OBJECTIVE: To estimate the rate of vaginal delivery after successful external cephalic version for breech presentation in women with compared with without a previous cesarean birth. DATA SOURCES: We searched MEDLINE, Scopus, EMBASE, CINAHL, ClinicalTrials.gov, and Cochrane Central Register of Controlled Trials for studies comparing the mode of delivery after successful external cephalic version in women with and without a previous cesarean birth. METHODS OF STUDY SELECTION: Two reviewers independently identified studies, extracted data, and evaluated study quality. The rate of vaginal delivery after successful external cephalic version in women with and without a previous cesarean birth was compared, and odds ratios (ORs) with 95% CIs were estimated. TABULATION, INTEGRATION, AND RESULTS: Six cohort studies and two case–control studies, reporting on 14,515 women were identified. The median point prevalence of a successful external cephalic version was 74% (interquartile range 63–81%) in women with a previous cesarean birth compared with 69% (interquartile range 64–83%) in women without a previous cesarean birth. The overall success rate of external cephalic version in women with a previous cesarean birth was similar compared with women without a previous cesarean birth (pooled OR 0.84, 95% CI 0.61–1.15). The median point prevalence of a vaginal delivery was 75% (interquartile range 61–84%) in women with a previous cesarean birth compared with 92% (interquartile range 85–95%) in women without a previous cesarean birth after a successful external cephalic version. The overall success rate of a vaginal delivery in women with a previous cesarean birth was less compared with women without a previous cesarean birth (pooled OR 0.26, 95% CI 0.14–0.50). A planned subgroup analysis on studies that included only multiparous women in the control group (parity one or greater) noted the overall success rate of external cephalic version in women with a previous cesarean birth 76% (853/1,123) was lower compared with multiparous women without a previous cesarean birth 84% (9,911/11,855) (pooled OR 0.70, 95% CI 0.54–0.89, I2 37%). The overall success rate of a vaginal delivery in women with a previous cesarean birth 83% (666/806) was less compared with women without a previous cesarean birth 97% (9,449/9,746) (pooled OR 0.21, 95% CI 0.12–0.39, I2 73%). CONCLUSION: Women with previous cesarean birth have similar rates of successful external cephalic version when compared with women without a cesarean birth. Although the rate of vaginal delivery is lower, the majority of patients have a successful vaginal birth after cesarean. SYSTEMATIC REVIEW REGISTRATION: PROSPERO, CRD42020160145.
OBJECTIVE: Chorioamniotic membrane senescence mediated by p38 mitogen activated kinase (p38 MAPK) in response to oxidative stress (OS) is associated with human parturition. In vivo, term labor fetal membranes showed OS, p38 MAPK activation, senescence and senescence associated inflammation. These findings are recapitulated in vitro in primary amnion epithelial cells (AECs) from term not in labor membranes exposed to OS induced by cigarette smoke extract (CSE). Our objective was to determine p38 induced senescence activation in response to other pathologic (LPS -infection; TNF-ainflammation) signals associated with preterm birth. STUDY DESIGN: AECs from fetal amniotic membranes at term, not in labor were exposed to tumor necrosis factor-alpha (TNF-a 50ng/mL) and lipopolysaccharide (LPS 100ng/mL) for 30 minutes or one hour. CSE (1:10) was used as positive control. Western blot analysis was performed for active and total p38 MAPK followed by densitometric analysis. Senescence was determined by flow cytometry using 5-Dodecanoylaminofluorescein di-b-D-galactopyranoside (C 12 FDG), a fluorogenic substrate for senescence associated b-galactosidase (SA-b-gal). Data were confirmed by cytological evaluation. Analysis was performed using the Mann-Whitney U test. RESULTS: p38 MAPK activation was increased in cells treated with TNF-a and CSE, but not LPS compared to untreated cells (control)(p¼0.04, p¼0.007 , p¼0.56 respectively; Figure A). The number of senescent cells as detected by C 12 FDG fluorescence were increased by all stimulants compared to control cells (p<0.05; Figure C). Senescence was confirmed with cytologic staining (Figure B). CONCLUSION: TNF-a, an inflammatory cytokine produced in response to various preterm birth-associated risk factors, and CSE induced senescence of AECs through the p38 MAPK pathway. LPS induction of senescence was independent of the p38MAPK pathway. Infectious and inflammatory factors may cause premature fetal cell senescence contributing to preterm birth pathophysiology.
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