Deep Infiltrating Endometriosis Linked to Higher Placenta and Newborn Risks in Pregnancy

Women whose endometriosis penetrates deeply into pelvic tissues face measurably greater risks during pregnancy than those with disease confined to the surface of the pelvic lining, according to a retrospective cohort study published in Reproductive Sciences. The research, led by İsmail Baglar and colleagues at the University of Health Sciences Kartal Lütfi Kırdar City Hospital in Istanbul, tracked 268 singleton pregnancies between 2015 and 2024 and found that deep infiltrating endometriosis, often abbreviated DIE, doubled the odds of placenta previa and significantly raised the likelihood that a newborn would require intensive care. The findings sharpen a question that has long troubled obstetricians: whether endometriosis should be treated as a single diagnosis or split into biologically distinct forms that each carry their own pregnancy risk profile.

Endometriosis affects an estimated ten percent of women of reproductive age worldwide and occurs when tissue resembling the uterine lining grows outside the uterus. For decades, clinicians have recognized that the disease is not uniform. Superficial endometriosis involves implants resting on the peritoneum, the membrane lining the pelvis, whereas deep infiltrating endometriosis describes lesions that invade at least five millimeters beneath the surface, often embedding into the rectovaginal septum, bowel, bladder, or uterosacral ligaments. These lesion types differ in anatomy, hormonal behavior, pain burden, and fertility impact. Yet most studies of pregnancy outcomes have lumped all forms together, leaving open whether the more aggressive phenotype genuinely worsens perinatal prognosis or whether previously reported risks reflect confounding by infertility treatments and surgical history.

The Istanbul team addressed that gap by restricting their analysis to women whose diagnoses were surgically confirmed, eliminating the imaging-based ambiguity that clouds many registry studies. They compared 102 pregnancies in women with deep infiltrating disease against 166 pregnancies in women with superficial disease, all delivered at a single tertiary referral center. The primary endpoints were deliberately practical: placenta previa, the condition in which the placenta covers the cervical opening, and preterm birth before 37 completed weeks of gestation. Secondary outcomes spanned a broader basket of placental complications, maternal perinatal events, and measures of newborn morbidity, including admission to the neonatal intensive care unit.

Because the two patient groups differed in ways that could independently influence pregnancy, the researchers employed multivariable logistic regression, a statistical technique that estimates the effect of one factor while holding others constant. Their models adjusted for maternal age, pre-pregnancy body mass index, parity, the use of assisted reproductive technology, the presence of adenomyosis, and previous uterine surgery. This matters because women with deep disease are more likely to undergo major pelvic operations and fertility procedures, both of which have been linked in earlier literature to abnormal placentation. Without such adjustment, any apparent association between lesion depth and placental pathology could simply have been a proxy for treatment history.

The adjusted results were striking. Placenta previa occurred significantly more often in the deep infiltrating group and remained independently associated with the condition after correction, yielding an adjusted odds ratio of 2.41 with a 95 percent confidence interval spanning 1.02 to 5.68. In clinical terms, women with DIE had roughly two and a half times the odds of this dangerous placental location compared with women whose disease was superficial. Preterm birth also trended upward in the deep disease group, but that association lost statistical significance once confounders were removed, suggesting the raw difference owed something to the population characteristics rather than the lesion biology alone.

Perhaps the most consequential finding concerned the composite placenta-related outcome, which combined placenta previa and placental abruption, the premature detachment of the placenta from the uterine wall. Even after full statistical adjustment, this composite remained independently associated with deep infiltrating endometriosis. The pattern points toward disordered placentation as the central mechanism linking deep pelvic disease to obstetric harm. Researchers have proposed several pathways: chronic inflammation within the pelvis may alter uterine receptivity and vascular remodeling, prior excision of bowel or vaginal lesions can disturb the lower uterine segment and cervix, and molecular changes in endometrial tissue may impair the normal invasion of trophoblast cells that anchor and feed the placenta.

Neonatal outcomes reinforced the picture. Admission to the neonatal intensive care unit was more frequent among babies born to mothers with DIE, and the association survived adjustment with an odds ratio of 1.89 and a confidence interval of 1.01 to 3.54. A confidence interval that begins just above one signals a robust but borderline result; it means the true effect could plausibly range from a near-negligible increase to nearly a fourfold rise in NICU admission risk. Because the analysis was confined to singleton pregnancies, the neonatal signal cannot be explained by the prematurity and low birth weight that commonly accompany twin gestations conceived through assisted reproduction.

The study carries the honest limitations typical of its design. As a single-center retrospective cohort drawing on medical records rather than prospective data collection, it inherits the risk of misclassification and of undetected confounders, such as smoking, medication exposure, or the precise surgical extent of lesion excision. The sample size of 268 pregnancies, while respectable for a surgically confirmed cohort of deep disease, limits statistical power for rarer outcomes like abruption, which is why the investigators bundled it into a composite endpoint. Reverse causation also cannot be excluded: the same severity of disease that drives women to major surgery may itself reflect a more biologically aggressive process that independently affects placentation. The authors accordingly frame their results as hypothesis-generating rather than definitive, calling for lesion-based phenotyping in larger, multicenter, prospective cohorts.

Nevertheless, the clinical implications are immediate and actionable. Endometriosis already affects as many as one in ten women, and the deep infiltrating subtype, historically underdiagnosed because of its insidious symptoms and the expertise required to identify it laparoscopically, is being recognized with increasing frequency at specialized centers. If lesion depth can be confirmed before conception, whether through surgical notes, magnetic resonance imaging, or transvaginal ultrasound mapping, obstetric teams could stratify patients early, schedule growth scans and placental localization studies with greater vigilance, and deliver in centers equipped for hemorrhage management and advanced neonatal care. Placenta previa in particular demands anticipation, since it complicates delivery planning and carries substantial risk of massive postpartum bleeding.

The broader scientific message may prove even more important than the odds ratios. Endometriosis is a disease of phenotypes, and the Istanbul data add pregnancy physiology to the growing list of outcomes, from pain and infertility to ovarian cancer risk, in which lesion biology matters more than diagnosis labels. A woman with superficial implants may be reassured that her obstetric risk profile resembles that of the general population far more closely than the averages reported in older studies that merged all disease forms. A woman with deep disease, by contrast, deserves a conversation about placental monitoring during her first prenatal visit. As surgical mapping and noninvasive phenotyping improve, the researchers argue that lesion-specific risk stratification could transform endometriosis from a static diagnosis into a dynamic perinatal risk model, one that follows each patient from her first pelvic scan to her delivery room.

Subject of Research: Obstetric and neonatal outcomes in pregnancies complicated by deep infiltrating versus superficial endometriosis

Article Title: Obstetric and Neonatal Outcomes in Deep Infiltrating Versus Superficial Endometriosis: A Retrospective Cohort Study

Article References: Baglar, İ., Topaloglu, T., Keles, E., Yılmaz, A., Kopuk, S. Y., Civi, B. Y., Guliyeva, K. A., Nokay, E., Karahan, M., & Agir, D. (2026). Obstetric and Neonatal Outcomes in Deep Infiltrating Versus Superficial Endometriosis: A Retrospective Cohort Study. Reproductive Sciences. https://doi.org/10.1007/s43032-026-02215-3

Image Credits: AI Generated

DOI: 10.1007/s43032-026-02215-3

Keywords: deep infiltrating endometriosis, superficial endometriosis, placenta previa, preterm birth, pregnancy outcomes, neonatal intensive care, placental abruption, retrospective cohort study, obstetrics, reproductive medicine, endometriosis phenotyping, adjusted odds ratio