Endometriosis During Pregnancy: Maternal and Fetal Considerations

Endometriosis is a chronic inflammatory condition traditionally viewed as hormonally suppressed during pregnancy. However, growing evidence indicates that pregnancy does not uniformly mitigate disease activity and that endometriosis may have clinically relevant implications for both maternal and fetal health. This chapter provides a comprehensive overview of endometriosis in the context of pregnancy, integrating current knowledge on pathophysiology, clinical course, diagnostic challenges, maternal complications, and fetal and neonatal outcomes. Particular emphasis is placed on the heterogeneity of the disease, highlighting how pregnancy risks vary according to endometriosis phenotype, disease extent, and prior surgical history. The chapter also addresses management strategies during pregnancy, postpartum considerations, and the importance of individualized risk stratification and multidisciplinary care. While many women with endometriosis experience uncomplicated pregnancies, those with deep infiltrating or extensive disease may face increased risks of placental dysfunction, preterm birth, and operative delivery. Persistent gaps in evidence, including limited prospective data and a lack of phenotype-specific guidelines, are discussed alongside future research priorities. Overall, this chapter reframes endometriosis as a condition of obstetric relevance and underscores the need for tailored, evidence-informed approaches to optimize maternal and fetal outcomes throughout pregnancy and the postpartum period.

- endometriosis - pregnancy - maternal complications - fetal outcomes - placental dysfunction 1. Introduction Endometriosis is a chronic, estrogen-dependent inflammatory disorder characterized by the presence of endometrial-like tissue outside the uterine cavity, most commonly affecting the ovaries, pelvic peritoneum, and deep pelvic structures [1]. It is estimated to affect approximately 6%–10% of women of reproductive age and up to 30%–50% of women experiencing infertility or chronic pelvic pain [2]. Despite its high prevalence and substantial impact on quality of life, endometriosis remains a heterogeneous condition with variable clinical presentation, disease progression, and response to treatment. Historically, pregnancy has been regarded as a state that confers symptomatic relief or temporary remission of endometriosis. This assumption was largely based on the progesterone-dominant hormonal environment of pregnancy and the decidualization of ectopic endometrial tissue [3]. Consequently, for decades, endometriosis during pregnancy received limited scientific attention and was often considered clinically irrelevant once conception occurred. However, accumulating evidence over the past two decades has challenged this traditional view, demonstrating that endometriosis may persist, progress, or contribute to significant obstetric complications during pregnancy [4]. With advances in assisted reproductive technologies (ARTs) and the increasing maternal age at first pregnancy, a growing proportion of pregnant women now have a known history of endometriosis or have undergone surgical or medical treatment for the disease prior to conception. Parallel to this demographic shift, large population-based cohort studies and systematic reviews – most notably those synthesizing national registry data – have consistently reported associations between endometriosis and adverse pregnancy outcomes, including placenta previa, preterm birth, hypertensive disorders of pregnancy, cesarean delivery, and postpartum hemorrhage [4, 5]. These observations suggest that endometriosis should no longer be viewed solely as a fertility-related condition, but rather as a disease with potential implications throughout gestation and the perinatal period. From a biological perspective, several mechanisms have been proposed to explain the link between endometriosis and pregnancy-related complications. These include chronic systemic and local inflammation, altered immune tolerance at the maternal–fetal interface, impaired decidualization, abnormal placentation, and vascular dysfunction [3, 6]. Importantly, these mechanisms may exert differential effects depending on disease phenotype, lesion location, and prior surgical history, highlighting the need for individualized risk assessment and antenatal surveillance. Despite the growing body of literature, significant gaps remain in the understanding of how endometriosis influences maternal and fetal health during pregnancy. Existing studies vary considerably in design, diagnostic criteria, and outcome definitions, and many do not differentiate between superficial, ovarian, and deep infiltrating endometriosis (DIE). Furthermore, evidence-based clinical guidelines addressing the management of pregnant women with endometriosis remain limited, and standardized recommendations for surveillance and delivery planning are still evolving. The aim of this chapter is to provide a comprehensive and up–to-date overview of endometriosis during pregnancy, with a specific focus on maternal and fetal considerations. By integrating current evidence on pathophysiology, clinical course, diagnostic challenges, and pregnancy outcomes, this chapter seeks to reframe endometriosis as a condition of obstetric relevance. In doing so, it aims to support clinicians in recognizing high-risk scenarios, optimizing multidisciplinary care, and ultimately improving pregnancy outcomes for women affected by this complex disease. 2. Pathophysiology of endometriosis in the context of pregnancy Pregnancy induces profound endocrine, immunological, and vascular adaptations that are essential for successful implantation, placentation, and fetal development. These adaptations include sustained progesterone dominance, tightly regulated immune tolerance at the maternal–fetal interface, and extensive vascular remodeling within the uterus and placenta. In women with endometriosis, however, these physiological processes unfold against a background of chronic inflammation, altered immune regulation, and impaired endometrial receptivity. Consequently, pregnancy does not uniformly suppress disease activity, and in certain clinical contexts, it may instead reveal or exacerbate underlying pathophysiological mechanisms associated with endometriosis. A central feature of endometriosis is progesterone resistance, which persists even during pregnancy despite markedly elevated systemic progesterone levels. Histopathological and molecular studies have demonstrated reduced expression and altered function of progesterone receptors – particularly progesterone receptor B – in both ectopic and eutopic endometrial tissue [7]. This receptor-level resistance attenuates the anti-inflammatory, anti-proliferative, and differentiating effects of progesterone, allowing inflammatory signaling pathways to remain active throughout gestation. As a result, the expected suppressive effect of pregnancy on ectopic endometrial tissue is incomplete and highly variable across patients. In parallel, local estrogen biosynthesis within endometriotic lesions remains active during pregnancy. Increased aromatase expression and impaired estrogen inactivation sustain a localized estrogen-dominant microenvironment that is largely independent of systemic hormonal suppression. Koninckx et al. [8] emphasized that this intracrine estrogen production contributes to lesion persistence, enhanced vascularity, and tissue fragility during pregnancy. This mechanism provides a biological explanation for clinical observations such as lesion enlargement, pain exacerbation, bleeding, and acute abdominal events in pregnant women with endometriosis, despite a progesterone-rich systemic milieu. Pregnancy also induces decidualization of ectopic endometriotic tissue, a process analogous to the physiological decidualization of the eutopic endometrium. While decidualization is typically reversible and benign, decidualized endometriotic lesions may exhibit exaggerated vascular proliferation and increased friability. Imaging–pathology correlation studies and clinical case series have shown that such lesions may rapidly increase in size, develop prominent vascular features, and mimic malignant transformation on ultrasound or magnetic resonance imaging (MRI) [9]. Clinically, these changes have been associated with serious complications, including spontaneous hemoperitoneum, bowel obstruction, and enlargement of adnexal masses during pregnancy. Importantly, decidualization does not equate to biological quiescence; particularly in cases of DIE, lesions may remain hormonally active and pro-inflammatory, underscoring the heterogeneity of lesion-specific responses to gestational hormones. Beyond hormonal mechanisms, immune dysregulation plays a pivotal role in the pathophysiology of endometriosis during pregnancy. Endometriosis is characterized by a pro-inflammatory pelvic environment enriched with activated macrophages, elevated cytokines, and altered immune cell profiles. Successful pregnancy requires a finely balanced immune state that permits tolerance toward the semi-allogeneic fetus while maintaining host defense. In women with endometriosis, this balance may be disrupted by pre-existing immune abnormalities [10]. Immunological studies have identified overlapping alterations in uterine natural killer cell activity, regulatory T-cell populations, and macrophage polarization patterns in both endometriosis and placentation disorders. These shared immune disturbances may impair trophoblast invasion and spiral artery remodeling, thereby contributing to defective placentation and an increased risk of hypertensive disorders of pregnancy and placental complications [11]. Angiogenesis and vascular dysfunction further represent key mechanistic links between endometriosis and adverse pregnancy outcomes. Aberrant angiogenic signaling, driven in part by the overexpression of vascular endothelial growth factor (VEGF) and related mediators, is a hallmark of endometriotic lesions. Although angiogenesis is fundamental to normal placental development, dysregulated vascular signaling in endometriosis may lead to abnormal placental implantation and impaired uteroplacental perfusion [12]. Experimental and clinical studies have linked excessive or disorganized VEGF activity to inadequate spiral artery remodeling, providing a mechanistic explanation for the increased incidence of placenta previa, placental abruption, fetal growth restriction (FGR), and preterm birth reported in this population. In addition, vascular fragility within decidualized lesions may predispose affected women to hemorrhagic complications during pregnancy and delivery. Importantly, the pathophysiological impact of endometriosis during pregnancy extends beyond the pelvis. Growing evidence supports the characterization of endometriosis as a systemic inflammatory condition with metabolic and vascular consequences. Chronic low-grade inflammation and endothelial dysfunction associated with endometriosis may influence maternal cardiovascular adaptation to pregnancy, contributing to altered uteroplacental blood flow and an increased susceptibility to hypertensive disorders [13]. Recent meta-analytic data linking endometriosis to long-term cardiovascular risk reinforce the concept of systemic vascular involvement, suggesting that pregnancy-related complications arise from a complex interplay of endocrine, immune, and vascular mechanisms operating at both local and systemic levels. Taken together, these mechanisms illustrate that the interaction between endometriosis and pregnancy is neither uniform nor benign. Rather than inducing universal disease quiescence, pregnancy may modulate endometriosis in a phenotype-dependent manner, with hormonal resistance, immune dysregulation, and vascular maladaptation collectively shaping maternal and placental physiology. This integrated pathophysiological framework provides a biologically plausible basis for the heterogeneous obstetric risks observed in women with endometriosis and underscores the importance of individualized risk assessment during pregnancy. 3. Clinical course of endometriosis during pregnancy The clinical course of endometriosis during pregnancy is highly variable and often unpredictable. While pregnancy has traditionally been viewed as a period of symptomatic remission, contemporary evidence indicates that symptom trajectories differ substantially among affected women. Prospective cohort studies and observational series demonstrate that some women experience partial or complete symptom relief, whereas others report persistent symptoms, disease-related complications, or the emergence of new clinical challenges during gestation. Importantly, this heterogeneity is not random but reflects differences in disease phenotype, lesion location, prior treatment history, and individual biological responses to pregnancy-related hormonal and immunological changes. From a symptomatic perspective, sustained progesterone exposure and amenorrhea during pregnancy are associated with reduced pelvic pain and cyclic symptomatology in a subset of women, particularly during the second and third trimesters [14]. However, this improvement is neither universal nor durable. In routine clinical practice, many pregnant women with endometriosis continue to report non-cyclic pelvic pain, sensations of pelvic pressure, bowel-related discomfort, or urinary symptoms. Observational studies indicate that persistent or worsening symptoms are disproportionately observed in women with DIE or extensive adhesive disease, especially when lesions involve the bowel, bladder, or uterosacral ligaments [15]. Mechanical factors, such as uterine enlargement, stretching of pelvic structures, and increased vascular congestion, may exacerbate pain originating from fibrotic or deeply infiltrating lesions. Notably, pain during pregnancy is frequently underreported or attributed to physiological gestational changes, which may delay recognition of endometriosis-related morbidity. Although uncommon, acute complications of endometriosis during pregnancy represent a clinically significant subset of presentations and may be life-threatening. Reported complications include spontaneous hemoperitoneum in pregnancy, bowel obstruction, adnexal torsion, rupture of decidualized endometriomas, and acute abdomen of unclear etiology [16]. Decidualized endometriotic lesions are particularly vulnerable to bleeding due to increased vascularity and tissue friability. Nationwide surveillance studies and IVF-based cohort analyses consistently identify endometriosis as a major underlying risk factor for spontaneous hemoperitoneum in pregnancy, a rare but severe condition thought to arise from the rupture of fragile utero-ovarian or peritoneal vessels adjacent to endometriotic implants [17]. Clinically, these events typically occur in the second or third trimester and present with sudden abdominal pain, hemodynamic instability, and signs of fetal compromise, often necessitating urgent surgical intervention. Diagnostic uncertainty is common, as imaging findings may mimic malignancy or other surgical emergencies, complicating timely management. Contrary to earlier assumptions, pregnancy does not universally suppress disease activity. Disease persistence and silent progression have been increasingly recognized, even in women who remain asymptomatic throughout gestation. Case series and intraoperative reports describe hormonally active, fibrotic, or inflammatory endometriotic lesions identified incidentally during cesarean delivery in women without antenatal symptoms [18]. This silent persistence has important clinical implications, as it may contribute to postpartum symptom recurrence, adhesion progression, and challenges in future fertility or surgical management. Inflammatory mediators and altered tissue remodeling during pregnancy may allow fibrosis and adhesion formation to continue despite the absence of overt clinical manifestations. Diagnosis of endometriosis during pregnancy is further complicated by diagnostic masking. Pregnancy-related anatomical and physiological changes – such as nausea, constipation, pelvic discomfort, and abdominal distension – overlap substantially with symptoms attributable to endometriosis. Consequently, clinicians may underestimate the contribution of endometriosis to patient complaints, particularly in women without a known pre-pregnancy diagnosis [19]. Population-based studies indicate that a significant proportion of women receive their first diagnosis of endometriosis only after delivery, highlighting the extent to which disease manifestations may be concealed during gestation. Additionally, the restricted use of invasive diagnostic procedures and contrast-enhanced imaging during pregnancy limits diagnostic certainty, reinforcing the need for heightened clinical vigilance in women with known endometriosis or prior pelvic surgery. The clinical trajectory of endometriosis during pregnancy is strongly phenotype-dependent. Women with superficial peritoneal disease are more likely to experience symptom improvement, whereas those with ovarian endometriomas or DIE face a higher likelihood of persistent symptoms and pregnancy-related complications [15, 20]. Phenotype-stratified analyses consistently show that deep infiltrating lesions, particularly those involving the bowel or bladder, are least responsive to gestational hormonal modulation and may remain mechanically problematic throughout pregnancy. Ovarian endometriomas may enlarge due to decidualization, occasionally mimicking malignant ovarian tumors on ultrasound or MRI, further complicating clinical assessment and management. Prior treatment and surgical history also play a pivotal role in shaping the clinical course during pregnancy. Although surgical intervention may reduce lesion burden and improve preconception symptoms, it may also result in adhesions, altered pelvic anatomy, and compromised uterine or ovarian vascularization. Retrospective cohort studies demonstrate that women with a history of extensive endometriosis surgery experience higher rates of pregnancy-related pain and operative delivery, reflecting both residual disease and long-term surgical sequelae [21]. These anatomical and functional changes may influence placental implantation, pain perception, and delivery planning. Women who conceive following ARTs often represent a subgroup with more severe disease and combined disease and treatment-related risks, necessitating closer antenatal surveillance. While pregnancy-related symptom modulation is a central feature of the clinical course, it is important to recognize that symptom relief is frequently transient. Many women experience recurrence or exacerbation of endometriosis-related symptoms within months postpartum, particularly following the resumption of ovulatory cycles. Longitudinal follow-up studies suggest that the postpartum recurrence phenotype often mirrors pre-pregnancy disease characteristics, emphasizing the importance of anticipatory counseling and early postpartum management planning. Recognition of this trajectory is essential to ensure continuity of care beyond delivery and will be addressed in detail in subsequent sections. 4. Diagnostic challenges of endometriosis in pregnant women Diagnosing endometriosis during pregnancy represents a substantial clinical challenge due to the convergence of pregnancy-related physiological changes, restricted diagnostic modalities, and the altered biological behavior of endometriotic lesions under gestational hormonal influence. Both symptom-based assessment and imaging interpretation are complicated by the normal adaptations of pregnancy, frequently resulting in delayed diagnosis, misdiagnosis, or incidental detection during delivery or surgical intervention. As a consequence, disease-related morbidity may remain unrecognized throughout gestation, particularly in women without a documented pre-pregnancy diagnosis. From a clinical standpoint, symptom-based evaluation is inherently limited during pregnancy. Many hallmark manifestations of endometriosis – pelvic pain, abdominal discomfort, bloating, bowel irregularities, and urinary frequency – overlap extensively with common physiological features of normal gestation. As pregnancy progresses, uterine enlargement, ligamentous stretching, and increasing pelvic vascular congestion further obscure symptom attribution [22]. Moreover, the absence of cyclic pain patterns during pregnancy diminishes the diagnostic utility of symptom chronology, which is a key feature in non-pregnant populations. Physical examination also offers limited discriminatory value, as bimanual pelvic assessment becomes less informative with advancing gestational age and may be avoided because of patient discomfort or obstetric concerns. Consequently, clinicians often rely on indirect indicators – such as a known history of endometriosis, prior pelvic surgery, or unexplained persistent pain – to raise diagnostic suspicion. Observational studies suggest that this indirect approach contributes to delayed or missed diagnoses, particularly in women without a pre-existing diagnosis. Imaging plays a central yet imperfect role in the diagnostic pathway. Ultrasound remains the first-line imaging modality during pregnancy due to its safety profile, availability, and real-time assessment capability. Transvaginal and transabdominal ultrasound may identify ovarian endometriomas, pelvic masses, or indirect signs of adhesions. However, decidualization of endometriomas during pregnancy frequently produces sonographic changes – including increased wall thickness, papillary projections, and altered echogenicity – that closely resemble features of ovarian malignancy [23]. Single-center and multicenter imaging series have identified these pregnancy-related changes as a major source of diagnostic uncertainty and unnecessary oncologic referral. Furthermore, DIE involving the bowel, bladder, or uterosacral ligaments is commonly underdiagnosed by ultrasound, particularly as the enlarging uterus displaces pelvic anatomy and limits visualization. Diagnostic accuracy is, therefore, highly operator-dependent, and the absence of standardized pregnancy-specific ultrasound criteria further constrains reliability. When ultrasound findings are inconclusive, MRI without gadolinium contrast serves as an important second-line modality. MRI is considered safe during pregnancy and provides superior soft-tissue contrast, enabling improved delineation of deep infiltrating lesions and differentiation between decidualized endometriomas and malignant ovarian tumors [24]. Nevertheless, MRI interpretation in pregnancy requires specialized expertise. Decidualized tissue often exhibits high signal intensity on T2-weighted sequences and may increase lesion complexity, raising the risk of misinterpretation. Radiologic–pathologic correlation studies indicate that diagnostic errors are most likely when MRI findings are evaluated in isolation, without longitudinal imaging or adequate clinical context. The absence of contrast limits vascular characterization, and fetal motion artifacts may further degrade image quality, particularly in late gestation. Diagnostic complexity is further amplified in cases of acute abdomen during pregnancy, where endometriosis-related complications must be differentiated from a broad spectrum of obstetric and non-obstetric conditions. Differential diagnoses include appendicitis, ovarian torsion, degenerating fibroids, placental abruption, uterine rupture, and gastrointestinal pathology. Among these, spontaneous hemoperitoneum in pregnancy, although rare, has a particularly strong association with endometriosis and may present with nonspecific features such as sudden abdominal pain, anemia, and hemodynamic instability [25]. Clinical audits and case series consistently report that endometriosis-associated hemoperitoneum is seldom diagnosed preoperatively, reflecting the nonspecific nature of its presentation and the diagnostic limitations imposed by pregnancy. Reluctance to use invasive procedures or ionizing radiation-based imaging further compounds diagnostic uncertainty, and surgical exploration is sometimes undertaken with incomplete preoperative clarity, underscoring the importance of multidisciplinary decision-making. One of the most challenging diagnostic dilemmas arises from malignancy mimicry. Decidualized endometriomas frequently exhibit imaging characteristics that overlap with ovarian cancer, generating significant anxiety and often prompting extensive diagnostic evaluation or surgical intervention [23, 26]. Multiple ultrasound and MRI series have demonstrated that decidualized endometriomas account for a substantial proportion of adnexal masses initially suspected to be malignant during pregnancy. Distinguishing benign decidualization from malignancy relies on careful longitudinal imaging, assessment of lesion stability, absence of ascites, and integration of clinical history. Tumor markers such as CA-125 have limited diagnostic value in pregnancy because of physiological elevation, particularly during the first trimester, and should, therefore, be interpreted with caution. In a considerable proportion of cases, endometriosis is diagnosed incidentally during cesarean delivery, postpartum sterilization procedures, or emergency laparotomy. Surgeons may encounter adhesions, endometriotic implants, or decidualized lesions that remained clinically silent throughout pregnancy [27]. Retrospective surgical series indicate that such incidental intraoperative detection is common even in women without antenatal suspicion of disease, highlighting the inherent limitations of prenatal diagnostic pathways. While incidental diagnosis provides retrospective confirmation of disease persistence, it also reflects missed opportunities for antenatal risk stratification, counseling, and tailored surveillance. When feasible, thorough documentation and histopathological confirmation are essential to guide postpartum management and long-term follow-up. Overall, diagnostic uncertainty has meaningful clinical consequences. Failure to recognize endometriosis during pregnancy may lead to inadequate pain control, delayed identification of complications, or suboptimal delivery planning. Conversely, overdiagnosis or misinterpretation of imaging findings may result in unnecessary interventions, exposing both mother and fetus to avoidable risk. Given these challenges, a heightened index of suspicion is warranted in pregnant women with known endometriosis, prior pelvic surgery, or unexplained persistent pelvic pain. Multidisciplinary collaboration among obstetricians, radiologists, surgeons, and anesthesiologists is essential to balance diagnostic accuracy with maternal–fetal safety and to ensure proportionate, individualized clinical decision-making. 5. Maternal complications associated with endometriosis Endometriosis is increasingly recognized as a condition with clinically meaningful implications for maternal health during pregnancy. Beyond its well-established association with infertility and chronic pelvic pain, a growing body of evidence indicates that endometriosis is linked to a broad spectrum of obstetric complications, some of which carry substantial maternal morbidity. Large population-based cohort studies and meta-analyses consistently demonstrate that these risks persist after adjustment for maternal age, parity, and mode of conception, suggesting an intrinsic disease-related effect rather than confounding by demographic or treatment-related factors. Proposed mechanisms include chronic systemic and local inflammation, immune dysregulation, altered uterine and placental vascularization, and anatomical distortion resulting from adhesions or prior surgical intervention. One of the most frequently reported maternal complications is persistent or exacerbated pain during pregnancy. Although cyclic pain typically diminishes with amenorrhea, non-cyclic pelvic pain associated with deep infiltrating lesions, adhesions, or bowel and bladder involvement often persists or intensifies as pregnancy progresses [28]. Prospective observational studies indicate that pain persistence is most pronounced in women with deep infiltrating disease, supporting the concept that fibrotic lesions exhibit limited responsiveness to gestational hormonal modulation. Progressive uterine enlargement and increased intra-abdominal pressure may exacerbate traction on adhesions and fibrotic nodules, leading to mechanically mediated pain. Pain management in this context is particularly challenging, as many pharmacological agents commonly used for endometriosis-related pain are contraindicated or restricted during pregnancy. As a result, suboptimal pain control may adversely affect maternal quality of life, sleep, mobility, and psychological well-being. Endometriosis is also consistently associated with an increased risk of obstetric hemorrhagic complications, including antepartum bleeding, postpartum hemorrhage, and, in rare cases, spontaneous hemoperitoneum during pregnancy [29]. Decidualized endometriotic lesions are characterized by increased vascularity and tissue friability, rendering them susceptible to bleeding in response to mechanical stress or vascular remodeling. Nationwide registry studies have confirmed a significantly higher incidence of postpartum hemorrhage among women with endometriosis, even after controlling for delivery mode and other confounders [30]. In addition, extensive pelvic adhesions may complicate surgical access and hemostasis during cesarean delivery, contributing to prolonged operative time, increased blood loss, and higher transfusion requirements. Among placental complications, the association between endometriosis and placenta previa is one of the most robust and consistently reported findings. Meta-analyses indicate a twofold to fourfold increased risk of placenta previa in women with endometriosis compared with unaffected controls [31]. This association has been observed across both spontaneous and assisted conceptions, supporting a disease-related mechanism rather than an effect mediated solely by fertility treatment. Impaired endometrial receptivity, altered uterine peristalsis, and abnormal decidualization are thought to influence implantation site selection, predisposing to low placental implantation. Clinically, placenta previa substantially increases the likelihood of cesarean delivery and is associated with severe hemorrhage, blood transfusion, and, in extreme cases, peripartum hysterectomy, thereby representing a major contributor to maternal morbidity in this population. Evidence also supports a modest but statistically significant association between endometriosis and hypertensive disorders of pregnancy, including gestational hypertension and pre-eclampsia [32]. Meta-analytic data indicate that this relationship persists after adjustment for shared risk factors such as maternal age and parity. Proposed biological mechanisms include chronic inflammation, endothelial dysfunction, and defective spiral artery remodeling, all of which overlap with key elements of pre-eclampsia pathophysiology. Although the absolute increase in risk is relatively small, the clinical implications are considerable, given the potential severity of hypertensive complications and their downstream effects on both maternal and fetal health. Consistent with the increased burden of obstetric complications, women with endometriosis demonstrate higher rates of cesarean delivery compared with the general obstetric population [30, 33]. This increased prevalence reflects a combination of factors, including higher rates of placenta previa, fetal malpresentation, and intrapartum complications. Population-based analyses suggest that both elective and emergency cesarean deliveries are more common in women with moderate to severe disease, reflecting anticipatory surgical decision-making as well as emergent obstetric indications. Elective cesarean delivery may be preferentially selected in women with severe pelvic adhesions or a history of extensive endometriosis surgery due to concerns regarding labor progression or the technical difficulty of emergency intervention. However, cesarean delivery in this population is often surgically challenging, with increased operative time, blood loss, and risk of intraoperative injury to adjacent organs, such as the bladder or bowel [34]. From a procedural perspective, surgical and anesthetic challenges represent an important component of maternal risk. Pelvic adhesions arising from endometriosis or prior surgical treatment may significantly distort anatomy, obscure surgical planes, and increase the likelihood of organ injury during abdominal or pelvic surgery. Multicenter surgical series report a higher incidence of intraoperative complexity in women with a history of DIE, particularly during cesarean delivery [34]. These challenges may necessitate advanced surgical expertise, careful preoperative planning, and multidisciplinary involvement, especially in emergency settings. Anesthetic management may also be complicated by chronic pain syndromes and prior surgical exposure, which can influence analgesic requirements and perioperative risk assessment. Beyond physical morbidity, endometriosis during pregnancy imposes a substantial psychological and quality-of-life burden. Persistent pain, fear of obstetric complications, and uncertainty regarding pregnancy outcomes may contribute to heightened anxiety and emotional distress. Systematic reviews demonstrate higher rates of anxiety and depressive symptoms among pregnant women with endometriosis compared with unaffected controls, underscoring the need for psychological support as an integral component of comprehensive prenatal care [35]. These psychosocial dimensions are clinically relevant, as maternal mental health influences pain perception, treatment adherence, and overall pregnancy experience, and should therefore be actively addressed within multidisciplinary care models. 6. Fetal and neonatal outcomes In recent years, endometriosis has emerged as a maternal condition with clinically relevant implications for fetal development and neonatal health. Earlier paradigms regarded pregnancy as a protective state that neutralized the effects of endometriosis; however, accumulating evidence challenges this assumption. Contemporary data indicate that endometriosis may influence placental development and function, fetal growth trajectories, and the timing of birth, even in pregnancies that appear otherwise uncomplicated. These associations underscore the importance of viewing endometriosis not only as a gynecologic condition but also as a modifier of the intrauterine environment. Among adverse outcomes, preterm birth represents one of the most consistently reported findings in pregnancies affected by endometriosis. Meta-analyses and large cohort studies demonstrate a significantly increased risk of both spontaneous and medically indicated preterm delivery compared with the general obstetric population [36, 37]. This association has been replicated across diverse healthcare systems and study designs, supporting its robustness. Several pathophysiological mechanisms have been proposed, including chronic intrauterine inflammation, altered cytokine profiles, and dysregulated prostaglandin synthesis, all of which may promote uterine contractility and cervical remodeling. In addition, defective placentation and placental insufficiency may necessitate early delivery for maternal or fetal indications. Notably, the risk of preterm birth appears to be particularly pronounced in women with DIE and in those who conceive via ARTs, suggesting an interaction between disease severity and reproductive pathway [38]. Closely related to prematurity, low birth weight and FGR occur more frequently in neonates born to mothers with endometriosis. Population-based studies consistently report an increased likelihood of delivering infants who are small for gestational age, even after adjustment for maternal age, parity, and smoking status [39]. Importantly, several registry-based analyses suggest that this association persists independently of hypertensive disorders of pregnancy, pointing toward a distinct underlying mechanism. Impaired uteroplacental perfusion is widely regarded as central to this process. Endometriosis-associated abnormalities in spiral artery remodeling, endothelial dysfunction, and placental inflammation may compromise nutrient and oxygen transfer to the fetus. The observation that growth impairment may occur in the absence of overt maternal hypertension further supports the concept of an endometriosis-specific placental phenotype. Placental dysfunction provides a unifying biological framework linking endometriosis to multiple adverse fetal outcomes. Histopathological studies reveal increased rates of placental lesions consistent with maternal vascular malperfusion in pregnancies complicated by endometriosis [40]. These structural abnormalities are mirrored by functional findings, including altered uteroplacental Doppler indices, suggesting impaired placental perfusion. Clinically, placental dysfunction may manifest as chronic fetal hypoxia, reduced growth velocity, and increased susceptibility to intrapartum fetal distress. Such compromise is often detected through abnormal fetal surveillance findings, including reduced fetal movements, non-reassuring cardiotocography, or abnormal Doppler velocimetry, frequently prompting intensified monitoring or early delivery. Although stillbirth and perinatal mortality remain rare outcomes, several studies report a modestly increased risk of stillbirth among women with endometriosis [36, 41]. The absolute risk increase is small; nevertheless, the association is biologically plausible, given established links between endometriosis, placental insufficiency, and FGR. Interpretation of these data is complicated by limited statistical power and insufficient adjustment for disease phenotype and severity in many studies, which may contribute to variability in reported risk estimates. Despite these limitations, the potential for severe outcomes reinforces the importance of vigilant fetal surveillance in pregnancies affected by moderate to severe endometriosis. Neonatal morbidity in this population appears to be largely mediated by prematurity and growth restriction rather than by direct teratogenic effects of endometriosis. Preterm infants born to mothers with endometriosis exhibit higher rates of neonatal intensive care unit admission, respiratory distress, and feeding difficulties [37, 39]. However, when analyses are adjusted for gestational age and birth weight, endometriosis itself does not independently increase the risk of congenital anomalies or long-term neurodevelopmental impairment. This distinction has important clinical implications, as it suggests that optimization of obstetric management – particularly prevention or mitigation of preterm birth – may substantially reduce neonatal morbidity associated with maternal endometriosis. Emerging evidence indicates that fetal risk is strongly influenced by the endometriosis phenotype. DIE and extensive disease involving the uterosacral ligaments or bowel are more consistently associated with adverse fetal outcomes than superficial peritoneal disease [38, 42]. Phenotype-stratified analyses highlight disease depth and anatomical extent as key determinants of placental dysfunction and fetal compromise. Ovarian endometriomas may also contribute to adverse outcomes, particularly in the context of prior surgical intervention, which may further disrupt pelvic and uterine vascular integrity. These findings support the concept that fetal risk in endometriosis is not uniform but varies according to disease characteristics. From a clinical perspective, these observations have direct implications for antenatal fetal surveillance. Given the increased risk of preterm birth and fetal growth abnormalities, pregnancies complicated by endometriosis – particularly those involving severe or deep disease – may benefit from enhanced monitoring strategies. These may include serial fetal growth assessments, Doppler evaluation of uteroplacental circulation, and individualized timing of delivery based on combined maternal and fetal status. Increasing expert consensus favors a selective, phenotype-informed surveillance approach rather than universal classification of all endometriosis pregnancies as high risk. While routine high-risk labeling is not warranted for women with mild disease, those with severe endometriosis, prior obstetric complications, or additional risk factors may require closer follow-up to optimize fetal and neonatal outcomes. 7. Endometriosis phenotypes and pregnancy outcomes Endometriosis is a heterogeneous disorder encompassing distinct phenotypes that differ in anatomical distribution, biological behavior, symptom burden, and responsiveness to hormonal modulation. Accumulating evidence indicates that pregnancy outcomes are not uniform across these phenotypes; rather, obstetric risk varies according to lesion type, depth of infiltration, disease extent, and prior surgical intervention. Phenotype-stratified analyses from large cohort studies increasingly support this differential risk profile, underscoring the importance of recognizing phenotype-specific patterns when counseling pregnant women with endometriosis and planning antenatal surveillance. Women with superficial peritoneal endometriosis, characterized by lesions confined to the peritoneal surface without deep tissue invasion, generally represent the lowest-risk phenotype during pregnancy. These lesions are often associated with milder symptoms and limited anatomical distortion. During gestation, superficial implants are more likely to undergo hormonal quiescence or partial regression, reflecting relative sensitivity to the progesterone-dominant intrauterine environment [43]. After adjustment for maternal and obstetric confounders, large retrospective analyses consistently report pregnancy outcomes comparable to those of the general obstetric population, with no clinically meaningful increase in preterm birth, FGR, or placental complications [44]. Accordingly, isolated superficial peritoneal disease alone does not usually warrant classification as a high-risk pregnancy, although routine clinical vigilance remains appropriate. In contrast, ovarian endometriomas constitute a phenotype with more complex implications for pregnancy. These cystic ovarian lesions may persist or undergo decidualization during gestation, occasionally enlarging or developing imaging features that raise concern for malignancy. Although many endometriomas remain asymptomatic, complications such as cyst rupture, torsion, or hemorrhage may occur, particularly in the second and third trimesters [45]. Imaging-based observational studies identify decidualized endometriomas as one of the most common adnexal masses evaluated during pregnancy, highlighting their diagnostic and clinical relevance. From an obstetric perspective, ovarian endometriomas have been associated with increased risks of placenta previa, preterm birth, and cesarean delivery [46]. These associations are likely multifactorial, involving altered ovarian and uterine vascularization, local inflammatory signaling, and, in many cases, the sequelae of prior surgical treatment. Women with surgically treated endometriomas appear to represent a higher-risk subgroup, as postoperative adhesions and compromised pelvic anatomy may influence placental implantation and labor dynamics. Among all phenotypes, DIE is most strongly and consistently associated with adverse pregnancy outcomes. Defined by lesions penetrating more than 5 mm beneath the peritoneal surface, DIE commonly involves the uterosacral ligaments, rectovaginal septum, bowel, bladder, and pelvic nerves, resulting in marked fibrosis and anatomical distortion. Multiple studies demonstrate that women with DIE face substantially increased risks of placenta previa, preterm birth, hypertensive disorders of pregnancy, and obstetric hemorrhage [47]. These associations remain robust across tertiary-center cohorts and population-based analyses, reinforcing their clinical significance. FGR and abnormal placentation are also more frequently observed, supporting the hypothesis that DIE exerts systemic and uterine effects that extend beyond local lesion burden. During pregnancy, DIE lesions often persist despite hormonal changes, reflecting pronounced progesterone resistance and sustained inflammatory activity. Mechanical interaction between the enlarging uterus and rigid fibrotic lesions may further exacerbate pain, bowel symptoms, and obstetric complications. Women with multisite or extensive endometriosis, involving combinations of superficial lesions, ovarian endometriomas, and deep infiltrating disease, represent a particularly high-risk subgroup. These patients frequently have a history of infertility, multiple surgical interventions, and prolonged disease duration. Cumulative risk modeling from cohort studies suggests that obstetric risk increases in parallel with overall lesion burden and anatomical extent, rather than being driven by any single phenotype in isolation. Pregnancies in this group are associated with higher rates of preterm delivery, placental abnormalities, cesarean section, and neonatal morbidity [48]. The interaction between widespread inflammation, surgical sequelae, and altered uterine physiology underscores the need for intensified antenatal surveillance and multidisciplinary management in this population. Importantly, the influence of disease phenotype on pregnancy outcomes cannot be fully understood without considering prior surgical treatment. While surgery may reduce lesion burden and improve fertility, it may also introduce adhesions, disrupt pelvic innervation, and alter uterine or ovarian blood supply. Surgical cohort studies indicate that women with prior extensive excision for deep infiltrating disease experience higher rates of abnormal placental implantation and operative delivery, highlighting the long-term obstetric consequences of surgical intervention [49]. Conversely, more conservative surgical approaches may preserve anatomical integrity but leave residual disease that continues to influence pregnancy physiology. These observations emphasize that both phenotype and surgical history must be integrated into comprehensive risk assessment. Collectively, emerging data support a move toward phenotype-specific obstetric risk stratification in women with endometriosis. Rather than treating endometriosis as a uniform condition, clinicians should incorporate lesion type, disease extent, and surgical history into individualized antenatal care plans. This tailored approach facilitates targeted fetal growth monitoring, early identification of placental complications, and proactive delivery planning, thereby optimizing maternal and neonatal outcomes while avoiding unnecessary medicalization of low-risk pregnancies. 8. Surgical history of endometriosis and pregnancy implications Surgical treatment constitutes a central component of endometriosis management, particularly in women with severe symptoms, deep infiltrating disease, or infertility. As an increasing proportion of women conceive following surgical intervention, understanding how prior endometriosis surgery modifies pregnancy course and outcomes has become clinically essential. Evidence from surgical cohorts and obstetric outcome studies consistently indicates that surgical history acts as an independent modifier of pregnancy risk. These effects are mediated through anatomical distortion, vascular and neural disruption, and functional alterations of the pelvis and uterus, with consequences that may extend well beyond the immediate goal of lesion removal. Endometriosis surgery encompasses a broad spectrum of procedures, ranging from conservative excision or ablation of superficial lesions to complex resections involving the bowel, bladder, ureters, or pelvic ligaments. Common interventions include ovarian cystectomy for endometriomas, excision of deep infiltrating nodules, adhesiolysis, and, in selected cases, segmental bowel resection. Although the primary objectives of surgery are pain relief and fertility enhancement, the extent and anatomical location of surgical intervention vary considerably. Surgical series consistently demonstrate that increasing procedural complexity is associated with greater disruption of pelvic anatomy and tissue integrity, a factor that is critically relevant when evaluating subsequent pregnancy risks [50]. From a reproductive and obstetric standpoint, prior surgery may influence uterine integrity and placental implantation. While endometriosis surgery rarely involves direct uterine incision, extensive dissection in proximity to the uterosacral ligaments, posterior cervix, or lower uterine segment may alter myometrial perfusion, local inflammatory signaling, and tissue compliance. Cohort studies focusing on women with a history of DIE surgery report higher rates of abnormal placental implantation, and multiple analyses suggest an association between prior extensive surgery – particularly for deep disease – and increased risk of placenta previa or abnormal placental attachment [51]. These observations support the hypothesis that surgical disruption of the endometrial–myometrial interface and surrounding vascular networks may influence implantation site selection and placental development. Postoperative adhesions represent one of the most common and clinically significant sequelae of endometriosis surgery. Adhesions may involve the uterus, ovaries, bowel, bladder, and abdominal wall, leading to distorted pelvic anatomy and reduced organ mobility. During pregnancy, progressive uterine enlargement may place tension on adhesive bands, contributing to pain, bowel symptoms, or urinary obstruction. From an obstetric perspective, adhesions may also complicate labor and delivery. Intraoperative reports describe dense adhesions as a major determinant of technical difficulty during cesarean delivery, as anterior or posterior adhesions can restrict uterine expansion, interfere with fetal descent, and obscure surgical planes. These challenges are associated with prolonged operative time, increased blood loss, and an elevated risk of bladder or bowel injury [52]. Consistent with these anatomical considerations, women with a history of extensive endometriosis surgery exhibit higher rates of cesarean delivery, both elective and emergent. This increased prevalence reflects a combination of obstetric indications – such as placenta previa or fetal malpresentation – and anticipatory surgical decision-making driven by concerns regarding the technical difficulty of emergency intervention [53]. Population-based analyses demonstrate that cesarean delivery rates rise in parallel with the surgical extent and with prior involvement of the bowel or bladder. Cesarean section in this context requires meticulous preoperative planning, as adhesions may distort the lower uterine segment, obscure anatomical landmarks, and necessitate alternative incision strategies. In women with prior bowel resection or bladder surgery, multidisciplinary surgical support may be required to ensure maternal safety. A substantial proportion of women who conceive following endometriosis surgery do so through ARTs. ART pregnancies constitute a distinct clinical subgroup characterized by higher baseline obstetric risk, including increased rates of preterm birth and placental complications. Studies examining ART cohorts indicate that the effects of endometriosis, prior surgical treatment, and ARTs are additive rather than independent. Women with surgically treated endometriosis who conceive via ARTs demonstrate higher rates of placenta previa, hypertensive disorders of pregnancy, and cesarean delivery compared with women without endometriosis undergoing ART [54]. These findings underscore the importance of integrating surgical history into counseling, risk stratification, and monitoring strategies for ART pregnancies. Importantly, not all surgical sequelae manifest immediately. Long-term effects of surgery, including fibrosis, altered pelvic innervation, and subtle vascular changes, may influence uterine function and placental perfusion throughout pregnancy. Longitudinal follow-up studies suggest that these changes may persist for years after intervention, even in women who are otherwise asymptomatic. Because such sequelae are not readily detectable by routine imaging, their contribution to abnormal placentation or impaired fetal growth may be underrecognized. Consequently, women with a history of extensive endometriosis surgery, particularly procedures involving deep infiltrating disease, may benefit from enhanced antenatal surveillance. This may include serial fetal growth assessments, careful evaluation of placental location, and individualized delivery planning informed by detailed operative reports. Despite these considerations, it is essential to emphasize that endometriosis surgery remains a valuable and often indispensable intervention. Its potential implications for future pregnancy highlight not a contraindication to surgery, but rather the need for careful surgical planning, judicious patient selection, and thorough documentation. Expert consensus increasingly emphasizes the role of preconception counseling in women of reproductive age undergoing extensive endometriosis surgery. Such counseling should include discussion of potential obstetric implications, anticipated surveillance needs, and delivery considerations. Close collaboration between gynecologic surgeons and obstetric care providers is fundamental to optimizing both reproductive success and pregnancy outcomes in this complex patient population. 9. Management strategies during pregnancy Management of endometriosis during pregnancy requires a careful balance between symptom control, prevention of disease-related and obstetric complications, and protection of maternal–fetal safety. Therapeutic options are inherently constrained by pregnancy-related physiological considerations, and evidence guiding management is largely derived from observational studies, expert consensus, and cautious extrapolation from non-pregnant populations. As such, management strategies should be predominantly conservative, individualized, and informed by disease phenotype, symptom severity, obstetric risk profile, and prior surgical history rather than by the diagnosis alone. A fundamental principle of care is risk stratification, which allows clinicians to distinguish women who may benefit from enhanced surveillance from those likely to experience uncomplicated pregnancies. Although endometriosis has been associated with adverse maternal and fetal outcomes, risk is not uniformly distributed. Cohort-based analyses demonstrate that clinically meaningful risk is concentrated among women with deep infiltrating disease, extensive multisite involvement, or a history of major pelvic surgery, whereas women with superficial disease and minimal symptoms frequently have uneventful gestations [55]. Accordingly, management should avoid routine high-risk classification for all women with endometriosis and instead rely on careful clinical assessment early in pregnancy, ideally informed by a detailed preconception history. For the majority of patients, conservative and expectant management represents the cornerstone of care. Pregnancy-related hormonal adaptations often stabilize disease activity, and unnecessary diagnostic or therapeutic interventions may expose both mother and fetus to avoidable risk. In asymptomatic or mildly symptomatic women, standard obstetric follow-up with heightened clinical awareness is generally sufficient. Observational data suggest that excessive intervention in low-risk phenotypes does not improve outcomes and may inadvertently increase anxiety and symptom perception. Education, reassurance, and clear communication regarding expected symptom trajectories are, therefore, integral components of conservative management. Clinicians should remain vigilant for signs of complications while avoiding unnecessary medicalization of otherwise low-risk pregnancies. Pain management during pregnancy poses a particular challenge due to the limited range of pharmacological options considered safe for fetal exposure. Paracetamol remains the first-line analgesic throughout gestation and is generally well-tolerated. Nonsteroidal anti-inflammatory drugs may be used with caution in early pregnancy but should be avoided in the second and third trimesters because of established fetal risks. Opioid analgesics may be considered for severe, refractory pain, but their use should be restricted in duration and closely supervised, given the potential for maternal side effects and neonatal withdrawal. Given these limitations, non-pharmacological strategies assume a central role. Clinical experience and small interventional studies support the use of pregnancy-adapted physiotherapy, posture-focused interventions, activity pacing, and psychosocial support to improve pain control and functional capacity. A multimodal approach integrating physical and psychological interventions often provides the most effective and safest strategy for symptom management. Surgical intervention during pregnancy is uncommon and should be reserved for clearly defined indications. These include acute complications such as ovarian torsion, rupture of an endometrioma, bowel obstruction, spontaneous hemoperitoneum, or suspicion of malignancy that cannot be excluded through noninvasive evaluation. When surgery is unavoidable, the second trimester is generally regarded as the optimal timing, balancing maternal safety with lower risks of miscarriage and preterm labor [56]. Surgical case series consistently emphasize that outcomes are most favorable when procedures are performed in experienced centers within a multidisciplinary framework involving obstetricians, surgeons, anesthesiologists, and neonatologists. Decisions regarding laparoscopic versus open approaches should be individualized, considering gestational age, disease extent, maternal stability, and institutional expertise. In selected patients, enhanced antenatal surveillance may be warranted. Women with moderate to severe endometriosis, deep infiltrating disease, prior extensive pelvic surgery, or evidence of placental dysfunction may benefit from tailored monitoring strategies. These may include serial fetal growth assessments, evaluation of placental location, and Doppler studies of uteroplacental circulation. Cohort studies suggest that selective, risk-adapted surveillance improves early detection of placental insufficiency without increasing unnecessary intervention, supporting this targeted approach. Importantly, routine intensified monitoring for all women with endometriosis is not supported by current evidence and may contribute to overmedicalization. Delivery planning and intrapartum management should be guided by obstetric indications rather than by the diagnosis of endometriosis alone. Vaginal delivery is feasible and appropriate for many women, including those with a history of mild to moderate disease. Cesarean delivery may be indicated in the presence of placenta previa, severe pelvic adhesions, or anticipated technical difficulty related to prior extensive surgery [55]. Retrospective obstetric series highlight the importance of anticipating distorted anatomy and adhesions in women with advanced disease. Careful preoperative planning, review of prior operative reports, availability of senior surgical expertise, and preparedness for potential complications such as hemorrhage or organ injury are key components of safe intrapartum care. Optimal management of endometriosis during pregnancy is inherently multidisciplinary. Collaboration among obstetricians, radiologists, gynecologic surgeons, pain specialists, physiotherapists, and mental health professionals enables comprehensive care that addresses both the physical and psychological dimensions of the disease. Evaluations of multidisciplinary care models in chronic gynecologic conditions demonstrate improved patient satisfaction and symptom control, supporting this integrated approach. Transparent counseling, shared decision-making, and anticipatory guidance regarding symptom expectations, obstetric risks, and postpartum recurrence are essential to empower women and promote adherence to individualized management plans. 10. Conclusions Endometriosis is increasingly recognized as a condition whose clinical relevance extends well beyond infertility and chronic pelvic pain, encompassing important dimensions of maternal, placental, and fetal health during pregnancy. Accumulating epidemiological, clinical, and mechanistic evidence challenges the long-standing assumption that pregnancy uniformly suppresses disease activity or confers protection against endometriosis-related morbidity. Instead, pregnancy should be understood as a dynamic physiological state in which the interaction between gestational adaptations and pre-existing disease processes may result in heterogeneous clinical trajectories, ranging from symptom attenuation to persistence of disease activity and increased obstetric risk. The evidence synthesized throughout this chapter highlights the marked heterogeneity of endometriosis and its differential impact on pregnancy outcomes. While many women with superficial peritoneal disease experience largely uncomplicated pregnancies, those with deep infiltrating or multisite endometriosis, a history of extensive pelvic surgery, or conception via ARTs consistently demonstrate higher risks of placental dysfunction, preterm birth, obstetric hemorrhage, and operative delivery. These phenotype-specific associations, recurrently observed across cohort, registry-based, and meta-analytic studies, underscore the limitations of uniform risk categorization and emphasize the need for phenotype-informed, individualized assessment throughout pregnancy. From a clinical standpoint, the management of endometriosis during pregnancy should be anchored in careful risk stratification, conservative symptom control, and selectively intensified antenatal surveillance. A nuanced approach is required to balance vigilance against overmedicalization, ensuring timely identification of clinically meaningful complications while avoiding unnecessary intervention in low-risk pregnancies. Multidisciplinary collaboration among obstetricians, gynecologic surgeons, radiologists, pain specialists, physiotherapists, and mental health professionals is central to this approach, enabling integrated care that addresses both the physical and psychological dimensions of the disease. Equally important is the recognition of the postpartum period as a critical transitional window, during which symptom recurrence is common and opportunities arise for long-term disease management, counseling, and future reproductive planning. Despite growing recognition of the pregnancy-related implications of endometriosis, important gaps remain in the current evidence base. Much of the available literature is retrospective in nature, with limited granularity regarding disease phenotype, surgical history, and longitudinal maternal–fetal outcomes. The scarcity of prospective and interventional studies constrains the development of robust, evidence-based clinical guidelines and limits our ability to refine risk prediction models. Addressing these limitations through well-designed, phenotype-specific prospective studies and translational research will be essential to improve mechanistic understanding and inform targeted preventive and therapeutic strategies. In conclusion, endometriosis should be regarded as a pregnancy-relevant condition that warrants integrated obstetric and gynecologic consideration rather than isolated management within reproductive medicine alone. By embracing individualized, evidence-informed care pathways and advancing focused research efforts, clinicians and researchers can better support women with endometriosis across the continuum of pregnancy, childbirth, and the postpartum period, ultimately improving both maternal and neonatal outcomes. Acknowledgments The author acknowledges the use of ChatGPT for language polishing.

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