左卡尼汀对柯萨奇A16型病毒感染手足口病的心肌保护作用

目的探讨左卡尼汀对柯萨奇病毒A16型感染所致手足口病(HFMD)的心肌保护作用及机制。方法 60例心肌酶谱异常的HFMD患儿随机分为左卡尼汀治疗组(左卡组)和1,6-二磷酸果糖治疗组(果糖组),每组30例,在抗病毒、退热等基础上分别给予左卡尼汀或果糖二磷酸钠治疗,并以同期体检的健康儿童30例为对照组。比较HFMD患儿治疗前后的心肌酶谱、丙二醛(MDA)、超氧化物岐化酶(SOD)、细胞凋亡因子sFas和sFasL的变化。结果两组HFMD患儿治疗有效性的差异无统计学意义(P0.05),仅果糖组1例进展为危重型。治疗前,左卡组和果糖组心肌酶谱、MDA、sFas、sFasL水平高于对照组(P0.05),SOD低于对照组(P0.05),但HFMD的两组间心肌酶谱、MDA、SOD、sFas、sFasL的差异无统计学意义(P0.05)。治疗后,左卡组和果糖组的心肌酶谱以及MDA、sFas、sFasL浓度均下降(P0.05),SOD水平增高(P0.05);治疗后除果糖组的CK高于对照组和左卡组,其余心肌酶指标及MDA、sFas、sFasl在两组间及与对照组的差异均无统计学意义(P0.05)。SOD水平与AST、LDH、CK、CK-MB呈负相关(r分别为-0.437、-0.364、-0.397、-0.519,P0.05),MDA水平与LDH、CK-MB呈正相关(r分别为0.382、0.411,P0.05)。结论左卡尼汀对柯萨奇病毒A16型感染所致HFMD有较好的心肌保护作用,可能与清除氧自由基和抑制心肌细胞凋亡有关。

Myocardial protective effect of L-carnitine in children with hand, foot and mouth disease caused by Coxsackie A16 virus

Objective To investigate the myocardial protective effect of L-carnitine in children with hand, foot and mouth disease (HFMD) caused by Coxsackie A16 virus and possible mechanisms. Methods A total of 60 HFMD children with abnormal myocardial enzyme after Coxsackie A16 virus infection were enrolled and randomly divided into L-carnitine group and fructose-1,6-diphosphate group (fructose group), with 30 children in each group. The two groups were given L-carnitine or fructose diphosphate in addition to antiviral and heat clearance treatment. Another 30 healthy children who underwent physical examination were enrolled as control group. The changes in myocardial zymogram, malondialdehyde (MDA), superoxide dismutase (SOD), and apoptosis factors sFas and sFasL after treatment were compared between groups. Results There was no significant difference in treatment response between the L-carnitine group and the fructose group (P>0.05). One child in the fructose group progressed to critical HFMD, which was not observed in the L-carnitine group. Before treatment, the L-carnitine group and the fructose group had significantly higher indices of myocardial zymogram and levels of MDA, sFas, and sFasL and a significantly lower level of SOD than the control group (P<0.05), while there were no significant differences in these indices between the L-carnitine group and the fructose group (P>0.05). After treatment, the L-carnitine group and the fructose group had significant reductions in the indices of myocardial zymogram and levels of MDA, sFas, and sFasL and a significant increase in the level of SOD (P<0.05); the fructose group had a significantly higher level of creatine kinase (CK) than the control group and the L-carnitine group, and there were no significant differences in other myocardial enzyme indices, MDA, sFas, and sFasL between the L-carnitine group and the fructose group, as well as between the L-carnitine and fructose groups and the control group (P>0.05). SOD level was negatively correlated with aspartate aminotransferase, lactate dehydrogenase (LDH), CK, and creatine kinase-MB (CK-MB) (r=-0.437, -0.364, -0.397, and -0.519 respectively; P<0.05), and MDA level was positively correlated with LDH and CK-MB (r=0.382 and 0.411 respectively; P<0.05). Conclusions L-carnitine exerts a good myocardial protective effect in children with HFMD caused by Coxsackie A16 virus, possibly by clearing oxygen radicals and inhibiting cardiomyocyte apoptosis.