levetiracetam and Atherosclerosis

The aim of the study was to investigate the risk of subclinical atherosclerosis independent from obesity and high blood lipid levels in pediatric patients with idiopathic epilepsy receiving valproic acid or levetiracetam monotherapy by evaluating carotid intima-media thickness (CIMT) and Epicardial adipose tissue thickness (EATT).. A total of 75 patients (38 males, 37 females; mean age 127.2 ± 37.9 months) with epilepsy receiving either valproic acid or levetiracetam monotherapy for more than 12 months (Epilepsy Group) and 75 sex, age, body mass index (BMI) matched healthy children (40 males, 35 females; mean age 133.8 ± 38.7 months) (Control Group) were included in the study. The mean duration of therapy was 27.6 ± 10.5 months. Serum lipid levels (total cholesterol, triglycerides, low density lipoprotein, high density lipoprotein) and CIMT-EATT of the patients and controls were assessed. Also, epilepsy group were divided according to antiepileptic drugs (valproic acid group and levetiracetam group).. The CIMT was determined as 0.6 ± 0.08 mm in epilepsy group and 0.49 ± 0.15 mm in control group (p < 0.001). The EATT was measured as 5.96 ± 0.8 mm in epilepsy group and 3.7 ± 0.5 mm in control group (p < 0.001). Of epileptic patients, 45 were using valproic acid monotherapy and 30 were on levetiracetam monotherapy. There was no significant difference in terms of CIMT between valproic acid and levetiracetam groups (0.61 ± 0.09 mm vs. 0.57 ± 0.07 mm; p = 0.07). EATT measurements were significantly higher in valproic acid group compared to levetiracetam group (6.14 ± 0.8 mm vs. 5.7 ± 0.7 mm; p = 0.02). CIMT and EATT values were not associated with the dosage and duration of each antiepileptic drug.. Non-obese children with epilepsy receiving valproic acid or levetiracetam monotherapy might have an increased risk for developing subclinical atherosclerosis despite normal lipid levels. The effect of valproic acid was more evident especially on EATT.

Topics: Adipose Tissue; Anticonvulsants; Atherosclerosis; Body Mass Index; Carotid Arteries; Carotid Intima-Media Thickness; Child; Epilepsy; Female; Humans; Levetiracetam; Male; Pericardium; Risk Factors; Valproic Acid

Although it is well documented that long-term therapy with older antiepileptic drugs (AEDs) leads to an increase in risk for atherosclerosis, there has been only limited information regarding the vascular risk in patients who are treated with new AEDs. We therefore conducted a prospective longitudinal study to assess the potential effects of new AEDs on the circulatory markers for vascular risk in patients with newly diagnosed epilepsy. We recruited adult patients with epilepsy who began to receive monotherapy with one of the new AEDs, including levetiracetam (LEV), oxcarbazepine (OXC), and topiramate (TPM). Circulatory markers of vascular risk were measured twice before and after 6 months of AED monotherapy. A total of 109 patients completed the study (LEV, n = 40; OXC, n = 40; TPM, n = 29). Six months of monotherapy resulted in significant increases in low-density lipoprotein cholesterol (LEV, from 90.2 to 98.5 mg/dl, 9.2% increase, p = 0.025; OXC, from 96.5 to 103.2 mg/dl, 7.0% increase, p = 0.049), homocysteine (LEV, from 7.9 to 10.4 μm, 31.6% increase, p = 0.001; OXC, from 8.7 to 11.5 μm, 32.2% increase, p < 0.001; TPM, from 8.3 to 12.3 μm, 48.2% increase, p < 0.001), apolipoprotein B (LEV, from 63.6 to 77.4 mg/dl, 21.7% increase; OXC, from 67.0 to 83.2 mg/dl, 24.2% increase; TPM, from 66.7 to 84.4 mg/dl, 26.5% increase; all p < 0.001), and apolipoprotein B/apolipoprotein A1 ratio (LEV, from 0.51 to 0.61, 19.6% increase; OXC, from 0.52 to 0.67, 28.8% increase; TPM, from 0.50 to 0.67, 34.0% increase; all p < 0.001). Serum apolipoprotein A1 and folate were significantly decreased in TPM (from 139.1 to 132.1 mg/dl, 5.0% decrease, p = 0.014) and OXC (from 8.1 to 6.4 ng/ml, 21.0% decrease, p = 0.046) groups, respectively. There were no significant changes in total cholesterol, triglyceride, high-density lipoprotein cholesterol, lipoprotein(a), and vitamin B12 in all three groups. Our findings suggest that treatment with some new AEDs might be associated with alterations in circulatory markers of vascular risk, which could contribute to the acceleration of atherosclerosis and increased risk of vascular diseases.

Topics: Adult; Anticonvulsants; Apolipoprotein A-I; Apolipoproteins B; Atherosclerosis; Biomarkers; Carbamazepine; Cholesterol, LDL; Epilepsy; Female; Fructose; Homocysteine; Humans; Levetiracetam; Male; Oxcarbazepine; Piracetam; Prospective Studies; Risk Factors; Topiramate