Abstract
BackgroundNumerous studies have shown that long term treatment with anticonvulsants may be an important risk factor for the onset of atherosclerosis, or worsening of its symptoms. There are many contradictory reports regarding these effects.ObjectivesWe performed a systematic review and meta-analysis of the published studies in order to see whether the atherogenic outcomes could be related to any serum biochemical abnormalities.Materials and MethodsPublished articles indexed in PubMed, ISI web of science, Science Direct and Scopus databases from 1990 to 2011 were retrieved using a comprehensive search strategy. After omitting the unrelated articles and duplicates, articles met the eligibility criteria for critical appraisal were included in the analysis. Data were summarized in standard data abstraction forms and subjected to analysis by STATA software.ResultsFinally, ten published studies were included in the meta-analysis. Results showed that carbamazepine and sodium valproate consumption are associated with a significant elevation of the serum homocysteine levels. On the other hand, medication with carbamazepine is associated with a reduction of the level of folate in the serum and that of sodium valproate is associated with a reduction of serum level of vitamin B12.ConclusionsAccording to the results of this study, as carbamazepine and valproate sodium consumption can result in elevated serum levels of homocysteine and decreased levels of folate and vitamin B12, and the atherogenic effect of increased serum homocysteine level is well established, the patients under these medications should be monitored for possible atherogenic effects.
Highlights
Numerous studies have shown that long term treatment with anticonvulsants may be an important risk factor for the onset of atherosclerosis, or worsening of its symptoms
Epidemiological studies have shown that in adults suffering from epilepsy, risk of development of atherogenic ischemic heart disease (IHD) and fatal cardiovascular disease increase to 34% and 68%, respectively [2]
In regards to treatment with sodium valproate, the results showed that it was significantly associated with increased serum homocysteine levels (P < 0.001) (p for heterogeneity = 0.003; I-squared = 72.1%; no publication bias in funnel plot, no significant Egger’s test [P > 0.05]), but was not associated with reduction of the serum folate levels (P = 0.52) (p for heterogeneity = 0.01; I-squared=65.7%; no publication bias in funnel plot, no significant Egger’s test [P > 0.05])
Summary
Numerous studies have shown that long term treatment with anticonvulsants may be an important risk factor for the onset of atherosclerosis, or worsening of its symptoms. Conclusions: According to the results of this study, as carbamazepine and valproate sodium consumption can result in elevated serum levels of homocysteine and decreased levels of folate and vitamin B12, and the atherogenic effect of increased serum homocysteine level is well established, the patients under these medications should be monitored for possible atherogenic effects. Impairment of endothelial function is another possible mechanism, which has been presumed to be the result of epilepsy itself, or side effects of long term treatment with antiepileptic agents. This may induce the process of atherogenesis and result in arterial obstructive diseases leading to stroke, myocardial infarction, etc. Among the serum biochemical changes, alterations of the serum homocysteine, folate, and B12 following anticonvulsant therapy and their relationship to atherosclerosis is a subject of controversy [5,6,7,8]as the metabolism of these biochemical factors are inter-related and deficiency of either folate or vitamin B12 increases the serum homocysteine level
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