-FABP (18.17±13.38 ng/mL vs 6.25±1.70 ng/mL; P<0.01) and cTnI (0.27±0.22 ng/mL vs 0.11±0.02 ng/mL; P<0.05) in the KD group was significantly higher than those in the control group. There was no significant difference in serum CK-MB concentrations between the two groups. Twenty-six patients (65%) and eight patients (20%) showed abnormally increased h-FABP and cTnI levels respectively in the KD group, but none of the control group showed increased levels of both. In the KD group, the percentage of patients with increased h-FABP was significantly higher than those with increased CTnI (P<0.01). The patients with coronary artery lesions had higher serum h-FABP level than those without (28.14±14.26 ng/mL vs 11.52±6.28 ng/mL; P<0.01). CONCLUSIONS: Serum levels of h-FABP and cTnI increase and can be used as the biomarkers of myocardial damage in children with KD. h-FABP appears to be more sensitive and specific. Detection of serum h-FABP level is useful for diagnosis of KD and coronary artery lesions secondary to KD.