Key result
L-carnitine significantly reduced creatine kinase levels compared to fructose-1,6-diphosphate and demonstrated a good myocardial protective effect in children with hand, foot and mouth disease caused by Coxsackie A16 virus.
Why the study?
Does L-carnitine improve myocardial enzyme and oxidative stress markers in children with HFMD caused by Coxsackie A16 virus compared to fructose-1,6-diphosphate?
RCT (n=90)
Randomly divided
No
Does L-carnitine improve myocardial enzyme and oxidative stress markers in children with HFMD caused by Coxsackie A16 virus compared to fructose-1,6-diphosphate?
L-carnitine provides myocardial protection in children with Coxsackie A16-induced HFMD, potentially by reducing oxidative stress and cardiomyocyte apoptosis.
Answers are grounded in this paper and cite their sources.
Supports adjunctive L-carnitine in Coxsackie A16 HFMD; extends RCT evidence to pediatric viral myocarditis.
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.
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Cui et al. (2017) conducted an RCT in Hand, foot and mouth disease (HFMD) with abnormal myocardial enzymes (n=90). L-carnitine vs. Fructose-1,6-diphosphate was evaluated on Creatine kinase (CK) level after 7 days of treatment (IU/L) (p=<0.05). L-carnitine significantly reduced creatine kinase levels compared to fructose-1,6-diphosphate and demonstrated a good myocardial protective effect in children with hand, foot and mouth disease caused by Coxsackie A16 virus.
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