Thyroid hormones may contribute to vascular risk factors and atherosclerosis

İngilizce (OpenAlex)

To the Editors: The recent article from Chuang et al. (2012) confirms the long-term drug-specific effects of monotherapy with both nonenzyme-inducing antiepileptic drugs (lamotrigine), enzyme inducers (carbamazepine and phenytoin), and enzyme inhibitors (valproic acid) on serologic biomarkers and quantified common carotid artery intima media thickness in patients with epilepsy. Based on common carotid artery intima media thickness measurements, these authors demonstrated that the duration of monotherapy with carbamazepine, phenytoin, or valproic acid is significantly associated with acceleration of atherosclerosis in patients with epilepsy, albeit via different underlying mechanisms. Some potential underlying mechanisms, such as inflammation (carbamazepine and phenytoin) and oxidative stress (valproic acid), were discussed in this article. However, the authors omitted a potentially important role of thyroid hormones on the vascular system. Recently, we investigated the mechanism of the effect of carbamazepine, valproic acid, and valproic acid plus carbamazepine by determining serum levels of oxidized low-density lipoprotein, apolipoprotein A1, homocysteine, folic acid, vitamin B12, paraoxonase-1 activity, total antioxidant capacity, malondialdehyde, nitric oxide, and thyroid hormones in 59 children with epilepsy who were treated with antiepileptic drugs for at least 6 months, and 23 controls (Yildiz et al., 2010). For technical reasons (body height <120 cm, and body weight <30 kg), the arterial distensibility was assessed by automatic carotid-femoral (aortic) pulse-wave velocity measurement (the Complior Colson device – Createch Industrie, France) in 39 subjects. This measurement is the safest and simplest method for atherosclerotic evaluation (Asmar et al., 1995; Mansia et al., 2007). In our study, we showed that serum lipid profiles, homocysteine, folic acid, vitamin B12, oxidative stress, total antioxidant capacity, nitric oxide, oxidized low-density lipoprotein, apolipoprotein A1, and paraoxanase-1 activity were not affected, but free T4 level was decreased in children with epilepsy using valproic acid, carbamazepine, and valproic acid plus carbamazepine. A significant increase in thyroid stimulating hormone (TSH) levels was also detected in epileptic children using valproic acid. These results suggest that antiepileptic drugs may induce atherogenesis though an effect on thyroid hormones (Ojamaa et al., 1996; Duman et al., 2007; Yildiz et al., 2010). I have no conflicts of interest to disclose. I confirm that I have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.