Comparison of the effects of alendronate and risedronate on bone mineral density and bone turnover markers in postmenopausal osteoporosis.

The aim of the study was to compare the effects of once-weekly alendronate sodium and daily risedronate sodium treatment on bone mineral density (BMD) and bone turnover markers in postmenopausal osteoporotic subjects. For this purpose, 50 patients were included in this study and randomly classified into two groups. Group I (n=25) received risedronate (5 mg/day) and group II (n=25) received alendronate Na (70 mg/week). The study duration was limited to 12 months. The efficacy of the treatment was evaluated by BMD measurements at spine and hip at 6th and 12th months of the treatment, as well as by the measurement of bone turnover markers such as serum osteocalcin (OC), bone-specific alkaline phosphatase (BASP), urine deoxypyridinoline (DPD) and calcium/creatine ratio in 24-h urine at 1st, 3rd, 6th and 12th months. The evaluation of the changes in BMD in all regions revealed a significant increase in BMD in both groups compared to baseline values except for spine (L2-L4) in alendronate group at 6th and 12th month and femoral neck in risedronate group at 6th month. However, the difference in percentage increase in BMD measurements was not statistically significant between the two groups at 6th and 12th months. In both groups, serum OC, BSAP and urine DPD were found to be significantly attenuated at 1st month of the treatment period, and continued to be lowered throughout the 3rd, 6th and 12th months (P<0.05). However, there was no statistically-significant difference between both groups of patients (P>0.05). In conclusion, our results suggest that both treatment protocols provide treatment options of similar efficiency for postmenopausal osteoporosis, and have almost-similar effects in enhancing the BMD and in slowing the bone turnover. Risedronate seems to have a more potent effect in the spinal region than that of alendronate, although this potency was not statistically significant.

Endothelial dysfunction in preeclampsia. Increased homocysteine and decreased nitric oxide levels.

Endothelial dysfunction underlies the pathogenesis of preeclampsia, but its mechanism has not yet been completely understood. Elevated oxygen free radicals may partially explain the endothelial cell damage. In this study, we have aimed to measure homocysteine (Hcy) and nitric oxide (NO) levels as endothelial dysfunction markers in preeclamptic women. Nineteen preeclamptic (33.9 +/- 1.4 weeks) and 15 gestational-age-matched normal pregnant women (35.5 +/- 0.7 weeks) were included in the study. Mean NO level was significantly lower (p < 0.001) and mean Hcy level was significantly higher (p < 0.001) in the preeclamptic group. Elevated Hcy and oxygen free radical levels could decrease NO levels due to the reaction with each other and reduced NO may increase blood pressure and ischemia in preeclamptic patients. We have concluded that increased Hcy and oxygen free radical levels, and decreased NO levels are closely associated with preeclampsia-related endothelial dysfunction.

Atherogenic profile in preeclampsia.

Atherosis is accepted to underlie the pathogenesis of preeclampsia, therefore we aimed to determine malonyldialdehyde (MDA) levels as a marker of lipid peroxidation, and lipoprotein(a) (Lp(a)), apolipoprotein A-1 (Apo A-1) and apolipoprotein B (Apo B) levels as a marker of atherogenic profile in preeclamptic and normal pregnant women. Twenty preeclamptic and 20 gestational-age matched normal pregnant patients were enrolled in the study, mean gestational ages for the preeclamptic and the control group were 33.9+/-1.4 and 35.5+/-0.7 weeks, respectively. Blood was withdrawn from the patients soon after diagnosis, and from the controls at their routine prenatal visits. MDA levels was significantly higher in preeclamptic patients (P=0.0003), but no difference was observed in Apo A-1 and Apo B and Lp(a) levels between the 2 groups. We consider that higher MDA was due to oxidative stress seen in preeclampsia, and similar Apo A-1 and Apo B and Lp(a) levels were due to lack of systemic atherosis.