Drug-induced pertubation of the aminothiol redox-status in patients with epilepsy: Improvement by B-vitamins

Transient Protective Effect of B-Vitamins in Experimental Epilepsy in the Mouse Brain

“…Oxidative stress can activate molecular cascades resulting in apoptotic cell death as reviewed in Mooney et al (2009). The presence of pyridoxine leads to an anti-oxidative environment and seems to contribute to an attenuation of the consequences of neurodegenerative stimulation (Apeland et al 2008). As reviewed in Scalabrino et al (2008), a deficiency of cobalamine (vitamin B 12 ) in the central nervous system results in upregulation of cytokines and growth factors such as tumor necrosis factor (TNF) or nerve growth factor followed by leukoneuropathy.…”

“…Complex mechanisms are known to induce or attenuate pathways leading to cell death following appropriate stimulation. Bvitamins were reported to attenuate degenerating processes in the nervous system and therefore have been clinically administered in a combination of B 1 (thiamine), B 6 (pyridoxine), and B 12 (cobalamine; Apeland et al 2008). There are some indications that B-vitamin supplementation counteracts abnormal aminothiol redox-status and genomic DNA methylation reactions (Apeland et al 2008).…”

“…Bvitamins were reported to attenuate degenerating processes in the nervous system and therefore have been clinically administered in a combination of B 1 (thiamine), B 6 (pyridoxine), and B 12 (cobalamine; Apeland et al 2008). There are some indications that B-vitamin supplementation counteracts abnormal aminothiol redox-status and genomic DNA methylation reactions (Apeland et al 2008). In humans, epidemiological studies indicate that hyperhomocysteinemia, in combination with B-vitamin deficiency, is associated with several degenerative processes, resulting in, e.g., cognitive dysfunction, neurological and psychiatric diseases, and other clinical manifestations.…”

Concentrations of the Selected Biomarkers of Endothelial Dysfunction in Response to Antiepileptic Drugs: A Literature Review

“…48 Literature data indicate that pharmacotherapy with AEDs affects HCys concentration, both in adult and pediatric patients. 7,8 Hyperhomocysteinemia is observed in more than 15% of children treated with AEDs, and its risk may increase during polytherapy (combination of 2 AEDs such as CBZ, VPA, PHT, VGB, OXC, TPM, LTG, and clobazam). 17 In the group of 78 epileptic children from the south of Italy (45% treated with monotherapy), the mean HCys value in patients was significantly higher than the mean in the control group (12.11 vs 7.4 mmol/L) and the decreased folate concentration was significantly correlated with increased HCys levels.…”

“…On the one hand, it has been demonstrated that there is a relationship between the use of AEDs and the levels of biochemical parameters (including HCys, folic acid, or lipids), which may influence the development of atherosclerosis. [7][8][9] On the other hand, there are data according to which this relationship does not exist. 10 Based on the comparative measurement of the intima-media thickness (IMT) in the common carotid artery in the group of epileptic adults, it has been demonstrated that the duration of AED therapy with some drugs significantly accelerates the process of atherosclerosis.…”