Prenatal psychological state and the use of drugs in labor.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Eighty patients with a Bishop score of less than or equal to 4 were randomly administered vaginal triacetin gel containing placebo or prostaglandin E2 in 1, 2, and 3 mg doses. Twelve to sixteen hours later, those not in labor underwent oxytocin induction. Increasing doses of prostaglandin were effective in ripening the cervix, and the higher doses were associated with significant success in inducing labor.
In a double-blind controlled multicentric study involving 94 patients with an intrauterine fetal death, we investigated the efficacy and tolerance of mifepristone (RU 486), a steroid compound that antagonizes progesterone action at the receptor level. Success of treatment was defined as the occurrence of fetal expulsion within 72 hours after the first drug intake. Mifepristone treatment (600 mg per day for 2 days) was considered to be effective in 29 of 46 patients (63%). There were only eight successes in 48 patients (17.4%) in the placebo group (p = 0.001, chi 2 test). Tolerance was good in the mifepristone group. In the placebo group, disseminated intravascular coagulation occurred in one woman for whom the investigator waited several weeks for spontaneous expulsion. This large double-blind controlled study provides evidence that mifepristone is of interest in the management of intrauterine fetal death. It could provide a pharmacologic alternative to the use of prostaglandins in this indication.
OBJECTIVE: Our purpose was to compare the efficacy, safety, and cost of commercially available dinoprostone cervical gel 0.5 mg with a hospital-compounded formulation. STUDY DESIGN: One hundred thirty-four patients undergoing labor induction were randomly assigned to one of two cervical ripening groups. Commercially available dinoprostone gel 0.5 mg or a compounded formulation of 0.5 mg of prostaglandin E2 gel was administered endocervically. On the basis of cervical scores, gel was reapplied at 6-hour intervals for a maximum of three doses. Physicians managing labor were blinded as to treatment group allocation. RESULTS: Among 134 patients evaluated, 70 were allocated to the commercially available gel and 64 to the compounded gel. No statistically significant differences were noted between the treatment groups with respect to start-to-delivery interval, number of doses, amount of oxytocin, or neonatal adverse outcomes. However, cesarean delivery was performed less frequently in patients in the group receiving the commercially available gel (12.9%) than in the group receiving the compounded gel (28.1%) (p = 0.03). Because of the higher cesarean delivery rate in the compound group, use of this formulation was not associated with cost savings. CONCLUSIONS: The two prostaglandin E2 formulations appeared equivalent with respect to efficacy. An unexplained higher cesarean section rate, however, was associated with the use of the compounded preparation.
OBJECTIVE: Our purpose was to compare the safety and efficacy of intravaginal prostaglandin E1, misoprostol, with that of intracervical prostaglandin E2 (Prepidil gel) for labor induction. STUDY DESIGN: One hundred three patients with an indication for induction of labor were randomly assigned to induction with prostaglandin E1, 50 micrograms intravaginally, or with Prepidil gel, 0.5 mg intracervically, every 4 hours until active labor. RESULTS: Four patients were excluded, leaving 49 patients who received prostaglandin E1 and 50 who received prostaglandin E2. The time from start of induction to vaginal delivery was significantly shorter in the prostaglandin E1 group (11.4 vs 18.9 hours, p < 0.001), and fewer patients in the prostaglandin E1 group required oxytocin augmentation (23% vs 55%, p < 0.005). No significant differences were noted in mode of delivery or in adverse maternal, fetal, or neonatal effects. CONCLUSION: Intravaginal prostaglandin E1 is a more effective, lower-cost agent for induction of labor than is intracervical prostaglandin E2 gel and is comparable in safety.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Prostaglandins E1, prostaglandin E2, 3-oxa-methano-prostaglandin I1 (SM-10906), a stable prostaglandin I2 analog, and dibutyryl cyclic AMP suppressed the production of tumor necrosis factor and interleukin-1 in lipopolysaccharide-stimulated rat pleural resident monocytic cells, whereas they enhanced the production of interleukin-6 and cytokine-induced neutrophil chemoattractant (CINC), a rat interleukin-8-like chemokine, in these cells. SM-10906 also inhibited the in vivo production of tumor necrosis factor and interleukin-1 in pleural exudates, when injected into the rat pleural cavity concomitantly with carrageenin. The cyclic AMP (cAMP) level in the lipopolysaccharide-stimulated resident cells was increased when the cells were incubated in the presence of prostaglandin E1, prostaglandin E2 or SM-10906. Prostaglandin I2 showed only slight effects. The addition of pentoxifylline, a phosphodiesterase inhibitor, to the incubation mixture increased the cAMP level and also enhanced the effect of prostaglandins, indicating that these regulating actions of prostaglandins may be exerted partly through a mechanism involving an increased intracellular cAMP level.
Explore the source record for details and available documents.