Postmenopausal Bladder Endometriosis Without Exogenous Estrogen: a case report and literature review

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This paper reports a rare case of postmenopausal bladder endometriosis in a 59-year-old woman who was 6 years postmenopausal, had a normal BMI, and had no history of exogenous estrogen or hormone replacement therapy. Using symptom evaluation plus transvaginal ultrasound and pelvic CT, the authors identified an anterior uterine–posterior bladder wall lesion and confirmed the diagnosis after laparoscopic partial cystectomy with total hysterectomy and bilateral salpingo-oophorectomy, with histopathology showing endometrial glands/stroma in the bladder and weak estrogen/progesterone receptor positivity. The authors propose that coexisting hepatitis B-related cirrhosis (impaired estrogen metabolism) and type 2 diabetes (chronic inflammation) may sustain a pro-inflammatory environment that enables local estrogen activity, while explicitly acknowledging that conclusions are limited by the nature of a single case. This paper is centrally about endometriosis — specifically postmenopausal bladder endometriosis without exogenous estrogen and with proposed systemic factors supporting lesion persistence.

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Abstract Background Endometriosis is a common estrogen-dependent disorder that typically affects women of reproductive age and generally resolves following menopause. This report describes a rare case of postmenopausal bladder endometriosis occurring in a woman with a normal body mass index and no history of exogenous estrogen use. Case presentation : A postmenopausal woman with a normal body mass index and no history of estrogen replacement therapy presented with dysuria. Clinical examination and imaging suggested bladder endometriosis. The patient underwent laparoscopic partial cystectomy with total hysterectomy and bilateral salpingo-oophorectomy. Postoperative histopathology confirmed the diagnosis of endometriosis. Conclusions This case demonstrates that BE can occur in postmenopausal women in the absence of exogenous oestrogen or obesity. The coexistence of liver cirrhosis, associated with impaired oestrogen metabolism, and diabetes, characterized by chronic inflammation, may synergistically contribute to a pro-inflammatory microenvironment that sustains local oestrogen activity, enabling lesion persistence. Clinicians should consider such systemic factors in non-obese postmenopausal women presenting with symptoms suggestive of endometriosis.
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Postmenopausal Bladder Endometriosis Without Exogenous Estrogen: a case report and literature review | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Postmenopausal Bladder Endometriosis Without Exogenous Estrogen: a case report and literature review Namei Wu, Yuxuan He, Yazhuo Jia, Guoyun Wang This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9091288/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 23 You are reading this latest preprint version Abstract Background Endometriosis is a common estrogen-dependent disorder that typically affects women of reproductive age and generally resolves following menopause. This report describes a rare case of postmenopausal bladder endometriosis occurring in a woman with a normal body mass index and no history of exogenous estrogen use. Case presentation : A postmenopausal woman with a normal body mass index and no history of estrogen replacement therapy presented with dysuria. Clinical examination and imaging suggested bladder endometriosis. The patient underwent laparoscopic partial cystectomy with total hysterectomy and bilateral salpingo-oophorectomy. Postoperative histopathology confirmed the diagnosis of endometriosis. Conclusions This case demonstrates that BE can occur in postmenopausal women in the absence of exogenous oestrogen or obesity. The coexistence of liver cirrhosis, associated with impaired oestrogen metabolism, and diabetes, characterized by chronic inflammation, may synergistically contribute to a pro-inflammatory microenvironment that sustains local oestrogen activity, enabling lesion persistence. Clinicians should consider such systemic factors in non-obese postmenopausal women presenting with symptoms suggestive of endometriosis. Postmenopausal Endometriosis Urinary bladder Liver cirrhosis Diabetes mellitus Case report Figures Figure 1 Figure 2 Figure 3 Figure 4 Introduction Bladder endometriosis (BE), defined as the presence of ectopic endometrial glands and stroma infiltrating the detrusor muscle, is an uncommon yet clinically significant subtype of deep infiltrating endometriosis (DIE). 1 , 2 While DIE affecting the urinary tract accounts for approximately 1% of all endometriosis cases, BE is the most prevalent form (70–85%), followed by ureteral involvement. 2 , 3 The pathophysiology of BE remains incompletely elucidated, with prevailing theories including coelomic metaplasia, lymphatic/vascular dissemination, and iatrogenic implantation; however, the most widely accepted mechanism involves retrograde menstruation of viable endometrial cells with subsequent invasion and proliferation within the bladder wall, often associated with adhesions from anterior DIE. 4 – 6 Postmenopausal endometriosis, affecting 2–5% of postmenopausal women, has been described predominantly in case reports, with a paucity of large-scale studies. 7 Endometriotic lesions persist and progress within a systemic low-oestrogen environment through local oestrogen synthesis enabled by enzymes such as aromatase, 17β-hydroxysteroid dehydrogenase, and steroidogenic acute regulatory protein within the lesion microenvironment. 7 , 8 Case presentation A 59-year-old woman (6 years postmenopausal) presented with a five-day history of dysuria reporting dull, intermittent, lower abdominal pain. She denied having haematuria or fever and had never received hormone replacement therapy. Her body mass index (BMI) was 23.2 kg/m². Her menstrual history was notable for menarche at age 14, natural menopause at age 53, and regular cycles (occurring every 27 days with a 5-day duration) prior to menopause; her obstetric history included two spontaneous vaginal deliveries and no miscarriages (gravida 2, para 2), and she reported a history of tolerable dysmenorrhea. She had a seven-year history of type 2 diabetes mellitus with suboptimal glycaemic control (highest recorded postprandial glucose level, 13 mmol/L), managed without pharmacotherapy. Her gynaecological history included intrauterine device (IUD) retention for > 20 years, and bilateral tubal ligation performed 10 years before presentation. The patient had a long-standing history of hepatitis B-related cirrhosis. Laboratory tests revealed significantly elevated liver enzymes, with aspartate aminotransferase (AST) at 122 U/L and alanine aminotransferase (ALT) at 189 U/L, accompanied by a mildly reduced serum albumin level of 35 g/L. Serum hormonal assays revealed the following: luteinizing hormone, 23.3 mIU/mL (postmenopausal reference: 14.4–62.2 mIU/mL); follicle-stimulating hormone, 45.9 (36.6–168.8) mIU/mL; oestradiol 5.61 (< 20) pg/mL; progesterone, 0.06 (< 1) ng/mL; and anti-Müllerian hormone < 0.02 ng/mL. Serum hormone levels confirmed postmenopausal status. Urine occult blood 0.03 mg/dL Gynecologic examination revealed a normal vulva and patent vagina. A tender mass approximately 2 cm in size with limited mobility was palpated in the anterior fornix. The uterus and bilateral adnexa were unremarkable.Transvaginal ultrasonography revealed a hypoechoic nodule(4.1×3.5×1.9cm) between the anterior uterine and posterior bladder walls, suggestive of DIE(Fig. 1 ). A hypoechoic nodule (4.1×3.5×1.9 cm) with indistinct borders and irregular morphology is observed between the anterior uterine wall and the posterior bladder wall, suggestive of deep infiltrating endometriosis. The findings also included a postmenopausal uterus and IUD. Abdominal computed tomography revealed normal excretion and no upper urinary tract dilatation. The bladder was adequately filled, but the posterior wall appeared irregular. Pelvic computed tomography (plain and contrast) revealed a morphologically normal uterus with heterogeneous myometrial density and an IUD in situ. The anterior uterine and posterior bladder walls were indistinct, with the latter showing slight thickening, local irregularity, and mild heterogeneous contrast enhancement(Fig. 2 ). Non-contrast CT demonstrates an indistinct interface between the anterior uterine wall and the posterior bladder wall, with mild thickening of the latter. The uterine morphology is grossly normal, and an intrauterine device is visible in the uterine cavity. The patient underwent laparoscopic surgery including hysterectomy, bilateral salpingo-oophorectomy, and excision of the endometriotic bladder lesion with concurrent cystoscopic placement of double-J ureteral stents — under general anaesthesia(Fig. 3 ). Dense adhesions are present between the posterior bladder wall and the anterior uterine wall. The lesion appears as a grayish-white, firm mass within the bladder wall, with ill-defined borders and no intact capsule. The postoperative regimen comprised antibiotic prophylaxis; haemostatic agents; continuous catheter drainage with bladder irrigation; insulin for diabetes management; and hepatoprotective and symptomatic support. Histopathological examination revealed endometrial stroma-like tissue with focal foamy histiocyte infiltration in the bladder lesion, consistent with endometriosis, whereas the uterus and adnexa exhibited an atrophic endometrium, chronic cervicitis, and absence of pathological abnormalities. Immunohistochemistry demonstrated weak positivity for the oestrogen and progesterone receptors(Fig. 4 ). (a) Hematoxylin-eosin staining shows typical endometrial glands and stroma within the bladder muscularis propria, consistent with endometriosis. (b) Partial bladder epithelium is observed adjacent to the lesion. (c) Immunohistochemical staining reveals weak positive expression of estrogen receptor in the glandular epithelial cells. (d) Immunohistochemical staining shows weak positive expression of progesterone receptor in the glandular epithelial cells. Follow-up bladder ultrasonography on postoperative day seven demonstrated suboptimal bladder distension with a regular wall contour and an indwelling catheter showing the inflated balloon. The catheter was removed after three weeks of continuous drainage. Vaginal cuff examination one month postoperatively revealed complete healing. Discussion and conclusions This case report describes a rare presentation of postmenopausal bladder endometriosis. The case is notable because the patient had no history of exogenous oestrogen therapy and maintained a normal body mass index yet had comorbid viral hepatitis-induced mild liver cirrhosis and poorly controlled type 2 diabetes. This clinical profile raises important pathophysiological questions regarding the mechanisms sustaining endometriosis after menopause. Mantilidewi et al. (2025) reported a similar case of postmenopausal endometriosis in a patient who did not receive prior hormone replacement therapy. 9 In contrast to our patient, the patient described in that study was obese. While postmenopausal ovaries cease oestrogen production, adipose tissue can convert androgens to oestrogen via aromatization, which may contribute to the pathogenesis in such cases. 9 , 10 A normal BMI (23.2 kg/m²) ruled out a substantial pathogenic contribution from adipose-derived oestrogen, in contrast to obesity-related cases wherein adipocyte aromatization sustains the ectopic endometrium. Table 1 summarizes the clinical characteristics of previously reported cases of postmenopausal bladder endometriosis. Case Age Years since menopause Symptoms Urologic involvement HRT use BMI (kg/m²) Ref Vorstman 64 NR Painless hematuria Posterior bladder wall No NR [10] Stewart 65 NR Intermittent painless hematuria Bladder dome No NR [11] Habuchi 68 15 Persistent pyuria Bladder dome No NR [12] Maeda 65 NR Intermittent painless hematuria Posterior bladder wall Yes NR [13] Garavan 53 2 Intermittent painful hematuria Posterior bladder wall + ovary No NR [14] Abbreviations: HRT, hormone replacement therapy; NR, not reported; TUR, transurethral resection. To date, only a few case reports have been documented in the literature 10-14 (Table1),with patient ages ranging from 53 to 68 years. Among these known cases, patients typically presented with hematuria or pyuria, with the bladder dome or posterior wall being the most common sites of involvement. Evidence suggests that postmenopausal endometriosis does not completely regress, with over 60% of patients remaining symptomatic 15 , indicating that local estrogen synthesis may play a promoting role in lesion recurrence or growth. 16 The clinical presentation of postmenopausal bladder endometriosis is atypical. In this case, the patient presented with dysuria as the initial symptom, which increased the risk of misdiagnosis. Therefore, for nonspecific lower urinary tract symptoms occurring in postmenopausal women, differential diagnosis should include conditions such as urothelial carcinoma, interstitial cystitis, cystitis glandularis, urinary tract tuberculosis, and pelvic lipomatosis. Cystoscopic biopsy and histopathological examination are essential for definitive diagnosis. 17,18 Transvaginal ultrasonography is a critical screening tool for DIE. 2,19 Computed tomography urography provides supplementary evaluation of renal function and ureteral involvement. Although cystoscopy enables direct visualization and biopsy, it often fails to detect microscopic lesions. 18 Histopathological examination combined with immunohistochemistry thus constituting the definitive diagnostic approach. 16 A multidisciplinary collaboration (urology, gynaecology, radiology, and pathology) is essential for accurate diagnosis, optimal surgical planning, and effective management. In this case of postmenopausal bladder endometriosis, we hypothesize that the co-existing conditions—mild hepatic impairment secondary to cirrhosis and metabolic dysregulation associated with type 2 diabetes—may synergistically contribute to a state of chronic inflammation. 20 This inflammatory state may disrupt local oestrogen metabolic homeostasis in the postmenopausal setting, thereby creating a permissive microenvironment for the persistence of ectopic endometrial lesions. For postmenopausal women presenting with symptoms suggestive of endometriosis, particularly those who are non-obese, clinical evaluation should extend beyond the gynaecological domain. A comprehensive assessment that integrates systemic comorbidities and their interaction with local oestrogen metabolism is therefore warranted. For non-obese postmenopausal women presenting with unexplained lower urinary tract symptoms, clinicians should maintain a high index of suspicion for endometriosis and conduct a comprehensive evaluation that includes assessment of systemic comorbidities—particularly those affecting hepatic function and inflammatory status—which may contribute to local estrogen bioavailability and lesion maintenance. Abbreviations BE Bladder endometriosis BMI Body mass index DIE Deep infiltrating endometriosis IUD Intrauterine device ER Oestrogen receptor PR Progesterone receptor Declarations Acknowledgements Not applicable. Contribution to authorship Namei Wu and Yuxuan He: study design, execution, analysis, manuscript drafting and critical discussion. Yazhuo Jia: study design, manuscript drafting and critical discussion. Guoyun Wang: study design, execution, analysis, manuscript drafting and critical discussion. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Availability of data and materials All data generated or analysed during this study are included in this published article. Ethics approval and consent to participate This study was approved by the Ethics Committee of Shandong Provincial Hospital Affiliated to Shandong First Medical University. Written informed consent was obtained from the patient for participation. Consent for publication Written informed consent was obtained from the patient for publication of this case report. Competing interests The authors declare that they have no competing interests. References Giudice LC, Kao LC, Endometriosis. Lancet. 2004;364:1789–99. Koninckx PR, Ussia A, Adamyan L, Wattiez A, Donnez J. Deep endometriosis: definition, diagnosis, and treatment. Fertil Steril. 2012;98:564–71. Berlanda N, Vercellini P, Carmignani L, Aimi G, Amicarelli F, Fedele L. Ureteral and vesical endometriosis. Two different clinical entities sharing the same pathogenesis. Obstet Gynecol Surv. 2009;64:830–42. Vercellini P, Frontino G, Pisacreta A, De Giorgi O, Cattaneo M, Crosignani PG. The pathogenesis of bladder detrusor endometriosis. Am J Obstet Gynecol. 2002;187:538–42. Fedele L, Piazzola E, Raffaelli R, Bianchi S. Bladder endometriosis: deep infiltrating endometriosis or adenomyosis? Fertil Steril. 1998;69:972–5. Pinkert TC, Catlow CE, Straus R. Endometriosis of the urinary bladder in a man with prostatic carcinoma. Cancer. 1979;43:1562–7. Ladanyi C, Boyd S, Sticco P, Mohling S. Postmenopausal endometriosis, where are we now? Curr Opin Obstet Gynecol. 2019;31:267–78. Hemsell DL, Grodin JM, Brenner PF, Siiteri PK, MacDonald PC. Plasma precursors of estrogen. II. Correlation of the extent of conversion of plasma androstenedione to estrone with age. J Clin Endocrinol Metab. 1974;38:476–9. Mantilidewi KI, Ridwan S, Kurniadi A, Harsono AB. Postmenopausal endometriosis. BMJ Case Rep. 2025;18:e260892. Vorstman B, Lynne C, Politano VA. Postmenopausal vesical endometriosis. Urology. 1983;22:540–2. Stewart WW, Ireland GW. Vesical endometriosis in a postmenopausal woman: a case report. J Urol. 1977;118(3):480–1. Habuchi T, Okagaki T, Miyakawa M. Endometriosis of bladder after menopause. J Urol. 1991;145(2):361–3. Maeda T, Uchida Y, Nakajima F. Vesical endometriosis following the menopause. Int Urogynecol J Pelvic Floor Dysfunct. 2009;20(12):1515–7. Garavan F, Grainger R, Jeffers M. Endometrioid carcinoma of the urinary bladder complicating vesical Mullerianosis: a case report and review of the literature. Virchows Arch. 2004;444(6):587–9. Haas D, Wurm P, Schimetta W, Schabetsberger K, Shamiyeh A, Oppelt P, et al. Endometriosis patients in the postmenopausal period: pre- and postmenopausal factors influencing postmenopausal health. Biomed Res Int. 2014;2014:746705. Bendon CL, Becker CM. Potential mechanisms of postmenopausal endometriosis. Maturitas. 2012;72:214–9. Habiba M, Brosens I, Benagiano G, Müllerianosis. Endocervicosis, and Endosalpingiosis of the Urinary Tract: A Literature Review. Reproductive sciences (Thousand Oaks, Calif). 2018;25(12):1607-18. Leone Roberti Maggiore U, Ferrero S, Candiani M, Somigliana E, Viganò P, Vercellini P. Bladder endometriosis: a systematic review of pathogenesis, diagnosis, treatment, impact on fertility, and risk of malignant transformation. Eur Urol. 2017;71:790–807. Exacoustos C, Malzoni M, Di Giovanni A, Lazzeri L, Tosti C, Petraglia F et al. Ultrasound mapping system for the surgical management of deep infiltrating endometriosis. Fertil Steril. 2014;102:143 – 50.e2. Monteiro R, Teixeira D, Calhau C. Estrogen signaling in metabolic inflammation. Mediators Inflamm. 2014;2014:615917. Additional Declarations No competing interests reported. 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07:26:33","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-9091288/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9091288/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":106068879,"identity":"baf009b8-f85c-434a-b75c-e408787e3e3a","added_by":"auto","created_at":"2026-04-03 06:21:15","extension":"jpeg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":31992,"visible":true,"origin":"","legend":"\u003cp\u003eTransvaginal ultrasonography of postmenopausal bladder endometriosis.\u003c/p\u003e","description":"","filename":"image1.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-9091288/v1/468ebeae6d31dd097c272da8.jpeg"},{"id":106068880,"identity":"1be67dcc-fb35-4591-9435-a05423d20245","added_by":"auto","created_at":"2026-04-03 06:21:15","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":1324391,"visible":true,"origin":"","legend":"\u003cp\u003eContrast-enhanced pelvic CT showing posterior bladder wall thickening and abnormal enhancement.\u003c/p\u003e","description":"","filename":"image2.png","url":"https://assets-eu.researchsquare.com/files/rs-9091288/v1/6fe2694619859b1722b06d22.png"},{"id":106068881,"identity":"87411c15-a973-4e74-afb4-8303884ccbe6","added_by":"auto","created_at":"2026-04-03 06:21:15","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":6750845,"visible":true,"origin":"","legend":"\u003cp\u003eLaparoscopic view of the bladder endometriotic lesion.\u003c/p\u003e","description":"","filename":"image3.png","url":"https://assets-eu.researchsquare.com/files/rs-9091288/v1/aa8f53037ab7d29cf8a1ade5.png"},{"id":106094477,"identity":"55d15aed-e192-4577-bc9a-a6de73a147b0","added_by":"auto","created_at":"2026-04-03 11:42:41","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":5013013,"visible":true,"origin":"","legend":"\u003cp\u003eHistopathological and immunohistochemical features of the bladder lesion.\u003c/p\u003e","description":"","filename":"image4.png","url":"https://assets-eu.researchsquare.com/files/rs-9091288/v1/4cf4c78c49d1fba66d79612f.png"},{"id":106095884,"identity":"4bc38ee0-af16-4c84-9fcf-4513a19d14ef","added_by":"auto","created_at":"2026-04-03 11:51:30","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":12623252,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9091288/v1/708634a1-4a51-450f-a559-b8cef8d196ce.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"\u003cp\u003ePostmenopausal Bladder Endometriosis Without Exogenous Estrogen: a case report and literature review\u003c/p\u003e","fulltext":[{"header":"Introduction","content":"\u003cp\u003eBladder endometriosis (BE), defined as the presence of ectopic endometrial glands and stroma infiltrating the detrusor muscle, is an uncommon yet clinically significant subtype of deep infiltrating endometriosis (DIE).\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e,\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e While DIE affecting the urinary tract accounts for approximately 1% of all endometriosis cases, BE is the most prevalent form (70\u0026ndash;85%), followed by ureteral involvement.\u003csup\u003e\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e,\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u003c/sup\u003e The pathophysiology of BE remains incompletely elucidated, with prevailing theories including coelomic metaplasia, lymphatic/vascular dissemination, and iatrogenic implantation; however, the most widely accepted mechanism involves retrograde menstruation of viable endometrial cells with subsequent invasion and proliferation within the bladder wall, often associated with adhesions from anterior DIE.\u003csup\u003e\u003cspan additionalcitationids=\"CR5\" citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003ePostmenopausal endometriosis, affecting 2\u0026ndash;5% of postmenopausal women, has been described predominantly in case reports, with a paucity of large-scale studies.\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e Endometriotic lesions persist and progress within a systemic low-oestrogen environment through local oestrogen synthesis enabled by enzymes such as aromatase, 17β-hydroxysteroid dehydrogenase, and steroidogenic acute regulatory protein within the lesion microenvironment.\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e,\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003eA 59-year-old woman (6 years postmenopausal) presented with a five-day history of dysuria reporting dull, intermittent, lower abdominal pain. She denied having haematuria or fever and had never received hormone replacement therapy. Her body mass index (BMI) was 23.2 kg/m\u0026sup2;.\u003c/p\u003e \u003cp\u003eHer menstrual history was notable for menarche at age 14, natural menopause at age 53, and regular cycles (occurring every 27 days with a 5-day duration) prior to menopause; her obstetric history included two spontaneous vaginal deliveries and no miscarriages (gravida 2, para 2), and she reported a history of tolerable dysmenorrhea.\u003c/p\u003e \u003cp\u003eShe had a seven-year history of type 2 diabetes mellitus with suboptimal glycaemic control (highest recorded postprandial glucose level, 13 mmol/L), managed without pharmacotherapy. Her gynaecological history included intrauterine device (IUD) retention for \u0026gt;\u0026thinsp;20 years, and bilateral tubal ligation performed 10 years before presentation. The patient had a long-standing history of hepatitis B-related cirrhosis. Laboratory tests revealed significantly elevated liver enzymes, with aspartate aminotransferase (AST) at 122 U/L and alanine aminotransferase (ALT) at 189 U/L, accompanied by a mildly reduced serum albumin level of 35 g/L.\u003c/p\u003e \u003cp\u003eSerum hormonal assays revealed the following: luteinizing hormone, 23.3 mIU/mL (postmenopausal reference: 14.4\u0026ndash;62.2 mIU/mL); follicle-stimulating hormone, 45.9 (36.6\u0026ndash;168.8) mIU/mL; oestradiol 5.61 (\u0026lt;\u0026thinsp;20) pg/mL; progesterone, 0.06 (\u0026lt;\u0026thinsp;1) ng/mL; and anti-M\u0026uuml;llerian hormone\u0026thinsp;\u0026lt;\u0026thinsp;0.02 ng/mL. Serum hormone levels confirmed postmenopausal status. Urine occult blood 0.03 mg/dL\u003c/p\u003e \u003cp\u003eGynecologic examination revealed a normal vulva and patent vagina. A tender mass approximately 2 cm in size with limited mobility was palpated in the anterior fornix. The uterus and bilateral adnexa were unremarkable.Transvaginal ultrasonography revealed a hypoechoic nodule(4.1\u0026times;3.5\u0026times;1.9cm) between the anterior uterine and posterior bladder walls, suggestive of DIE(Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eA hypoechoic nodule (4.1\u0026times;3.5\u0026times;1.9 cm) with indistinct borders and irregular morphology is observed between the anterior uterine wall and the posterior bladder wall, suggestive of deep infiltrating endometriosis.\u003c/p\u003e \u003cp\u003eThe findings also included a postmenopausal uterus and IUD. Abdominal computed tomography revealed normal excretion and no upper urinary tract dilatation. The bladder was adequately filled, but the posterior wall appeared irregular. Pelvic computed tomography (plain and contrast) revealed a morphologically normal uterus with heterogeneous myometrial density and an IUD in situ. The anterior uterine and posterior bladder walls were indistinct, with the latter showing slight thickening, local irregularity, and mild heterogeneous contrast enhancement(Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eNon-contrast CT demonstrates an indistinct interface between the anterior uterine wall and the posterior bladder wall, with mild thickening of the latter. The uterine morphology is grossly normal, and an intrauterine device is visible in the uterine cavity.\u003c/p\u003e \u003cp\u003eThe patient underwent laparoscopic surgery including hysterectomy, bilateral salpingo-oophorectomy, and excision of the endometriotic bladder lesion with concurrent cystoscopic placement of double-J ureteral stents \u0026mdash; under general anaesthesia(Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eDense adhesions are present between the posterior bladder wall and the anterior uterine wall. The lesion appears as a grayish-white, firm mass within the bladder wall, with ill-defined borders and no intact capsule.\u003c/p\u003e \u003cp\u003eThe postoperative regimen comprised antibiotic prophylaxis; haemostatic agents; continuous catheter drainage with bladder irrigation; insulin for diabetes management; and hepatoprotective and symptomatic support. Histopathological examination revealed endometrial stroma-like tissue with focal foamy histiocyte infiltration in the bladder lesion, consistent with endometriosis, whereas the uterus and adnexa exhibited an atrophic endometrium, chronic cervicitis, and absence of pathological abnormalities. Immunohistochemistry demonstrated weak positivity for the oestrogen and progesterone receptors(Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e(a) Hematoxylin-eosin staining shows typical endometrial glands and stroma within the bladder muscularis propria, consistent with endometriosis. (b) Partial bladder epithelium is observed adjacent to the lesion. (c) Immunohistochemical staining reveals weak positive expression of estrogen receptor in the glandular epithelial cells. (d) Immunohistochemical staining shows weak positive expression of progesterone receptor in the glandular epithelial cells.\u003c/p\u003e \u003cp\u003eFollow-up bladder ultrasonography on postoperative day seven demonstrated suboptimal bladder distension with a regular wall contour and an indwelling catheter showing the inflated balloon. The catheter was removed after three weeks of continuous drainage. Vaginal cuff examination one month postoperatively revealed complete healing.\u003c/p\u003e "},{"header":"Discussion and conclusions","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003cp\u003eThis case report describes a rare presentation of postmenopausal bladder endometriosis. The case is notable because the patient had no history of exogenous oestrogen therapy and maintained a normal body mass index yet had comorbid viral hepatitis-induced mild liver cirrhosis and poorly controlled type 2 diabetes. This clinical profile raises important pathophysiological questions regarding the mechanisms sustaining endometriosis after menopause.\u003c/p\u003e \u003cp\u003eMantilidewi et al. (2025) reported a similar case of postmenopausal endometriosis in a patient who did not receive prior hormone replacement therapy.\u003csup\u003e\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e\u003c/sup\u003e In contrast to our patient, the patient described in that study was obese. While postmenopausal ovaries cease oestrogen production, adipose tissue can convert androgens to oestrogen via aromatization, which may contribute to the pathogenesis in such cases.\u003csup\u003e\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e,\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u003c/sup\u003e A normal BMI (23.2 kg/m\u0026sup2;) ruled out a substantial pathogenic contribution from adipose-derived oestrogen, in contrast to obesity-related cases wherein adipocyte aromatization sustains the ectopic endometrium.\u003c/p\u003e \u003c/div\u003e\n\u003cp\u003eTable 1 summarizes the clinical characteristics of previously reported cases of postmenopausal bladder endometriosis.\u0026nbsp;\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"3\" cellpadding=\"0\"\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 58px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCase\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 26px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 73px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eYears since menopause\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 141px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eSymptoms\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 105px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eUrologic involvement\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 49px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eHRT use\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 55px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eBMI (kg/m\u0026sup2;)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 28px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eRef\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 58px;\"\u003e\n \u003cp\u003eVorstman\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 26px;\"\u003e\n \u003cp\u003e64\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 73px;\"\u003e\n \u003cp\u003eNR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 141px;\"\u003e\n \u003cp\u003ePainless hematuria\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 105px;\"\u003e\n \u003cp\u003ePosterior bladder wall\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 49px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 55px;\"\u003e\n \u003cp\u003eNR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 28px;\"\u003e\n \u003cp\u003e[10]\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 58px;\"\u003e\n \u003cp\u003eStewart\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 26px;\"\u003e\n \u003cp\u003e65\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 73px;\"\u003e\n \u003cp\u003eNR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 141px;\"\u003e\n \u003cp\u003eIntermittent painless hematuria\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 105px;\"\u003e\n \u003cp\u003eBladder dome\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 49px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 55px;\"\u003e\n \u003cp\u003eNR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 28px;\"\u003e\n \u003cp\u003e[11]\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 58px;\"\u003e\n \u003cp\u003eHabuchi\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 26px;\"\u003e\n \u003cp\u003e68\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 73px;\"\u003e\n \u003cp\u003e15\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 141px;\"\u003e\n \u003cp\u003ePersistent pyuria\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 105px;\"\u003e\n \u003cp\u003eBladder dome\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 49px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 55px;\"\u003e\n \u003cp\u003eNR\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 28px;\"\u003e\n \u003cp\u003e[12]\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 58px;\"\u003e\n \u003cp\u003eMaeda\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 26px;\"\u003e\n \u003cp\u003e65\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 73px;\"\u003e\n \u003cp\u003eNR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 141px;\"\u003e\n \u003cp\u003eIntermittent painless hematuria\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 105px;\"\u003e\n \u003cp\u003ePosterior bladder wall\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 49px;\"\u003e\n \u003cp\u003eYes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 55px;\"\u003e\n \u003cp\u003eNR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 28px;\"\u003e\n \u003cp\u003e[13]\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 58px;\"\u003e\n \u003cp\u003eGaravan\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 26px;\"\u003e\n \u003cp\u003e53\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 73px;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 141px;\"\u003e\n \u003cp\u003eIntermittent painful hematuria\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 105px;\"\u003e\n \u003cp\u003ePosterior bladder wall + ovary\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 49px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 55px;\"\u003e\n \u003cp\u003eNR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 28px;\"\u003e\n \u003cp\u003e[14]\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cstrong\u003eAbbreviations:\u003c/strong\u003e HRT, hormone replacement therapy; NR, not reported; TUR, transurethral resection.\u003c/p\u003e\n\u003cp\u003eTo date, only a few case reports have been documented in the literature \u003csup\u003e10-14\u003c/sup\u003e(Table1),with patient ages ranging from 53 to 68 years. Among these known cases, patients typically presented with hematuria or pyuria, with the bladder dome or posterior wall being the most common sites of involvement. Evidence suggests that postmenopausal endometriosis does not completely regress, with over 60% of patients remaining symptomatic \u003csup\u003e15\u003c/sup\u003e, indicating that local estrogen synthesis may play a promoting role in lesion recurrence or growth. \u003csup\u003e16\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eThe clinical presentation of postmenopausal bladder endometriosis is atypical. In this case, the patient presented with dysuria as the initial symptom, which increased the risk of misdiagnosis. Therefore, for nonspecific lower urinary tract symptoms occurring in postmenopausal women, differential diagnosis should include conditions such as urothelial carcinoma, interstitial cystitis, cystitis glandularis, urinary tract tuberculosis, and pelvic lipomatosis. Cystoscopic biopsy and histopathological examination are essential for definitive diagnosis. \u003csup\u003e17,18\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eTransvaginal ultrasonography is a critical screening tool for DIE.\u003csup\u003e2,19\u003c/sup\u003e Computed tomography urography provides supplementary evaluation of renal function and ureteral involvement. Although cystoscopy enables direct visualization and biopsy, it often fails to detect microscopic lesions.\u003csup\u003e18\u003c/sup\u003e Histopathological examination combined with immunohistochemistry thus constituting the definitive diagnostic approach.\u003csup\u003e16\u003c/sup\u003e A multidisciplinary collaboration (urology, gynaecology, radiology, and pathology) is essential for accurate diagnosis, optimal surgical planning, and effective management.\u003c/p\u003e\n\u003cp\u003eIn this case of postmenopausal bladder endometriosis, we hypothesize that the co-existing conditions\u0026mdash;mild hepatic impairment secondary to cirrhosis and metabolic dysregulation associated with type 2 diabetes\u0026mdash;may synergistically contribute to a state of chronic inflammation.\u003csup\u003e20\u0026nbsp;\u003c/sup\u003eThis inflammatory state may disrupt local oestrogen metabolic homeostasis in the postmenopausal setting, thereby creating a permissive microenvironment for the persistence of ectopic endometrial lesions.\u003c/p\u003e\n\u003cp\u003eFor postmenopausal women presenting with symptoms suggestive of endometriosis, particularly those who are non-obese, clinical evaluation should extend beyond the gynaecological domain. A comprehensive assessment that integrates systemic comorbidities and their interaction with local oestrogen metabolism is therefore warranted. For non-obese postmenopausal women presenting with unexplained lower urinary tract symptoms, clinicians should maintain a high index of suspicion for endometriosis and conduct a comprehensive evaluation that includes assessment of systemic comorbidities\u0026mdash;particularly those affecting hepatic function and inflammatory status\u0026mdash;which may contribute to local estrogen bioavailability and lesion maintenance.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eBE\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eBladder endometriosis\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eBMI\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eBody mass index\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eDIE\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eDeep infiltrating endometriosis\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eIUD\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eIntrauterine device\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eER\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eOestrogen receptor\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003ePR\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eProgesterone receptor\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003eAcknowledgements\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003eContribution to authorship\u003c/p\u003e\n\u003cp\u003eNamei Wu and Yuxuan He: study design, execution, analysis, manuscript drafting and critical discussion.\u003c/p\u003e\n\u003cp\u003eYazhuo Jia: study design, manuscript drafting and critical discussion.\u003c/p\u003e\n\u003cp\u003eGuoyun Wang: study design, execution, analysis, manuscript drafting and critical discussion.\u003c/p\u003e\n\u003cp\u003eFunding\u003c/p\u003e\n\u003cp\u003eThis research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.\u003c/p\u003e\n\u003cp\u003eAvailability of data and materials\u003c/p\u003e\n\u003cp\u003eAll data generated or analysed during this study are included in this published article.\u003c/p\u003e\n\u003cp\u003eEthics approval and consent to participate\u003c/p\u003e\n\u003cp\u003eThis study was approved by the Ethics Committee of Shandong Provincial Hospital Affiliated to Shandong First Medical University. Written informed consent was obtained from the patient for participation.\u003c/p\u003e\n\u003cp\u003eConsent for publication\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for publication of this case report.\u003c/p\u003e\n\u003cp\u003eCompeting interests\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eGiudice LC, Kao LC, Endometriosis. Lancet. 2004;364:1789\u0026ndash;99.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKoninckx PR, Ussia A, Adamyan L, Wattiez A, Donnez J. Deep endometriosis: definition, diagnosis, and treatment. Fertil Steril. 2012;98:564\u0026ndash;71.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBerlanda N, Vercellini P, Carmignani L, Aimi G, Amicarelli F, Fedele L. Ureteral and vesical endometriosis. Two different clinical entities sharing the same pathogenesis. Obstet Gynecol Surv. 2009;64:830\u0026ndash;42.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eVercellini P, Frontino G, Pisacreta A, De Giorgi O, Cattaneo M, Crosignani PG. The pathogenesis of bladder detrusor endometriosis. Am J Obstet Gynecol. 2002;187:538\u0026ndash;42.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFedele L, Piazzola E, Raffaelli R, Bianchi S. Bladder endometriosis: deep infiltrating endometriosis or adenomyosis? Fertil Steril. 1998;69:972\u0026ndash;5.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePinkert TC, Catlow CE, Straus R. Endometriosis of the urinary bladder in a man with prostatic carcinoma. Cancer. 1979;43:1562\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLadanyi C, Boyd S, Sticco P, Mohling S. Postmenopausal endometriosis, where are we now? Curr Opin Obstet Gynecol. 2019;31:267\u0026ndash;78.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHemsell DL, Grodin JM, Brenner PF, Siiteri PK, MacDonald PC. Plasma precursors of estrogen. II. Correlation of the extent of conversion of plasma androstenedione to estrone with age. J Clin Endocrinol Metab. 1974;38:476\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMantilidewi KI, Ridwan S, Kurniadi A, Harsono AB. Postmenopausal endometriosis. BMJ Case Rep. 2025;18:e260892.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eVorstman B, Lynne C, Politano VA. Postmenopausal vesical endometriosis. Urology. 1983;22:540\u0026ndash;2.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eStewart WW, Ireland GW. Vesical endometriosis in a postmenopausal woman: a case report. J Urol. 1977;118(3):480\u0026ndash;1.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHabuchi T, Okagaki T, Miyakawa M. Endometriosis of bladder after menopause. J Urol. 1991;145(2):361\u0026ndash;3.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMaeda T, Uchida Y, Nakajima F. Vesical endometriosis following the menopause. Int Urogynecol J Pelvic Floor Dysfunct. 2009;20(12):1515\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGaravan F, Grainger R, Jeffers M. Endometrioid carcinoma of the urinary bladder complicating vesical Mullerianosis: a case report and review of the literature. Virchows Arch. 2004;444(6):587\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHaas D, Wurm P, Schimetta W, Schabetsberger K, Shamiyeh A, Oppelt P, et al. Endometriosis patients in the postmenopausal period: pre- and postmenopausal factors influencing postmenopausal health. Biomed Res Int. 2014;2014:746705.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBendon CL, Becker CM. Potential mechanisms of postmenopausal endometriosis. Maturitas. 2012;72:214\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHabiba M, Brosens I, Benagiano G, M\u0026uuml;llerianosis. Endocervicosis, and Endosalpingiosis of the Urinary Tract: A Literature Review. Reproductive sciences (Thousand Oaks, Calif). 2018;25(12):1607-18.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLeone Roberti Maggiore U, Ferrero S, Candiani M, Somigliana E, Vigan\u0026ograve; P, Vercellini P. Bladder endometriosis: a systematic review of pathogenesis, diagnosis, treatment, impact on fertility, and risk of malignant transformation. Eur Urol. 2017;71:790\u0026ndash;807.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eExacoustos C, Malzoni M, Di Giovanni A, Lazzeri L, Tosti C, Petraglia F et al. Ultrasound mapping system for the surgical management of deep infiltrating endometriosis. Fertil Steril. 2014;102:143\u0026thinsp;\u0026ndash;\u0026thinsp;50.e2.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMonteiro R, Teixeira D, Calhau C. Estrogen signaling in metabolic inflammation. Mediators Inflamm. 2014;2014:615917.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-womens-health","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bmwh","sideBox":"Learn more about [BMC Women's Health](http://bmcwomenshealth.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bmwh/default.aspx","title":"BMC Women's Health","twitterHandle":"","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Postmenopausal, Endometriosis, Urinary bladder, Liver cirrhosis, Diabetes mellitus, Case report","lastPublishedDoi":"10.21203/rs.3.rs-9091288/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9091288/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eEndometriosis is a common estrogen-dependent disorder that typically affects women of reproductive age and generally resolves following menopause. This report describes a rare case of postmenopausal bladder endometriosis occurring in a woman with a normal body mass index and no history of exogenous estrogen use.\u003c/p\u003e\u003ch2\u003eCase presentation\u003c/h2\u003e \u003cp\u003e: A postmenopausal woman with a normal body mass index and no history of estrogen replacement therapy presented with dysuria. Clinical examination and imaging suggested bladder endometriosis. The patient underwent laparoscopic partial cystectomy with total hysterectomy and bilateral salpingo-oophorectomy. Postoperative histopathology confirmed the diagnosis of endometriosis.\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e \u003cp\u003eThis case demonstrates that BE can occur in postmenopausal women in the absence of exogenous oestrogen or obesity. The coexistence of liver cirrhosis, associated with impaired oestrogen metabolism, and diabetes, characterized by chronic inflammation, may synergistically contribute to a pro-inflammatory microenvironment that sustains local oestrogen activity, enabling lesion persistence. Clinicians should consider such systemic factors in non-obese postmenopausal women presenting with symptoms suggestive of endometriosis.\u003c/p\u003e","manuscriptTitle":"Postmenopausal Bladder Endometriosis Without Exogenous Estrogen: a case report and literature review","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-04-03 06:21:00","doi":"10.21203/rs.3.rs-9091288/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-04-06T06:51:13+00:00","index":"","fulltext":""},{"type":"reviewerAgreed","content":"265490206018701882001001618898478014237","date":"2026-04-04T15:52:27+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-04-02T17:17:55+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"71196991236171947235281221558854015553","date":"2026-04-01T11:51:10+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"331794782405015133479944709899963678129","date":"2026-03-31T21:18:12+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-31T19:26:39+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"83673714188312039195500831081528619998","date":"2026-03-31T19:20:42+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-31T18:34:00+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"235426439843961841885695326375164034793","date":"2026-03-31T17:59:16+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-31T15:59:53+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"115105396537189472878805300076540476778","date":"2026-03-31T15:56:29+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-31T13:57:08+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"45524546179194954236622856439433474031","date":"2026-03-31T13:30:40+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"80782830647046458786761624278885099410","date":"2026-03-31T11:28:16+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"60257320518576070824439417848383128331","date":"2026-03-31T08:55:31+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-30T06:12:16+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"215988311093430086071992885572142554704","date":"2026-03-30T04:33:47+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"95550991394957873920992753530638335526","date":"2026-03-29T13:36:09+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-03-29T11:33:17+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-03-18T15:01:52+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-03-16T06:57:17+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-03-16T06:57:06+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Women's Health","date":"2026-03-11T07:17:53+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-womens-health","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bmwh","sideBox":"Learn more about [BMC Women's Health](http://bmcwomenshealth.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bmwh/default.aspx","title":"BMC Women's Health","twitterHandle":"","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"601d8f87-7d23-425e-ba73-a10aa61fb4b6","owner":[],"postedDate":"April 3rd, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-05-04T07:40:27+00:00","versionOfRecord":[],"versionCreatedAt":"2026-04-03 06:21:00","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9091288","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9091288","identity":"rs-9091288","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}

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