Related Experiment Video
Updated: Jun 17, 2026

Induction of Maternal Immune Activation in Mice at Mid-gestation Stage with Viral Mimic Poly(I:C)
Published on: March 25, 2016
Labour induction with 25 micrograms versus 50 micrograms intravaginal misoprostol in full term pregnancies
Aruna Nigam1, Monika Madan, Manju Puri
1Department of Obstetrics and Gynaecology, Lady Hardinge Medical College, New Delhi 110001, India. prakasharuna@hotmail.com
Abstract:
We undertook this study in order to compare the efficacy of 25 microg versus 50 microg of intravaginal misoprostol for cervical ripening and labour induction at term. The study population consisted of 120 women with term singleton pregnancies in vertex presentation booked for caesarean section. They had a Bishop scoring of <6 and a reactive fetal heart rate tracing. They were randomized into two groups, A and B, to receive 25 microg and 50 microg of vaginal misoprostol, respectively, 4 hourly with a maximum of five doses until the patient had three contractions in 10 minutes. There was no significant difference in the induction delivery interval between the two groups (12.52+/- 7.05 h in the 25 microg group versus 11.72+/- 6.74 h in the 50 microg group; P = 0.58). Of the women in the 25 microg group, 83.3% delivered vaginally as did 71.67% of those in the 50 microg group, but the difference was not statistically significant (P = 0.128). There were significantly more women requiring oxytocin augmentation in the 25 microg group than in the 50 microg group (P = 0.03). However, there were no significant differences in the rates of caesarean and operative vaginal delivery, meconium stained liquor, fetal distress or in the incidences of hyperstimulation between the two groups. Neonatal outcomes were similar. The intravaginal administrations of 25 microg, as well as 50 microg of misprostol, are equally efficacious in inducing labour. The 25 microg group more often required oxytocin as an adjunct.
Related Concept Videos
Intrauterine Drug Delivery Systems
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...

