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Endometriosis

Endometriosis is a chronic, estrogen-dependent inflammatory disease defined by endometrial-like tissue outside the uterine lining, affecting approximately 10% of reproductive-age women (approximately 9 million in the U.S.). Endometriosis is a common cause of pelvic pain; in a cross-sectional survey of 940 women with surgically confirmed disease, 26.2% listed infertility among the symptoms leading to diagnosis.[1] There is currently no medical or surgical cure, and diagnosis is delayed an average of 5 to 12 years from symptom onset.[1]

Pathophysiology​

The most widely accepted theory is retrograde menstruation (Sampson's theory), in which shed endometrial tissue travels through the fallopian tubes into the peritoneal cavity, where it implants, proliferates, and provokes an inflammatory response.[3] Additional mechanisms include:

  • Epigenetic reprogramming of endometrial mesenchymal progenitor / stem cells, with overexpression of steroidogenic factor-1 driving excessive local estrogen production via estrogen receptor-β, and progesterone receptor deficiency causing progesterone resistance.[3]
  • Immune dysregulation with proinflammatory cytokines, altered circulating immune cell populations, and aberrant microRNA expression creating a systemic inflammatory environment.[4]
  • Neurogenesis within lesions, with new nerve fiber growth contributing to nociceptive and neuropathic pain mechanisms; central sensitization (nociplastic pain) explains why lesion burden correlates poorly with pain severity.[1]

Three pain mechanisms coexist and explain the disconnect between disease stage and symptom severity: nociceptive (lesion-driven inflammation), neuropathic (lesion-associated nerve fiber injury and infiltration), and nociplastic (central sensitization).

Clinical Presentation​

Approximately 90% of women with endometriosis report pelvic pain, and 50% report moderate to severe fatigue.[1] Symptoms include:

  • Dysmenorrhea. Progressive, often starting in adolescence
  • Nonmenstrual chronic pelvic pain
  • Deep dyspareunia
  • Dyschezia. Painful defecation, often cyclic
  • Dysuria. Cyclic
  • Infertility. Reported by 26.2% of 940 survey respondents with surgically confirmed endometriosis.[1]

Endometriosis exists in three phenotypes: superficial peritoneal lesions, ovarian endometriomas, and deep infiltrating endometriosis (involving the rectovaginal septum, bladder, ureters, or bowel).[2][4]

Diagnosis​

A clinical diagnosis can now be made based on symptoms, physical examination, and imaging; surgical confirmation is not required to initiate empiric treatment. ACOG 2026 supports a presumptive diagnosis and treatment while imaging evaluation continues.[1][5][7] Diagnostic considerations:

  • Physical examination. Tenderness in the posterior fornix, uterosacral nodularity, fixed retroverted uterus, or adnexal masses.[1]
  • Transvaginal ultrasound (TVUS) is first-line imaging and can identify endometriomas and deep infiltrating endometriosis in experienced hands. A negative scan does not exclude superficial disease.[19][5]
  • Pelvic MRI maps deep infiltrating endometriosis.[5]
  • Laparoscopy with biopsy can establish histology and treat disease when indicated, including when imaging is negative and empiric treatment has been unsuccessful or is inappropriate.[19][7]
  • Biomarkers. No serum biomarker, including CA-125, has sufficient sensitivity or specificity for clinical use.[3]

Treatment: Medical Management​

Hormonal therapy is the mainstay of treatment for endometriosis-associated pain in women not seeking immediate pregnancy. Treatments suppress ovarian activity, act locally on endometriotic tissue, or both; not every regimen reliably inhibits ovulation or provides contraception. A network meta-analysis of 15 RCTs (1,680 participants) found placebo-adjusted mean pain reductions of 12.6–17.7 points on a 0–100 VAS for the combined contraceptives, progestins, levonorgestrel IUD and GnRH agonists studied, with little difference among these regimens.[1]

First-Line Therapies​

  • Combined oral contraceptives (20–30 μg ethinyl estradiol). Continuous use provides better pain control than cyclic regimens. Mean pain reduction versus placebo: 15.1 points (95% CI, −20.8 to −9.3).[1][8]
  • Progestin-only options. Norethindrone acetate (oral), depot medroxyprogesterone acetate (IM), etonogestrel implant, or the 52-mg levonorgestrel IUD. The LNG-IUD reduced pain by 17.7 points versus placebo but does not suppress ovulation.[1][8]
  • NSAIDs. Commonly used adjunctively, though a Cochrane review found insufficient evidence that they significantly reduce endometriosis-specific pain.[8][9]

Second-Line Therapies: GnRH Agonists and Antagonists​

Two oral GnRH antagonist regimens are FDA-approved for endometriosis-associated pain: Orilissa (elagolix) and Myfembree (relugolix combination therapy).[10][21]

  • Elagolix (Orilissa). With normal liver function or mild hepatic impairment, low dose 150 mg daily (up to 24 months) or high dose 200 mg twice daily (up to 6 months).[10] Moderate hepatic impairment permits only 150 mg daily for up to 6 months; severe hepatic impairment and known osteoporosis are contraindications. In the phase 3 trials EM-1 and EM-2, month-3 dysmenorrhea response rates were 43–46% (150 mg daily) and 72–76% (200 mg twice daily) versus 20–23% with placebo.[10] In a phase 3 endometriosis-pain trial, oral elagolix 200 mg twice daily with add-back estradiol 1 mg / norethindrone acetate 0.5 mg once daily had efficacy and BMD data through 12 months.[1][10][11]
  • Relugolix combination therapy (Myfembree). Relugolix 40 mg plus estradiol 1 mg plus norethindrone acetate 0.5 mg, once daily.[21] At 24 weeks in the SPIRIT 1 and 2 trials, 75% met dysmenorrhea responder criteria versus 27–30% with placebo; a separate extension reported outcomes through 2 years among eligible trial completers.[12][13] Add-back reduces but does not eliminate bone loss: US treatment is limited to 24 months, with baseline and annual DXA for endometriosis.[1][12][13][21] Myfembree contraindications include current or prior thromboembolic disease or high thrombotic risk, known osteoporosis, and hepatic impairment; the label directs discontinuation 4–6 weeks before surgery with increased thromboembolic risk when feasible.[21]

A meta-analysis of five phase 3 trials (2,060 participants; elagolix 200 mg twice daily, relugolix combination therapy and linzagolix with add-back) found a pooled NNT of 2 for dysmenorrhea response and 5 for nonmenstrual pelvic pain response, with no statistical heterogeneity. Treatment lasted up to 24 weeks.[14]

GnRH agonists (leuprolide acetate) remain an option but require injection, cause an initial flare, and are limited to 12 months with add-back therapy due to bone loss concerns.[8][9][2]

These GnRH regimens are not contraceptives. The labels require pregnancy exclusion and nonhormonal contraception, and ovulation suppression or amenorrhea does not exclude pregnancy.[10][21]

Third-Line Therapy​

  • Aromatase inhibitors (off-label) block estrogen production within lesions and are reserved for refractory cases. In premenopausal patients, combine with an appropriate ovarian-suppression regimen to limit follicular stimulation; specialist selection is required. Limited by bone loss with prolonged use.[9][8]

Approximately 11–19% of patients have no pain reduction with hormonal medications, and 25–34% experience recurrent pain within 12 months of discontinuation.[1][8]

Treatment: Surgical Management​

Surgery may be considered when hormonal therapy is ineffective or contraindicated, for a large or suspicious endometrioma when symptoms, malignancy concern, or follicle access warrant intervention, or for deep lesions that threaten organ function.[5][8] For infertility, benefit depends on disease phenotype and the fertility plan: treating superficial disease may improve spontaneous pregnancy, whereas routine endometrioma surgery solely to improve ART live birth is not recommended.[1][19]

  • Laparoscopic excision or ablation is the standard surgical approach. For endometriomas at least 3 cm, excision may reduce one-year endometrioma recurrence versus drainage and ablation (OR 0.17, 95% CI 0.09–0.34; four RCTs, 264 women; low-certainty evidence).[32] CO₂ laser vaporization is another option, with ovarian-reserve tradeoffs.[19] Superficial-disease comparisons differ.[19]
  • Recurrence and repeat surgery are different outcomes. A July 2026 meta-analysis of 57 studies (22,644 patients) estimated approximately 11% repeat surgery, with very high heterogeneity and varying follow-up.[22] Postoperative suppression may be offered when immediate pregnancy is not desired.[22][6] ESHRE strongly recommends considering a postoperative 52-mg LNG-IUS or combined hormonal contraceptive for at least 18–24 months to prevent recurrent dysmenorrhea; after endometrioma surgery in women not immediately seeking conception, it strongly recommends long-term hormonal treatment to reduce endometrioma and symptom recurrence.[19] In the 405-participant PRE-EMPT trial after conservative surgery, long-acting progestogens (LNG-IUS or depot medroxyprogesterone acetate) and combined oral contraception yielded similar three-year pain scores; further surgery or second-line treatment occurred in 50 versus 61 women (73 versus 97 events; HR 0.67, 95% CI 0.44–1.00).[33]
  • Hysterectomy with excision of all visible lesions may be considered when conservative treatments fail and future pregnancy is not desired ; total hysterectomy is preferred as a good-practice point.[19] Approximately 25% of patients who undergo hysterectomy for endometriosis experience recurrent pelvic pain, and 10% undergo additional surgery to treat pain.[1] The ovarian-removal decision requires individualized counseling about recurrent disease, fertility goals, early menopause, and hormone therapy.[1][9]
  • Endometrioma excision and fertility. Cystectomy adversely affects ovarian reserve (lower AMH, reduced antral follicle counts), requiring careful risk-benefit discussion before surgery in women desiring fertility.[9]

In a large population-based cohort (n = 84,885, median follow-up 10 years), up to 1 in 4 women who underwent minor conservative surgery and 1 in 5 who underwent major conservative surgery with ovarian preservation required additional endometriosis surgery.[15]

Urologic involvement​

Urinary involvement may be silent. When deep endometriosis or an endometrioma is suspected, the 2025 DGGG/OEGGG/SGGG guideline calls for bilateral renal ultrasound (expert consensus) to detect silent obstruction. If preoperative imaging shows ureteral or renal-pelvic dilation, repeat upper-tract imaging three months after ureterolysis to document relief; hydronephrosis also warrants assessment of renal function.[30] Surgery should be planned with an experienced multidisciplinary team. Bladder lesions may require partial cystectomy; ureterolysis is appropriate in selected extrinsic disease, while obstructing intrinsic disease or failed ureterolysis may require resection with ureteroureterostomy or reimplantation according to location and length.[20][30] Extrinsic ureteral disease is confined to the adventitia, while intrinsic disease extends into the muscularis; this wall-layer distinction underlies the choice between ureterolysis and resection, though no validated depth threshold defines it.[23] Because deep posterior-compartment excision near the uterosacral ligaments and ureter can place the pelvic autonomic plexus at risk, a nerve-sparing dissection that separates the connective tissue and fascia surrounding the nerves from the underlying peritoneum and endometriotic lesions has been described; in one center's reported experience, none of 51 patients required intermittent self-catheterization after this technique. See Pelvic Neuroanatomy for the plexus anatomy.[24] Injection of sterile water or saline beneath an implant adjacent to bowel, bladder, or ureter has also been described to create a dissection plane and a heat sink that protects the underlying wall during laser vaporization or excision.[25] The ESGE/ESHRE/WES surgical recommendations advise renal ultrasound follow-up after ureteral surgery and during conservative management of suspected deep disease to avoid missing silent hydronephrosis.[20] See Ureteral Stricture and ureteral reconstruction.

Postoperative voiding dysfunction. Colorectal surgery for deep endometriosis carries a meaningful risk of lower urinary tract dysfunction that varies by technique. A systematic review included 60 studies in its qualitative synthesis; nine studies (792 patients) contributed to the meta-analysis of voiding dysfunction within 30 days. Disc excision was associated with higher odds than rectal shaving (OR 12.9, 95% CI 1.40-119.34), while segmental resection did not differ significantly from shaving (OR 3.05, 95% CI 0.55-16.87) or discoid resection (OR 0.99, 95% CI 0.54-1.85).[26] A 2020 meta-analysis of 13 studies found lower odds of postoperative voiding dysfunction with rectal shaving than segmental resection (OR 0.34, 95% CI 0.18–0.63) or discoid excision (OR 0.22, 95% CI 0.09–0.51), and less self-catheterization beyond one month than segmental resection (OR 0.30, 95% CI 0.14–0.66); discoid excision and segmental resection did not differ significantly.[27] A later 22-study meta-analysis estimated the shaving versus discoid comparison imprecisely (OR 0.44, 95% CI 0.07–2.84), while shaving was associated with less postoperative voiding dysfunction than segmental resection (OR 0.33, 95% CI 0.20–0.54).[31] The choice between techniques still depends on the anatomy of the disease. In a single-center retrospective cohort of 198 women who underwent surgery for posterior-compartment deep infiltrating endometriosis, 41% initially had voiding dysfunction (postvoid residual >100 mL at the second bladder scan); among the 17 who needed self-catheterization after discharge, the median time to a postvoid residual under 100 mL was 41 days.[28] Preoperative ENZIAN compartment-B nodules were associated with postoperative dysfunction (p = 0.001), and stage B3 (a compartment-B nodule >3 cm in lateral diameter) had the highest hazard ratio for elevated residual urine (HR 6.43, 95% CI 2.3-18.2).[28] A multicenter series identified persistent urinary retention (postvoid residual >100 mL requiring self-catheterization beyond 30 days) in 16 of 881 women (1.8%) after deep pelvic endometriosis surgery, compared with a 3.5%-14.3% range cited from prior posterior-compartment surgery literature; among the 16 retention cases, 93.8% underwent colorectal resection and 87.5% colpectomy, and the authors suggested that bilateral uterosacral-ligament resection with posterior colpectomy tended to increase risk.[29] Eleven of the 16 still required self-catheterization at one year.[29]

Endometriosis and Infertility​

Infertility occurs in 30–50% of women with endometriosis through multiple mechanisms: chronic inflammation impairing folliculogenesis and implantation, distorted pelvic anatomy, diminished ovarian reserve, and altered endometrial receptivity.[16][4]

  • Ovarian suppression and ART pretreatment. In infertile women with endometriosis, ESHRE strongly recommends against ovarian suppression to improve fertility. It also strongly recommends against extended GnRH-agonist pretreatment before ART to improve live birth because benefit is uncertain.[19]
  • Minimal–mild disease (rASRM I–II). Surgical excision or ablation may improve spontaneous pregnancy rates. Ovulation induction with IUI increases fecundity (limit to 3–4 cycles).[4][17]
  • Moderate–severe disease (rASRM III–IV). IVF is the most effective treatment. ART outcomes are similar to other causes of infertility in stage I–II disease but show reduced live birth rates and oocyte yields in stage III–IV.[16][18]
  • Endometriomas and IVF. ESHRE strongly recommends against routine endometrioma surgery solely to improve ART live birth because evidence shows no benefit and surgery is likely to reduce ovarian reserve. Consider surgery for pain, suspicious findings, or follicle access, with individualized counseling.[19]
  • The Endometriosis Fertility Index (EFI) can help guide management decisions after surgery.[16]

Systemic Comorbidities and Long-Term Risks​

Endometriosis is increasingly recognized as a systemic inflammatory disease with effects extending beyond the pelvis:[4][1]

  • Ovarian cancer. Risk is 93% greater overall, with a 3.4-fold risk of clear-cell and a 2.3-fold risk of endometrioid subtypes. Ovarian-cancer incidence is approximately 1.1% among all women, and the absolute risk in women with endometriosis remains low; guidelines do not recommend prophylactic bilateral salpingo-oophorectomy for normal-appearing ovaries.[1]
  • Cardiovascular disease. Significantly elevated risk of MI and stroke, partly mediated by chronic inflammation and partly by high rates of surgical menopause.[9][1]
  • Autoimmune conditions. Increased risk of SLE, rheumatoid arthritis, and other autoimmune diseases.[9][1]
  • Mental health. Depression and anxiety, with evidence of altered brain gene expression and decreased volume in emotional-processing regions.[4]
  • Coexisting pain conditions. Migraine, irritable bowel syndrome, interstitial cystitis / painful bladder syndrome, and fibromyalgia are common comorbidities, reflecting shared central-sensitization pathways.[9]

Emerging Concepts​

  • Classification. The revised ASRM staging system correlates poorly with symptoms and prognosis. Newer frameworks including the ENZIAN classification for deep endometriosis and the Endometriosis Fertility Index aim to better guide clinical decisions.[6][16]
  • Noninvasive diagnosis. Research into circulating biomarkers (miRNAs, proteomics) and advanced imaging continues, though none have reached clinical utility.[3][4]
  • Multimodal pain management. Because central sensitization contributes to pain, interdisciplinary approaches that incorporate pelvic-floor physical therapy, cognitive behavioral therapy and neuromodulatory agents are used alongside hormonal treatment.[1][9]

See Also​

  • Chronic Pelvic Pain. Biopsychosocial framework, central sensitization, and the multidisciplinary CPP workup.
  • IC/PBS. Frequent comorbidity through shared central-sensitization pathways.
  • Ureteral Stricture. Reconstructive approach for endometriosis-related ureteral obstruction.
  • UPJ Obstruction. Extrinsic compression by endometriotic implants.
  • Opportunistic Adnexal Surgery. Endometriosis-related adnexal surgery considerations.
  • GSM. Vaginal estrogen counseling after surgical menopause / oophorectomy for endometriosis.

Podcasts​

Advances in Endometriosis: Diagnosis & Management
BackTable OBGYN, Ep. 133 (2026) · Hugh Taylor, Nicole Faulkner
backtable.com

Videos​

Robotic Management of Ureteral Deep Infiltrating Endometriosis
Aydın E, et al. Urology Video Journal 2020 (CC BY-NC-ND 4.0)
Open source videoRead the article
Robotic Lich-Gregoir Ureteral Reimplantation for Endometriosis
Raimondo D, et al. Facts Views Vis ObGyn 2026
Read the article

References​

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10. U.S. Food and Drug Administration. "Orilissa (elagolix) prescribing information." Revised December 2025. DailyMed label.

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17. Practice Committee of the American Society for Reproductive Medicine. "Endometriosis and Infertility: A Committee Opinion." Fertil Steril. 2012;98(3):591-598. doi:10.1016/j.fertnstert.2012.05.031

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20. ESGE, ESHRE and WES working group. "Recommendations for the surgical treatment of endometriosis. Part 2: deep endometriosis." Hum Reprod Open. 2020. Full recommendations.

21. MYFEMBREE. US prescribing information. DailyMed label.

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23. Ceccaroni M, Ceccarello M, Caleffi G, et al. "Total Laparoscopic Ureteroneocystostomy for Ureteral Endometriosis: A Single-Center Experience of 160 Consecutive Patients." J Minim Invasive Gynecol. 2019;26(1):78-86. doi:10.1016/j.jmig.2018.03.031

24. Kanno K, Andou M, Aiko K, et al. "Fertility- and Nerve-sparing Laparoscopic Eradication of Deep Endometriosis with Total Posterior Compartment Peritonectomy: The Kurashiki Method." J Minim Invasive Gynecol. 2021;28(2):170-171. doi:10.1016/j.jmig.2020.05.028

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27. Vesale E, Roman H, Moawad G, et al. "Voiding Dysfunction after Colorectal Surgery for Endometriosis: A Systematic Review and Meta-analysis." J Minim Invasive Gynecol. 2020;27(7):1490-1502.e3. doi:10.1016/j.jmig.2020.07.019

28. Imboden S, Bollinger Y, Härmä K, et al. "Predictive Factors for Voiding Dysfunction after Surgery for Deep Infiltrating Endometriosis." J Minim Invasive Gynecol. 2021;28(8):1544-1551. doi:10.1016/j.jmig.2021.01.009

29. Azaïs H, Rubod C, Ghoneim T, et al. "Persistent Urinary Retention after Surgery for Deep Infiltrating Endometriosis: A Multi-center Series of 16 Cases." Arch Gynecol Obstet. 2015;291(6):1333-1339. doi:10.1007/s00404-014-3588-7

30. Burghaus S, Schäfer SD, Bär KJ, et al. "Diagnosis and Therapy of Endometriosis. Guideline of the DGGG, OEGGG and SGGG (S2k-Level, AWMF Registry No. 015/045, April 2025)." Geburtshilfe Frauenheilkd. 2026;86(2):133-188. doi:10.1055/a-2760-4867

31. Madar A, Crestani A, Eraud P, et al. "Voiding dysfunction after surgery for colorectal deep infiltrating endometriosis: an updated systematic review and meta-analysis." Updates Surg. 2025;77(3):739-748. doi:10.1007/s13304-025-02124-1

32. Kalra R, McDonnell R, Stewart F, Hart RJ, Hickey M, Farquhar C. "Excisional surgery versus ablative surgery for ovarian endometrioma." Cochrane Database Syst Rev. 2024;11(11):CD004992. doi:10.1002/14651858.CD004992.pub4

33. Cooper KG, Bhattacharya S, Daniels JP, et al. "Long acting progestogens versus combined oral contraceptive pill for preventing recurrence of endometriosis related pain: the PRE-EMPT pragmatic, parallel group, open label, randomised controlled trial." BMJ. 2024;385:e079006. doi:10.1136/bmj-2023-079006