Methods: This double-blind, randomized clinical trial recruited 60 patients with predisposing factors to PPROM. The women were randomly divided into two GDC-0973 datasheet groups of intervention and control and received vitamin C and placebo, respectively. The intervention group received 250 mg vitamin C twice a day and the controls received the placebo only. Unconjugated estriol was measured using the ELISA.

All data were extracted and recorded in a checklist and compared using descriptive statistics as well as the x2, Fisher exact, and t tests. Results: The demographic data showed no difference between the two groups. The mean level of serum unconjugated Inhibitors,research,lifescience,medical estriol was significantly lower in the intervention group than in the control group (P=0.044). Also, the frequency of PPROM was lower in the intervention Inhibitors,research,lifescience,medical group, but the difference was not significant (P>0.05). Unconjugated estriol levels were not significantly different between the healthy women and the PPROM patients. Conclusion: This study demonstrated that vitamin C administration decreased unconjugated estriol Inhibitors,research,lifescience,medical levels in the patients with PPROM. The findings of this study also indicated that administration of ascorbic acid was a safe and effective method to reduce the incidence of PPROM. Alteration in unconjugated estriol is an active mediator for

this effect. Key Words: Unconjugated, Estrio, Vitamin C Introduction Premature rupture of membrane (PROM) is the rupture of the chorioamniotic membrane and leakage of the amniotic fluid before delivery contractions.1 PROM is the commonest cause of premature delivery. Recent studies have reported that with occurrence rates of 6 to 19%, PROM is the leading cause of mortality Inhibitors,research,lifescience,medical in the prenatal period.2 Preterm PROM (PPROM), which leads to PROM

before the 37th week Inhibitors,research,lifescience,medical of pregnancy, is responsible for 40 to 50% preterm deliveries and necessitates hospitalization in the neonatal intensive care unit (NICU).3 Various causes have so far been propounded for PPROM – with a sizable bulk of evidence relating it to biochemical processes such as disorders of collagen synthesis in the extra-cellular matrix Metalloexopeptidase of amnion and chorion and planned death of cells in fetal tissues. It is suspected that mediators released from stretching membrane or infection and activation of destructive enzymes in the matrix lead to the rupture of the uterus or amniotic membranes.4 One of the factors involved in the activation of membrane destruction is the activity of reactive oxygen species (ROS). Because antioxidants suppress ROS by their chemical characteristic, consumption of materials like ascorbic acid or vitamin C is effective in the stability of the membrane and prevention of PROM and PPROM.5 Epidemiological studies, linking clinical conditions known to produce ROS or reduce antioxidant protection to PPROM, support this hypothesis.