The present study was undertaken to determine the change of blood lipid peroxide and antioxidant status in healthy nonpregnant women (n = 20), pregnant women in the third trimester (n = 20), pregnant women during delivery (n = 26) and fetal cord blood. Plasma and erythrocyte malondialdehyde (MDA) levels were found to be significantly higher and erythrocyte glutathione (GSH) levels were significantly lower in pregnant women in the third trimester than in nonpregnant women (p < 0.02, p < 0.03 and p < 0.001, respectively). The highest plasma and erythrocyte MDA levels and the lowest GSH levels were obtained from the pregnant women during delivery (6.99 ± 2.35 nmol/ml, 283.20 ± 43.81 nmol/g Hb, 6.73 ± 2.34 µmol/g Hb, respectively). Erythrocyte glutathione peroxidase (GSH-P) and glutathione reductase (GSH-R) activities were not different between the groups. Maternal plasma and erythrocyte MDA levels were significantly correlated with cord blood plasma and erythrocyte MDA levels (r = 0.63, p < 0.001, and r = 0.41, p < 0.001, respectively). There was a significant positive correlation in GSH-R and in GSH-P activities between maternal and cord blood erythrocytes (r = 0.81, p < 0.001, and r = 0.79, p < 0.001, respectively). A significant correlation was found between maternal erythrocyte GSH-P and both cord blood erythrocyte GSH-R activities (r = 0.74, p < 0.001) and cord erythrocyte GSH levels (r = 0.73, p < 0.001). There was also a significant negative correlation between maternal erythrocyte MDA and cord erythrocyte GSH-R levels (r = –0.9, p < 0.001). Our results suggest that lipid peroxidation and antioxidant status may be changed during delivery, and these changes may affect the fetus by creating oxidative stress.

Trichodynia is a commonly encountered symptom in patients with diffuse alopecia, and depression and somatoform dissociation disorders may play an important role in its aetiology. Our data provide no evidence that serum levels of zinc, folate or vitamin B(12) are involved in the pathogenesis of trichodynia.

BackgroundMigraine is a common headache disorder that may be associated with vascular disease and cerebral white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI) scan. High sensitivity C-reactive protein (hs-CRP) is a marker of inflammation that may predict subclinical atherosclerosis. However, the relation between migraine, vascular risks, and WMHs is unknown. We evaluated hs-CRP levels and the relation between hs-CRP level and WMHs in adult migraine patients.MethodsThis case–control study included 432 subjects (216 migraine patients [without aura, 143 patients; with aura, 73 patients]; 216 healthy control subjects without migraine; age range 18–50 y). Migraine diagnosis was determined according to the International Classification of Headache Disorders II diagnostic criteria. The migraine patients and control subjects had no known vascular risk factors, inflammatory disease, or comorbid disease. The presence and number of WMHs on MRI scans were determined, and serum hs-CRP levels were measured by latex-enhanced immunoturbidimetry.ResultsMean hs-CRP level was significantly greater in migraine patients (1.94 ± 2.03 mg/L) than control subjects (0.82 ± 0.58 mg/L; P ≤ .0001). The mean number of WMHs per subject and the presence of WMHs was significantly greater in migraine patients (69 patients [31.9%]; 1.68 ± 3.12 mg/dL) than control subjects (21 subjects [9.7%]; 0.3 ± 1.3; P ≤ .001). However, there was no correlation between hs-CRP level and WMHs in migraine patients (r = 0.024; not significant). The presence of WMHs was increased 4.35-fold in migraine patients (odds ratio 4.35, P ≤ .001).ConclusionsHigh hs-CRP level may be a marker of the proinflammatory state in migraine patients. However, the absence of correlation between hs-CRP level and WMHs suggests that hs-CRP is not causally involved in the pathogenesis of WMHs in migraine patients. The WMHs were located mostly in the frontal lobe and subcortical area.

Our results indicated that lipid peroxidation and the inadequacy of the defense system seem to play a crucial role in the pathogenesis of recurrent aphthous stomatitis.

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