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Published on: June 25, 2010
Homocysteine Metabolism and Hematological Parameters in Early Stage of Phenytoin Treated Epileptic Children
Insights
Phenytoin monotherapy in epileptic children significantly increases homocysteine and decreases folate and vitamin B12 levels early in treatment. Monitoring these metabolic changes is crucial for preventing cardiovascular complications.
Area of Science:
- Neurology
- Clinical Chemistry
- Pediatric Medicine
Background:
- Antiepileptic drug (AED) therapy, particularly long-term use, is linked to metabolic issues and increased atherosclerosis risk in epilepsy patients.
- Conflicting prior research exists on hematological parameters, homocysteine, folate, and vitamin B12 levels in epilepsy patients on phenytoin monotherapy.
Purpose of the Study:
- To evaluate homocysteine metabolism and hematological parameters in epileptic children during the early stages of phenytoin monotherapy.
Main Methods:
- Enrolled 64 newly diagnosed epileptic children; 50 completed the 3-month follow-up.
- Measured serum homocysteine via enzyme immunoassay and serum folate/vitamin B12 via competitive chemiluminescent enzyme immunoassay.
- Analyzed hematological parameters using a Sysmex XT-1800i automated hematology analyzer.
Main Results:
- No significant changes in anthropometric or hematological parameters were observed post-phenytoin therapy compared to baseline.
- Significantly increased serum homocysteine levels were detected after phenytoin monotherapy.
- Highly significant decreases in serum folate and vitamin B12 levels were observed post-phenytoin monotherapy.
Conclusions:
- Phenytoin monotherapy can rapidly increase serum homocysteine and decrease serum folate and vitamin B12 in epileptic children.
- These early metabolic alterations may contribute to a higher incidence of cardiovascular events in pediatric epilepsy patients on phenytoin.
- Early screening and management of elevated homocysteine, alongside regular monitoring of hematological parameters, are recommended for children on phenytoin to prevent atherosclerosis.
Background:
Long-term antiepileptic drug (AED) therapy has been associated with metabolic consequences that lead to an increase in risk of atherosclerosis in patients with epilepsy. Earlier published studies showed conflicting results about the levels of hematological parameters, serum homocysteine, folate, and vitamin B12, in epileptics treated with phenytoin monotherapy. Therefore, we evaluated homocysteine metabolism and hematological parameters in early stage of phenytoin treated epileptic children.
Methods:
A total of 64 newly diagnosed epileptic children with mean age 10.09 ± 2.56 years were enrolled at the start of study. However, after 3 months follow up, the final total sample size was only 50 epileptic children. Fourteen children dropped out of study due to poor follow up. Serum homocysteine levels were measured by enzyme immunoassay method. Serum folate and vitamin B12 levels were estimated by Competitive Chemiluminescent Enzyme Immunoassay method. Hematological parameters were analysed by an automated hematology analyzer (Cell counter), Sysmex XT-1800i, using commercially available reagents.
Results:
In our study the anthropometric and hematological parameters did not show any significant difference after phenytoin monotherapy as compared to before therapy in epileptic children. The serum homocysteine level in epileptic children was found to be significantly increased after phenytoin (PHT) monotherapy as compared to before therapy. Moreover, a highly significant decrease was observed in the serum folate and vitamin B12 levels after phenytoin monotherapy as compared to before therapy in epileptic children.
Conclusions:
Phenytoin monotherapy may cause a significant increase in the levels of serum homocysteine and a significant decrease in the serum folate and vitamin B12 levels in children with epilepsy, and the significant changes in above mentioned parameters occur early in the course of treatment. This could be responsible for a higher prevalence of cardiovascular incidents in epileptic children taking phenytoin monotherapy. Therefore, it may be useful to do early screening and treatment of increased serum homocysteine levels in epileptic children under phenytoin monotherapy to prevent atherosclerosis and its complications. Hematological parameters should also be strictly monitored regularly in individuals administered with PHT monotherapy. If there are persistent alterations, the administration of the drugs should be discontinued.
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