Abstract

Endometriosis is an inflammatory disease with a heterogeneous presentation that affects women of childbearing age. Given the limitations of previous retrospective studies, it is still unclear whether endometriosis has adverse implications for pregnancy outcomes. To evaluate the association between the presence of endometriosis and preterm birth and whether the risk varied according to the disease phenotype. This cohort study with exposed and unexposed groups was conducted in 7 maternity units in France from February 4, 2016, to June 28, 2018. Participants included women with singleton pregnancies who were followed up before 22 weeks' gestation along with their newborns delivered at or after 22 weeks' gestation. The final follow-up occurred in July 2019. Data were analyzed from October 7, 2020, to February 7, 2021. Women in the endometriosis group had a documented history of endometriosis and were classified according to 3 endometriosis phenotypes: isolated superficial peritoneal endometriosis (SUP), ovarian endometrioma (OMA; potentially associated with SUP), and deep endometriosis (DE; potentially associated with SUP and OMA). Women in the control group did not have a history of clinical symptoms of endometriosis before their current pregnancy. The primary outcome was preterm birth between 22 weeks and 36 weeks 6 days of gestation. Association between endometriosis and the primary outcome was assessed through univariate and multivariate logistic regression analyses and was adjusted for the following risk factors associated with preterm birth: maternal age, body mass index (calculated as weight in kilograms divided by height in meters squared) before pregnancy, country of birth, parity, previous cesarean delivery, history of myomectomy and hysteroscopy, and preterm birth. The same analysis was performed according to the 3 endometriosis phenotypes (SUP, OMA, and DE). Of the 1351 study participants (mean [SD] age, 32.9 [5.0] years) who had a singleton delivery after 22 weeks of gestation, 470 were assigned to the endometriosis group (48 had SUP [10.2%], 83 had OMA [17.7%], and 339 had DE [72.1%]) and 881 were assigned to the control group. No difference was observed in the rate of preterm deliveries before 37 weeks 0 days of gestation between the endometriosis and control groups (34 of 470 [7.2%] vs 53 of 881 [6.0%]; P = .38). After adjusting for confounding factors, endometriosis was not associated with preterm birth before 37 weeks' gestation (adjusted odds ratio, 1.07; 95% CI, 0.64-1.77). The results were comparable for the different disease phenotypes (SUP: 6.2% [3 of 48]; OMA: 7.2% [6 of 83]; and DE: 7.4% [25 of 339]; P = .84). This cohort study found no association between endometriosis and preterm birth, and the disease phenotype did not appear to alter the result. Monitoring the pregnancy beyond the normal protocols or changing management strategies for women with endometriosis may not be warranted to prevent preterm birth.

Highlights

  • Endometriosis is an inflammatory disease that affects 10% to 15% of women of reproductive age worldwide.[1]

  • This cohort study found no association between endometriosis and preterm birth, and the disease phenotype did not appear to alter the result

  • Meaning The findings suggest that modification of pregnancy monitoring or management strategies to prevent preterm birth for women with endometriosis may not be needed

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Summary

Introduction

Endometriosis is an inflammatory disease that affects 10% to 15% of women of reproductive age worldwide.[1]. Previous studies have yielded conflicting results regarding the implication of endometriosis for pregnancy outcomes.[2]. Various hypotheses have been proposed to explain the adverse implications of endometriosis for pregnancy, but the pathogenesis and the specific role of each disease phenotype remain unclear. Endometriosis is believed to adversely affect uterine functions, especially by compromising properties of the eutopic endometrium.[6]. These alterations could interfere with the normal process of decidualization that helps control trophoblast invasion at the maternal-fetal interface,[7-12] thereby potentially leading to severe placentation defects and obstetric complications.[10,13]. Considering endometriosis as an endometrial disease, a previous study documented the molecular alteration of the choriodecidual layer in women with DE, with molecular changes at the fetal-maternal interface.[14] These alterations could interfere with the normal process of decidualization that helps control trophoblast invasion at the maternal-fetal interface,[7-12] thereby potentially leading to severe placentation defects and obstetric complications.[10,13] Considering endometriosis as an endometrial disease, a previous study documented the molecular alteration of the choriodecidual layer in women with DE, with molecular changes at the fetal-maternal interface.[14]

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