Migraine is the most common neurological disorder, but the molecular basis is still not completely understood. An impairment of mitochondrial oxidative metabolism might play a role in the pathophysiology. The goal of this study was to investigate the differences in oxidative stress status with the measurement of erythrocyte superoxide dismutase (SOD), catalase activity, and malondialdehyde (MDA) levels in the migraine patients with or without aura and attack. There were 56 patients (46 female, 10 male) in the migraine group and 25 matched healthy subjects in the control group. The patients comprised 37 with migraine without aura (MWoA], 19 with migraine with aura (MWA), and 22 with headache attack. The MDA levels of patients in the migraine group were significantly higher than that in the control group. The SOD activity was significantly higher in the MWA as compared to MWoA. There was no significant correlation between these levels and headache attack period. Conclusively, in this preliminary study, we had found increased oxidative stress in the migraine patients especially the patients with MWA. Further knowledge about this issue may contribute the cause and complications of migraine and may be essential for development of treatment approaches.

Although the systemically measured levels of protein S, vWf, VEGF and IL-12 were found to be higher in patients of primary varicose veins, levels of protein C, fibrinogen, homocysteine and PGI2 were not found to be statistically significant. No systemic increased oxidative stress seems to be related to the early stages of chronic venous insufficiency. Further studies are warranted for understanding the role of molecules such as NO, oxidative stress parameters and cytokines.

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Alterations in thyroid function are associated with changes in body weight, metabolism, and low-grade inflammation. In several studies, plasma levels of visfatin were found to be associated with body mass index, diabetes, and metabolic syndrome. In our study we aimed to evaluate visfatin levels according to thyroid dysfunction. The study cohort comprised 56 Hashimoto thyroiditis patients with hypothyroidism (43.94+/-14.27 yr), 56 Graves patients with hyperthyroidism (45.87+/-13.28 yr), and 56 euthyroid healthy subjects (45.23+/-7.11 yr) as a control group. In addition, we evaluated the effect of therapy on plasma visfatin levels in 16 hypothyroid and in 25 hyperthyroid patients. Markedly low visfatin levels were found in hyperthyroid patients [9.44 (8.07- 10.8) ng/ml] compared with the hypothyroid [49.93 (40.72- 59.1) ng/ml] and control groups [38.6 (30.6-46.6) ng/ml] (p<0.001, p<0.001). Plasma visfatin levels in patients with hypothyroidism decreased significantly following treatment [58.58 (10.21-190.7) ng/ml vs 40.00 (10.01-102.6) ng/ml; p=0.001]. Plasma visfatin levels increased significantly after antithyroid therapy in patients with hyperthyroidism [7.86 (1.02-19.23) ng/ml vs 12.63 (3.48-110.9) ng/ml; p<0.001]. There were negative correlations between visfatin levels with free T3 (r=-0.719, p<0.001), and free T4 (r=-0.716, p<0.001) levels. There was a positive correlation between visfatin and TSH levels (r=0.701, p<0.001). There was a negative correlation between delta visfatin levels with delta free T3, delta free T4 (r=-0.686, p<0.001; r=-0.624, p<0.001). Visfatin thus seems to be regulated by thyroid hormones. While the influence of thyroid dysfunction on adipocytokine production and release is still poorly understood, the results of our study suggest that the effects of hyper- and hypothyroidism on various metabolic parameters may be partly mediated by visfatin.

Brimonidine and NAC supplementation provide antioxidative properties to retina and decrease retinal damage induced by ocular hypertension.