{"paper_id":"14cb1235-89d4-4450-8f0b-ed207dc90f17","body_text":"~ 1089 ~ \nInternational Journal of Clinical Obstetrics and Gynaecology 2026; 10(1): 1089-1093 \n \nISSN (P): 2522-6614 \nISSN (E): 2522-6622 \nIndexing: Embase \nImpact Factor (RJIF): 6.71 \n© Gynaecology Journal \nwww.gynaecologyjournal.com \n2026; 10(1): 1089-1093 \nReceived: 20-11-2025 \nAccepted: 24-12-2025 \n \nDr. Manisha Chaudhari \nSenior Resident, Department of \nObstetrics and Gynaecology, Banas \nMedical College and Research \nInstitute, Palanpur, Gujarat, India \n \nDr. Manisha Bhikhabhai Suthar \nAssociate Professor, Department of \nObstetrics and Gynaecology, Shree \nShankaracharya Institute of \nMedical Science, Bhilai, \nChhattisgarh, India \n \nDr. Jatin Pravin Patel \nResident (Gynecology), Shree \nChhotubhai A Patel Hospital and \nCHC, Mota Fofaliya, Gujarat, \nIndia \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \nCorresponding Author: \nDr. Jatin Pravin Patel \nResident (Gynecology), Shree \nChhotubhai A Patel Hospital and \nCHC, Mota Fofaliya, Gujarat, \nIndia \n \nObstetric outcomes in women with endometriosis: A \nretrospective cohort study \n \nManisha Chaudhari, Manisha Bhikhabhai Suthar and Jatin Pravin Patel \n \nDOI: https://www.doi.org/10.33545/gynae.2026.v10.i1m.1993  \n \nAbstract \nBackground: Endometriosis is a chronic gynecological condition affecting approximately 10% of \nreproductive-age women and has been increasingly associated with adverse pregnancy outcomes. However, \nthe extent to which endometriosis influences obstetric compl ications remains incompletely understood. \nThis study aimed to evaluate obstetric outcomes in women with a confirmed diagnosis of endometriosis \ncompared to women without the condition. \nMethods: A retrospective cohort study was conducted at a tertiary care h ospital between. A total of 684 \npregnant women were included: 228 with a confirmed diagnosis of endometriosis (exposed group) and 456 \nwithout endometriosis (unexposed group) , matched by age and parity in a 1:2 ratio. Obstetric outcomes \nincluding preterm bi rth, preeclampsia, placenta previa, cesarean delivery, small for gestational age (SGA) \nneonates, gestational diabetes mellitus (GDM), and postpartum hemorrhage (PPH) were compared between \ngroups. Statistical analyses included chi -square tests , independent t-tests, and multivariable logistic \nregression. \nResults: Women with endometriosis demonstrated significantly higher rates of preterm birth (18.4% vs. \n9.6%, p = 0.001) , placenta previa (6.1% vs. 1.8% , p = 0.003) , preeclampsia (12.7% vs. 7.0% , p = 0.014) , \nand cesarean delivery (58.3% vs. 39.0% , p<0.001). The mean gestational age at delivery was significantly \nlower in the endometriosis group (37.2 ± 2.8 weeks vs. 38.6 ± 1.9 weeks , p<0.001). After multivariable \nadjustment, endometriosis remained an independ ent predictor of preterm birth (aOR 2.14 , 95% CI 1.38 -\n3.32), placenta previa (aOR 3.47, 95% CI 1.52-7.93), and cesarean delivery (aOR 2.21, 95% CI 1.58-3.09). \nConclusion: Endometriosis is significantly associated with multiple adverse obstetric outcomes , \nparticularly preterm birth , placenta previa , and cesarean delivery. Enhanced antenatal surveillance and \nmultidisciplinary management are warranted for pregnant women with endometriosis. \n \nKeywords: Endometriosis, obstetric outcomes, preterm birth, placenta previa, cesarean delivery, \npregnancy complications, retrospective cohort study \n \n1. Introduction  \nEndometriosis is a chronic , estrogen-dependent inflammatory disorder characterized by the \npresence of endometrial -like tissue outside the uterine cavity , most com monly affecting the \novaries, peritoneum, and rectovaginal septum  [1]. It affects an estimated 6 -10% of women of \nreproductive age worldwide and represents one of the most prevalent gynecological conditions \nencountered in clinical practice  [2]. The cardinal symptoms include chronic pelvic pain , \ndysmenorrhea, dyspareunia, and subfertility, collectively contributing to substantial impairment \nin quality of life and significant healthcare expenditure [3]. \nWhile the relationship between endometriosis and infertili ty has been extensively investigated \nand well-established, the impact of endometriosis on obstetric outcomes has garnered increasing \nscientific attention over the past two decades  [4]. Several pathophysiological mechanisms have \nbeen proposed to explain how  endometriosis may adversely influence pregnancy , including \nimpaired decidualization, aberrant placentation, chronic inflammatory milieu, and altered uterine \ncontractility [5]. The eutopic endometrium of women with endometriosis exhibits molecular and \ncellular abnormalities that may compromise implantation and subsequent placental \ndevelopment, potentially predisposing to complications such as preeclampsia , placenta previa, \nand preterm birth [6]. \nA systematic review and meta -analysis by Zullo et al. (2017) d emonstrated that endometriosis \nwas associated with increased risks of preterm birth , cesarean section , and placenta previa , \nalthough substantial heterogeneity existed across included studies [7]. Similarly, a large  \n\n\nInternational Journal of Clinical Obstetrics and Gynaecology https://www.gynaecologyjournal.com \n~ 1090 ~ \npopulation-based cohort study from Sweden  reported elevated \nrisks of preeclampsia and antepartum hemorrhage among \nwomen with endometriosis  [8]. More recently , Berlac et al . \n(2017) found that women with endometriosis had higher rates of \ngestational hypertensive disorders and adverse perinatal \noutcomes, although the magnitude of associations varied by \nendometriosis phenotype [9]. A comprehensive meta -analysis by \nHorton et al . (2019) further confirmed these associations and \nemphasized the need for additional well -designed studies to \nclarify the independent contribution of endometriosis to obstetric \nmorbidity after controlling for confounders such as assisted \nreproductive technology (ART) utilization [10]. \nDespite the growing body of evidence, several gaps persist in the \nliterature. Many previous studies did not adequately differentiate \nbetween spontaneous and ART -conceived pregnancies, making \nit difficult to disentangle the independent effects of \nendometriosis from those attributable to fertility treatments  [11]. \nFurthermore, data from Middle Eastern a nd developing country \npopulations remain limited , and the influence of endometriosis \nstage and phenotype on specific obstetric outcomes requires \nfurther investigation  [12]. Additionally , postpartum outcomes \nsuch as postpartum hemorrhage have been inconsist ently \nevaluated across existing studies [13]. \nThe aim of this study was to compare obstetric outcomes \nbetween pregnant women with a confirmed diagnosis of \nendometriosis and those without endometriosis in a tertiary care \nsetting, while controlling for poten tial confounders including \nmode of conception, maternal age, body mass index (BMI) , and \nparity. \n \n2. Materials and Methods \n2.1 Study Design and Setting \nThis retrospective cohort study was conducted at the Department \nof Obstetrics and Gynecology of a tertiar y university -affiliated \nhospital.  \n \n2.2 Study Population \nThe exposed group comprised 228 women with a confirmed \ndiagnosis of endometriosis established prior to or during early \npregnancy. Diagnosis was based on surgical confirmation \n(laparoscopy or laparotomy) with or without histopathological \nverification, or imaging -confirmed endometriomas (≥2 cm) \nidentified on transvaginal ultrasonography or magnetic \nresonance imaging. The unexposed group consisted of 456 \nwomen without any documented history or cl inical evidence of \nendometriosis, matched to the exposed group in a 1:2 ratio by \nmaternal age (±2 years) and parity. \n \n2.3 Inclusion and Exclusion Criteria \nInclusion criteria were: singleton pregnancy , delivery at ≥24 \nweeks of gestation , and complete medical  records documenting \nantenatal, intrapartum, and postpartum course. Exclusion criteria \nincluded: multiple gestations , major fetal congenital anomalies , \nchronic hypertension diagnosed prior to pregnancy , pre-\ngestational diabetes mellitus, chronic renal disease, autoimmune \ndisorders requiring immunosuppressive therapy , and incomplete \nmedical records. \n \n2.4 Data Collection and Variables \nData were extracted from electronic health records by trained \nresearch assistants using a standardized data collection form. \nMaternal demographic variables included age , pre-pregnancy \nBMI, parity, smoking status , and mode of conception \n(spontaneous vs. ART). For the endometriosis group , additional \ndata regarding disease stage (revised American Society for \nReproductive Medicine [rA SRM] classification: stages I -II vs. \nIII-IV) and phenotype (peritoneal , ovarian endometrioma, deep \ninfiltrating endometriosis [DIE]) were recorded when available. \nPrimary obstetric outcomes included: preterm birth (<37 weeks \nof gestation), preeclampsia (defined per the International Society \nfor the Study of Hypertension in Pregnancy criteria) , placenta \nprevia (confirmed by ultrasound at >28 weeks) , cesarean \ndelivery, small for gestational age (SGA; birth weight <10th \npercentile for gestational age) , gestational diabetes mellitus \n(GDM; diagnosed by 75 -g oral glucose tolerance test per \nIADPSG criteria), and postpartum hemorrhage (PPH; estimated \nblood loss ≥500 mL for vaginal delivery or ≥1000 mL for \ncesarean delivery). Secondary outcomes included gestational age \nat delivery, neonatal birth weight, Apgar score at 5 minutes , and \nneonatal intensive care unit (NICU) admission. \n \n2.5 Statistical Analysis \nContinuous variables were expressed as mean ± standard \ndeviation (SD) and compared using independent -sample t-tests. \nCategorical variables were presented as frequencies and \npercentages and analyzed using chi-square tests or Fisher's exact \ntest as appropriate. Multivariable logistic regression analysis was \nperformed to identify independent associations between \nendometriosis and adverse obstetric outcomes after adjusting for \npotential confounders (maternal age , BMI, smoking, parity, \nmode of conception , and history of prior cesarean delivery). \nResults were reported as adjusted odds ratios (aOR) with 95% \nconfidence interval s (CI). A two -tailed p -value <0.05 was \nconsidered statistically significant. All analyses were performed \nusing SPSS version 28.0 (IBM Corporation , Armonk, NY, \nUSA). \n \n3. Results \n3.1 Baseline Characteristics \nA total of 684 women were included in the final an alysis: 228 in \nthe endometriosis group and 456 in the control group. Baseline \ndemographic and clinical characteristics are presented in  Table \n1. The two groups were comparable with respect to maternal \nage, parity, and smoking status. However , the endometri osis \ngroup had a significantly higher proportion of ART -conceived \npregnancies (34.2% vs. 8.1% , p<0.001) and a slightly higher \nmean BMI (26.3 ± 4.1 vs. 25.4 ± 3.8 kg/m², p = 0.006). \n \nTable 1: Baseline Demographic and Clinical Characteristics \n \nVariable Endometriosis (n = 228) Control (n = 456) p-value \nAge (years), mean ± SD 32.4 ± 4.6 31.9 ± 4.3 0.163 \nPre-pregnancy BMI (kg/m²), mean ± SD 26.3 ± 4.1 25.4 ± 3.8 0.006 \nNulliparous, n (%) 142 (62.3) 278 (61.0) 0.737 \nSmoking, n (%) 19 (8.3) 31 (6.8) 0.462 \nART conception, n (%) 78 (34.2) 37 (8.1) <0.001 \nPrior cesarean delivery, n (%) 38 (16.7) 64 (14.0) 0.362 \nrASRM Stage III-IV, n (%) 131 (57.5) — — \nDeep infiltrating endometriosis, n (%) 67 (29.4) — — \n \n\nInternational Journal of Clinical Obstetrics and Gynaecology https://www.gynaecologyjournal.com \n~ 1091 ~ \n3.2 Obstetric Outcomes \nComparison of obstetric outcomes between the two groups is \nsummarized in  Table 2 . Women with endometriosis had \nsignificantly higher rates of preterm birth (18.4% vs. 9.6% , p = \n0.001), preeclampsia (12.7% vs. 7.0% , p = 0.014) , placenta \nprevia (6.1% vs. 1.8% , p = 0.003), cesarean delivery (58.3% vs. \n39.0%, p<0.001), and PPH (9.6% vs. 5.5% , p = 0.038). The rate \nof GDM was numerically higher in the endometriosis group but \ndid not reach statistical significance (14.0% vs. 10.3% , p = \n0.151). The rate of SGA neonates was significantly higher in  the \nendometriosis group (13.2% vs. 8.1% , p = 0.036). Mean \ngestational age at delivery was significantly lower (37. 2 ± 2.8 \nvs. 38.6 ± 1.9 weeks , p<0.001), and mean neonatal birth weight \nwas also significantly lower (2 , 918 ± 548 g vs. 3 , 187 ± 462 g , \np<0.001) in the endometriosis group. NICU admission was more \nfrequent among neonates born to women with endometriosis \n(14.5% vs. 7.7%, p = 0.004). \n \nTable 2: Comparison of Obstetric and Neonatal Outcomes \n \nOutcome Endometriosis (n = 228) Control (n = 456) p-value \nPreterm birth (<37 weeks), n (%) 42 (18.4) 44 (9.6) 0.001 \nPreeclampsia, n (%) 29 (12.7) 32 (7.0) 0.014 \nPlacenta previa, n (%) 14 (6.1) 8 (1.8) 0.003 \nCesarean delivery, n (%) 133 (58.3) 178 (39.0) <0.001 \nGDM, n (%) 32 (14.0) 47 (10.3) 0.151 \nSGA (<10th percentile), n (%) 30 (13.2) 37 (8.1) 0.036 \nPPH, n (%) 22 (9.6) 25 (5.5) 0.038 \nGestational age at delivery (weeks), mean ± SD 37.2 ± 2.8 38.6 ± 1.9 <0.001 \nBirth weight (g), mean ± SD 2, 918 ± 548 3, 187 ± 462 <0.001 \nApgar <7 at 5 min, n (%) 12 (5.3) 15 (3.3) 0.208 \nNICU admission, n (%) 33 (14.5) 35 (7.7) 0.004 \n \n3.3 Multivariable Analysis \nAfter adjusting for maternal age, BMI, parity, smoking, mode of \nconception, and prior cesarean delivery, endometriosis remained \nindependently associated with several adverse outcomes (Table \n3). The strongest associations were observed for placenta  previa \n(aOR 3.47, 95% CI 1.52 -7.93, p = 0.003) and cesarean delivery  \n(aOR 2.21 , 95% CI 1.58 -3.09, p<0.001). Preterm birth (aOR \n2.14, 95% CI 1.38 -3.32, p = 0.001) , preeclampsia (aOR 1.82 , \n95% CI 1.06 -3.13, p = 0.029) , and SGA (aOR 1.71 , 95% CI \n1.03-2.84, p = 0.038) also remained statistically significant. The \nassociation with PPH was attenuated and became borderline \nsignificant after adjustment (aOR 1.68 , 95% CI 0.93 -3.04, p = \n0.086). \n \nTable 3: Multivariable Logistic Regression Analysis for Adverse \nObstetric Outcomes \n \nOutcome Adjusted OR 95% CI p-value \nPreterm birth 2.14 1.38-3.32 0.001 \nPreeclampsia 1.82 1.06-3.13 0.029 \nPlacenta previa 3.47 1.52-7.93 0.003 \nCesarean delivery 2.21 1.58-3.09 <0.001 \nSGA 1.71 1.03-2.84 0.038 \nPPH 1.68 0.93-3.04 0.086 \nGDM 1.34 0.82-2.19 0.241 \n \n4. Discussion \nThe findings of this retrospective cohort study demonstrate that \nwomen with endometriosis face significantly elevated risks of \nmultiple adverse obstetric outcomes , including preterm birth , \npreeclampsia, placenta previa , cesarean delivery , and SGA \nneonates. These associations persisted after multivariable \nadjustment for key confounders , including mode of conception , \nsupporting the concept that endometriosis exerts independent \ndeleterious effects on pregnancy outcomes through intrinsic \ndisease-related mechanisms. \nOur findings are consistent with the results of a landmark meta -\nanalysis by Zullo et al . (2017) , which reported significan tly \nincreased risks of preterm birth (OR 1.63) , placenta previa (OR \n3.03), and cesarean section (OR 1.57) among women with \nendometriosis [14]. The magnitude of our observed associations \nwas somewhat greater , particularly for placenta previa (aOR \n3.47), which may reflect the relatively high proportion of \nadvanced-stage disease (57.5% with rASRM stages III -IV) and \ndeep infiltrating endometriosis (29.4%) in our cohort , as disease \nseverity has been correlated with worse obstetric outcomes in \nprior investigations [15]. \nThe pathophysiology underlying the association between \nendometriosis and adverse obstetric outcomes is multifactorial. \nEndometriosis is characterized by a state of chronic pelvic \ninflammation with elevated levels of pro -inflammatory \ncytokines, including interleukin -6, tumor necrosis factor -alpha, \nand interleukin-1β, which may interfere with normal trophoblast \ninvasion and spiral artery remodeling , thereby predisposing to \ndefective placentation  [16]. This impaired placentation may \nmanifest clinically  as preeclampsia , fetal growth restriction , or \nplacental abruption. Furthermore , the eutopic endometrium of \nwomen with endometriosis exhibits progesterone resistance and \naltered gene expression profiles that compromise \ndecidualization, a process critical f or successful implantation \nand early placental development [17]. \nThe elevated rate of placenta previa observed in our study \ndeserves particular attention. Several studies have reported this \nassociation, and it has been hypothesized that endometriosis-\nrelated anatomical distortion of the pelvic structures , along with \naltered endometrial receptivity in the upper uterine segment , \nmay promote lower uterine segment implantation  [18]. \nAdditionally, prior surgical interventions for endometriosis , \nincluding laparoscopic excision or ablation , may contribute to \nuterine scarring and subsequent abnormal placentation [19]. \nThe significantly higher cesarean delivery rate in the \nendometriosis group (58.3% vs. 39.0%) aligns with previous \nreports and may b e attributable to multiple factors , including \nobstetrician awareness of potential complications , pelvic \nadhesive disease limiting labor progress , higher incidence of \nmalpresentation, and elective cesarean deliveries planned due to \nprior endometriosis surge ry [20]. Saraswat et al. (2017) similarly \nreported a cesarean delivery rate exceeding 50% among women \nwith endometriosis in a large Scottish population -based \nstudy [21]. \nThe borderline association between endometriosis and \n\nInternational Journal of Clinical Obstetrics and Gynaecology https://www.gynaecologyjournal.com \n~ 1092 ~ \npostpartum hemorrhage (aOR 1.68 , p = 0.086) is noteworthy , \nthough it did not achieve conventional statistical significance \nafter adjustment. This finding is consistent with the findings of \nMannini et al . (2022) , who reported a modest but inconsistent \nassociation between endometriosis and PPH across different \nstudy populations  [22]. The potential mechanisms may include \nimpaired myometrial contractility due to adenomyosis \n(frequently coexisting with endometriosis) , inflammatory \nmediator-related uterine atony , or surgical complications during  \ncesarean delivery in the setting of severe pelvic adhesions [23]. \nOur study did not find a statistically significant association \nbetween endometriosis and GDM (aOR 1.34 , p = 0.241), which \nis concordant with the majority of published literature. A recent \nsystematic review by Pérez -López et al . (2018) similarly \nconcluded that the evidence linking endometriosis to GDM is \ninconclusive, with most studies reporting null or weakly positive \nassociations [24]. \nAn important strength of this study is the adjustment for mode of \nconception, which a critical confounder is  given that ART itself \nhas been independently associated with adverse obstetric \noutcomes including preterm birth , preeclampsia, and placenta \nprevia [25]. Many prior studies failed to adequately account f or \nthis variable , making it challenging to determine whether \nobserved associations reflected the effects of endometriosis per \nse or ART -related factors. In our multivariable models , the \nassociations remained robust after including ART as a covariate , \nsuggesting that endometriosis contributes to adverse outcomes \nthrough pathways independent of fertility treatment. \nThis study has several limitations that must be acknowledged. \nFirst, the retrospective design is inherently susceptible to \nselection bias and resi dual confounding. Second , the diagnosis \nof endometriosis was based on surgical or imaging criteria , and \nwomen with undiagnosed or asymptomatic endometriosis in the \ncontrol group may have led to misclassification bias , potentially \nattenuating the observed a ssociations. Third , the study was \nconducted at a single tertiary referral center , which may limit \ngeneralizability, as the patient population likely represents a \nskewed distribution toward more severe disease. Fourth , the \nrelatively modest sample size prec luded robust subgroup \nanalyses by endometriosis stage or phenotype. Finally , \ninformation regarding endometriosis -specific treatments \nreceived prior to pregnancy (hormonal suppression , surgical \nexcision) was incompletely documented , limiting our ability to \nevaluate the potential modifying effect of preconception \ntreatment. \nFuture prospective multicenter studies with larger sample sizes \nand detailed phenotypic characterization of endometriosis are \nneeded to further delineate the impact of disease severity , \nphenotype, and prior treatment on specific obstetric outcomes. \nAdditionally, investigations into potential biomarkers that could \nidentify women with endometriosis at highest risk for obstetric \ncomplications would be of considerable clinical value. \n \n5. Conclusion \nThis retrospective cohort study demonstrates that endometriosis \nis independently associated with significantly increased risks of \npreterm birth, preeclampsia, placenta previa, cesarean delivery, \nand small for gestational age neonates. These findings \nunderscore the importance of recognizing endometriosis as a \nclinically significant risk factor for adverse obstetric outcomes. \nPregnant women with a history of endometriosis should be \nclassified as high -risk and may benefit from enhanced antenatal \nsurveillance, including serial ultrasonographic assessment of \nplacental location and fetal growth , along with multidisciplinary \ncare involving both gynecologists with expertise in \nendometriosis and maternal -fetal medicine specialists. Early \nidentification and proac tive management of potential \ncomplications may contribute to improved maternal and \nneonatal outcomes in this vulnerable population. \nAcknowledgement  \nNot available  \n \nAuthor’s Contribution  \nNot available  \n \nConflict of Interest \nNot available  \n \nFinancial Support  \nNot available \n \nReferences \n1. Giudice LC , Kao LC. Endometriosis. Lancet. \n2004;364(9447):1789-1799. doi:10.1016/S0140 -\n6736(04)17403-5. \n2. 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Pérez-López FR , Villagrasa-Boli P , Muñoz-Olarte M , \nMorera-Fumero AL , Chedraui P. Association between \nendometriosis and gestational dia betes mellitus: a meta -\nanalysis. Diabetes Res Clin Pract. 2018;135:100 -106. \ndoi:10.1016/j.diabres.2017.11.015. \n25. Qin JB, Sheng XQ, Wu D, et al. Worldwide prevalence of \nadverse pregnancy outcomes among singleton pregnancies \nafter in vitro  fertilization/intracytoplasmic sperm injection: \na systematic review and meta -analysis. Arch Gynecol \nObstet. 2017;295(2):285 -301. doi:10.1007/s00404 -016-\n4249-9. \n \nHow to Cite This Article \nChaudhari M, Suthar MB, Patel JP. Obstetric outcomes in women with \nendometriosis: A retrospective cohort study . International Journal of \nClinical Obstetrics and Gynaecology. 2026; 10(1): 1089-1093.  \n \n \nCreative Commons (CC) License \nThis is an open access journal , and articles are distributed under the terms \nof the Creative Commons Attribution -Non Commercial-Share Alike 4.0 \nInternational (CC BY -NC-SA 4.0) License , which allows others to rem ix, \ntweak, and build upon the work non -commercially, as long as appropriate \ncredit is given and the new creations are licensed under the identical terms.","source_license":"CC0","license_restricted":false}