目的 观察血浆心肌营养素-1(CT-1)在新生儿缺氧缺血性脑病(HIE)合并心肌损伤中的变化及临床意义.方法 选择HIE患儿45例(轻度15例、中度24例、重度6例)为观察组,根据有无心肌损伤分为心肌损伤组(19例)和无心肌损伤(26例)两个亚组.20例正常新生儿为对照组.采用双抗体夹心酶标免疫分析法检测血浆CT-1水平.同时检测血清肌酸激酶同工酶(CK-MB)和心肌肌钙蛋白I(CTnI)水平.结果 轻度、中/重度HIE组血浆 CT-1水平分别为169±20、287±44 pg/mL,均 高于对照组(30±8 pg/mL)(P<0.01),且中/重度HIE组高于轻度HIE组(P<0.01).HIE患儿急性期血浆CT-1水平与血清CK-MB、CTnI均呈显著正相关(r分别为0.565、0.621,均P<0.01).心肌损伤亚组血浆CT-1水平较非心肌损伤亚组升高(249±35 pg/mL vs 177±26 pg/mL;P<0.01).心肌损伤亚组急性期血浆CT-1水平(249±35 pg/mL)明显高于恢复期(157±19 pg/mL)(P<0.01).结论 检测HIE患儿血浆CT-1水平有助于HIE新生儿心肌损伤的诊断,且有助于判断HIE病情.

Objective To study the changes and significance of plasma cardiotrophin-1 (CT-1) in neonates with hypoxic-ischemic encephalopathy (HIE) complicated by myocardial ischemic injury. Methods Forty-five neonates with HIE (15 mild cases, 24 moderate cases and 6 severe cases) were enrolled and divided into two subgroups based on the presence of myocardial injury (n=19) and not (n=26). Twenty healthy neonates were used as the control group. Plasma CT-1 levels were measured using double-antibody sandwich enzyme immunoassay method. Serum creatinine kinase MB (CK-MB) and cardiac troponin I (CTnI ) levels were also measured. Results Plasma CT-1 levels in the mild HIE (169±20 pg/mL) and moderate/severe HIE subgroups (287±44 pg/mL) were significantly higher than those in the control group (30±8 pg/mL), and plasma CT-1 levels were associated with the severity of HIE (P<0.01). Plasma CT-1 levels were positively correlated with serum CK-MB and CTnI levels in neonates with HIE in the acute phase (r=0.565 and 0.621 respectively; P<0.01). Plasma CT-1 levels in neonates with myocardial injury were significantly higher than those without myocardial injury (249 ±35 pg/mL vs 177±26 pg/mL; P<0.01). Plasma CT-1 levels were significantly reduced in neonates with myocardial injury in the convalescent phase (157±19 pg/mL) compared with those in the acute phase (249±35 pg/mL; P<0.01). Conclusions Detection of plasma CT-1 levels may be useful in the diagnosis of myocardial ischemic injury and the severity evaluation of HIE.