No abstract

The purpose of this study was to evaluate the distinct pathogenic mechanisms underlying chronic hypertension in pregnancy and preeclampsia in terms of oxidative stress and vascular reactivity. A total of 17 women with uncomplicated pregnancies, 30 women with preeclampsia and 17 women with chronic hypertension were evaluated. We measured serum derivatives of reactive oxygen metabolites (d-ROMs; marker of oxygen free radicals), flow-mediated vasodilation (FMD; marker of endothelial function) and intima-media thickness in the carotid artery (IMT; marker of atherogenesis) during pregnancy and 1 month after delivery. Serum d-ROM concentrations were significantly higher in women with chronic hypertension and severe preeclampsia than in the control group during pregnancy. d-ROM concentrations in all groups significantly decreased to similar levels 1 month after delivery. FMD was significantly lower during pregnancy in preeclamptic and chronic hypertension groups compared with the control group. FMD in preeclamptic groups significantly increased and normalized to control levels after delivery. Similarly, FMD in the chronic hypertension group significantly increased after delivery but was still lower. IMT in the chronic hypertension group was significantly higher than that in control and preeclamptic groups. These findings suggest that endothelial dysfunction induced by enhanced oxidative stress is reversible in women with preeclampsia, whereas impaired vascular reactivity may be associated with atherosclerotic changes in women with chronic hypertension.

Visceral fat accumulation stimulates the production of adipocytokines in patients with metabolic syndrome. Excess body weight gain during pregnancy is a risk factor for preeclampsia. To evaluate whether the pathogenesis of preeclampsia is similar to that of metabolic syndrome, we measured plasma adipocytokine concentrations and investigated the association between plasma adiponectin concentrations and body weight gain or endothelial function in preeclamptic women. We investigated 15 preeclamptic and 17 women with uncomplicated pregnancies. Women with preeclampsia had significantly lower plasma concentrations of adiponectin (10.2 ± 2.0 vs. 7.3 ± 2.2 lg ml À1 , Po0.01), but higher concentrations of leptin, plasminogen activator inhibitor-1, interleukin-6, vascular cell adhesion molecule-1, E-selectin and C-reactive protein. Plasma triglyceride levels were significantly higher in preeclamptic patients, but the levels of other lipids did not differ significantly between the two groups. We found that flow-mediated vasodilation was significantly decreased in preeclamptic women compared with controls (10.6 ± 6.4 vs. 3.8 ± 2.0%, Po0.001). Plasma adiponectin concentrations correlated negatively with body mass index (r¼À0.50, Po0.05) and body weight gain during pregnancy (r¼À0.63, Po0.01), and positively with flow-mediated vasodilation (r¼0.50, Po0.05) in preeclamptic women, but not in women with uncomplicated pregnancies. Similar to the patients with metabolic syndrome, we found that dysregulation of adipocytokines, such as low adiponectin levels and high levels of other adipocytokines, and excess body weight gain during pregnancy, may decrease plasma adiponectin concentrations that are associated with endothelial dysfunction in preeclamptic women.

Our findings indicate that the severity of hypoxic changes and oxidative DNA damage are greater in the placenta of women with early-onset preeclampsia, and that the prolonged preeclamptic conditions may reduce placental blood flow, ultimately leading to FGR.

To identify predictive factors of prognosis after radiotherapy with concurrent steroid pulse therapy for thyroid eye disease, retrospective analyses were performed among 77 patients. Clinical activity score and magnetic resonance imaging were used to evaluate degrees of orbital inflammation. As a pre-treatment work-up, the thyroid-stimulating antibody (TSAb) level was measured. During a median follow-up of 25.0 months, the 2-year cumulative relapse-free rate (CRFR) was 80.9%. In the univariate analysis, a worse 2-year CRFR was significantly associated with the presence of optic neuropathy (P = 0.001), a higher TSAb rate (P = 0.001), and lower standard deviation (SD) of signal intensity at the extraocular muscle in T2-weighted images (P = 0.006). In the multivariate analysis, TSAb rate and SD affected the CRFR independently. When TSAb activity of 2800% was set as a cut-off at 2 years after treatment, the predictive sensitivity and specificity of relapse were 81.2% and 90.6%, respectively. With regard to SD, the respective sensitivity and specificity values were 81.2% and 82.7% when 100 was set as a cut-off. In conclusion, high TSAb and low SD were significant risk factors for cumulative relapse in orbital radiotherapy. Cut-off values of 2800% for TSAb and 100 for SD may be suitable.