Association between polycystic ovary syndrome and the risk of pregnancy complications

Yu, Haifeng; Chen, Hong-Su; Rao, Dapang; Gong, Jian

doi:10.1097/md.0000000000004863

Cited by 211 publications

(267 citation statements)

References 46 publications

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“…We confirm a prior meta‐analysis reporting a higher risk for miscarriage in PCOS . Prior research reports the risk factors for miscarriage, both in PCOS and in the general population, include obesity and ART use .…”

Section: Discussionsupporting

confidence: 87%

“…Women with PCOS have intrinsic insulin resistance (IR), which is mechanistically distinct from the IR associated with obesity, and obesity will further worsen both IR and the clinical presentation of PCOS . Women with PCOS are more likely to have increased oxidative stress, and to experience infertility requiring assisted conception, and when they conceive, there is also an increased risk for pregnancy and delivery complications …”

Section: Introductionmentioning

confidence: 99%

“…Despite empirical evidence for an increased prevalence of maternal pregnancy and delivery complications in women with PCOS, there are still significant gaps in understanding the potential pathophysiological pathways for these associations. This is likely because of both the complexity and heterogeneity of PCOS, the range of potential confounders for pregnancy complications, and the variable methodology of conducted studies with these factors often not considered in prior meta‐analyses.…”

Section: Introductionmentioning

confidence: 99%

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Increased maternal pregnancy complications in polycystic ovary syndrome appear to be independent of obesity—A systematic review, meta‐analysis, and meta‐regression

et al. 2019

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Summary Polycystic ovary syndrome (PCOS) is associated with an increased risk of maternal pregnancy and delivery complications. However, the impact of clinical features of PCOS and other potential risk factors in PCOS is still unknown. We aimed to investigate the association of PCOS with maternal pregnancy and delivery complications with consideration of risk factors and potential confounders. The meta‐analysis included 63 studies. PCOS was associated with higher miscarriage, gestational diabetes mellitus, gestational hypertension, pre‐eclampsia, induction of labour, and caesarean section. The association of PCOS with these outcomes varied by geographic continent, PCOS phenotypes, and study quality. Pre‐eclampsia and induction of labour were not associated with PCOS on body mass index‐matched studies. No outcome was associated with PCOS on assisted pregnancies. Age was significantly associated with higher miscarriage on meta‐regression. There were no studies assessing perinatal depression. We confirm that PCOS is associated with an increased risk of maternal pregnancy and delivery complications. The association of PCOS with the outcomes is worsened in hyperandrogenic PCOS phenotypes, in specific geographic continents, and in the highest quality studies but disappears in assisted pregnancies. Future studies in PCOS are warranted to investigate proper timing for screening and prevention of maternal pregnancy and delivery complications with consideration of clinical features of PCOS.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Increased maternal pregnancy complications in polycystic ovary syndrome appear to be independent of obesity—A systematic review, meta‐analysis, and meta‐regression

et al. 2019

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“…79 −82 When a pregnant mother with PCOS is subsequently diagnosed with hyperinsulinemia, hypertension, or hyperandrogenemia during pregnancy this increases maternal and fetal morbidity and mortality. 83 −85 The likelihood of developing obstetric complications during pregnancy such as gestational diabetes, preeclampsia, and early termination of pregnancy increase. 86 −89 While the etiology of metabolic derangement in PCOS women and their offspring is not well understood, this study describes a profile of cardiometabolic dysfunction that is associated with gut microbiota dysbiosis in offspring exposed to androgens prenatally.…”

Section: Discussionmentioning

confidence: 99%

Prenatal androgen exposure causes hypertension and gut microbiota dysbiosis

et al. 2018

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Background: Conditions of excess androgen in women, such as polycystic ovary syndrome (PCOS), often exhibit intergenerational transmission. One way in which the risk for PCOS may be increased in daughters of affected women is through exposure to elevated androgens in utero. Hyperandrogenemic conditions have serious health consequences, including increased risk for hypertension and cardiovascular disease. Recently, gut dysbiosis has been found to induce hypertension in rats, such that blood pressure can be normalized through fecal microbial transplant. Therefore, we hypothesized that the hypertension seen in PCOS has early origins in gut dysbiosis caused by in utero exposure to excess androgen. We investigated this hypothesis with a model of prenatal androgen (PNA) exposure and maternal hyperandrogenemia by single-injection of testosterone cypionate or sesame oil vehicle (VEH) to pregnant dams in late gestation. We then completed a gut microbiota and cardiometabolic profile of the adult female offspring. Results: The metabolic assessment revealed that adult PNA rats had increased body weight and increased mRNA expression of adipokines: adipocyte binding protein 2, adiponectin, and leptin in inguinal white adipose tissue. Radiotelemetry analysis revealed hypertension with decreased heart rate in PNA animals. The fecal microbiota profile of PNA animals contained higher relative abundance of bacteria associated with steroid hormone synthesis, Nocardiaceae and Clostridiaceae, and lower abundance of Akkermansia, Bacteroides, Lactobacillus, Clostridium. The PNA animals also had an increased relative abundance of bacteria associated with biosynthesis and elongation of unsaturated short chain fatty acids (SCFAs). Conclusions: We found that prenatal exposure to excess androgen negatively impacted cardiovascular function by increasing systolic and diastolic blood pressure and decreasing heart rate. Prenatal androgen was also associated with gut microbial dysbiosis and altered abundance of bacteria involved in metabolite production of short chain fatty acids. These results suggest that early-life exposure to hyperandrogenemia in daughters of women with PCOS may lead to long-term alterations in gut microbiota and cardiometabolic function.

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“…Several diseases have been reported to both impair decidualization and predispose to preeclampsia including polycystic ovarian syndrome [79–84], obesity [79, 80, 85, 86], diabetes mellitus [87–89], and endometriosis [90–92]. These comorbidities may exert their disruptive action on the endometrium through anomalous inflammation, exaggerated production of androgens, insulin, and homocysteine, as well as pathological epigenetic modifications [79, 91, 93–96].…”

Section: Potential Mechanisms Of Impaired Decidualization In Preeclammentioning

confidence: 99%

Emerging role for dysregulated decidualization in the genesis of preeclampsia

2017

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In normal human placentation, uterine invasion by trophoblast cells and subsequent spiral artery remodeling depend on cooperation among fetal trophoblasts and maternal decidual, myometrial, immune and vascular cells in the uterine wall. Therefore, aberrant function of anyone or several of these cell-types could theoretically impair placentation leading to the development of preeclampsia. Because trophoblast invasion and spiral artery remodeling occur during the first half of pregnancy, the molecular pathology of fetal placental and maternal decidual tissues following delivery may not be informative about the genesis of impaired placentation, which transpired months earlier. Therefore, in this review, we focus on the emerging prospective evidence supporting the concept that deficient or defective endometrial maturation in the late secretory phase and during early pregnancy, i.e., pre-decidualization and decidualization, respectively, may contribute to the genesis of preeclampsia. The first prospectively-acquired data directly supporting this concept were unexpectedly revealed in transcriptomic analyses of chorionic villous samples (CVS) obtained during the first trimester of women who developed preeclampsia 5 months later. Additional supportive evidence arose from investigations of Natural Killer cells in first trimester decidua from elective terminations of women with high resistance uterine artery indices, a surrogate for deficient trophoblast invasion. Last, circulating insulin growth factor binding protein-1, which is secreted by decidual stromal cells was decreased during early pregnancy in women who developed preeclampsia. We conclude this review by making recommendations for further prospectively-designed studies to corroborate the concept of endometrial antecedents of preeclampsia. These studies could also enable identification of women at increased risk for developing preeclampsia, unveil the molecular mechanisms of deficient or defective (pre)decidualization, and lead to preventative strategies designed to improve (pre)decidualization, thereby reducing risk for preeclampsia development.

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Association between polycystic ovary syndrome and the risk of pregnancy complications

Abstract: Supplemental Digital Content is available in the text

Cited by 211 publications

References 46 publications

Increased maternal pregnancy complications in polycystic ovary syndrome appear to be independent of obesity—A systematic review, meta‐analysis, and meta‐regression

Increased maternal pregnancy complications in polycystic ovary syndrome appear to be independent of obesity—A systematic review, meta‐analysis, and meta‐regression

Prenatal androgen exposure causes hypertension and gut microbiota dysbiosis

Emerging role for dysregulated decidualization in the genesis of preeclampsia

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