Results
Sixteen observational studies involving 14,917 women were included. EP prevalence among women with AM ranged from 4.3% to 34.6% across 12 studies. AM prevalence among women with EPs ranged from 3.9% to 91.9% across 11 studies and showed substantially greater dispersion. Among seven studies reporting both directions, six yielded higher estimates for AM among women with EPs than for EP among women with AM. In hysteroscopic polypectomy cohorts, AM prevalence was 3.9– 14.5%, while hysterectomy-based estimates were more variable and the two highest values, 55.9% and 91.9%, arose from selected surgical or pathology-enriched populations. This asymmetry was consistent with denominator structure, surgical selection, and intensity of myometrial assessment.
Conclusion
AM and EPs are repeatedly identified together across diverse gynecological pathways, but the observed likelihood of identifying the alternative lesion is strongly pathway-dependent. Identification of one lesion should not end diagnostic consideration when symptoms, imaging findings, infertility, or treatment response remain incompletely explained. Current evidence supports targeted consideration of the alternative lesion, with further evaluation guided by symptoms and clinical pathway, rather than universal dual-pathology screening.
Keywords
adenomyosis, endometrial polyps, coexistence, prevalence, clinical pathway, systematic review
Introduction
Adenomyosis (AM) and endometrial polyps (EPs) are common benign uterine disorders encountered in overlapping clinical contexts, including abnormal uterine bleeding, infertility evaluation, pelvic pain, and peri- or postmenopausal assessment.1–5 AM is characterized by endometrial glands and stroma within the myometrium and is commonly associated with dysmenorrhoea, abnormal uterine bleeding, chronic pelvic pain, and reproductive difficulties.6–8 EPs are focal intracavitary lesions that may cause abnormal uterine bleeding, infertility, or postmenopausal bleeding or may remain asymptomatic.8,9 Despite arising in different anatomical compartments and typically being identified through different diagnostic pathways, AM and EPs may occur in the same patient and contribute to overlapping clinical presentations.10,11
The clinical challenge is not simply whether these lesions coexist, but whether identification of one lesion adequately explains the patient’s presentation. In women with established AM, persistent or disproportionate bleeding, infertility, or a suspected intracavitary abnormality may indicate an additional EP. Conversely, in women with EPs, substantial dysmenorrhoea, uterine enlargement, persistent symptoms after treatment, or myometrial imaging abnormalities may suggest coexisting AM. As transvaginal ultrasonography permits assessment of both the endometrial cavity and the myometrium during the same examination, recognition of AM–EP coexistence may not require additional disease-specific diagnostic steps in many patients. More importantly, identifying concomitant disease may influence symptom attribution and subsequent clinical management. Clinically useful evidence must therefore clarify the settings in which coexistence is repeatedly detected and the circumstances in which consideration of the alternative lesion may be warranted.
Published evidence on AM–EP coexistence is fragmented across hysterectomy specimens, hysteroscopic or polypectomy cohorts, resectoscopy populations, fertility-preserving surgery, and studies using imaging, intraoperative assessment, or mixed clinical records. These settings differ in age distribution, symptoms, procedural indication, pre-test probability, and the opportunity to identify both lesions. Two complementary but distinct questions must also be preserved: how often EPs are identified among women with AM, and how often AM is identified among women with EPs. Although the same coexisting cases may contribute to both calculations within a study, the denominators and ascertainment opportunities differ. Direction-specific estimates therefore answer different clinical questions and should not be treated as interchangeable expressions of a single prevalence.
This systematic review synthesized bidirectional evidence on AM–EP coexistence while preserving direction-specific denominators. We aimed to determine whether coexistence was repeatedly observed across different gynaecological pathways, characterize direction-specific patterns and dispersion, and examine how source population, clinical entry pathway, and ascertainment method shaped the reported estimates. By linking each estimate to its original clinical context, we sought to provide a framework for targeted, symptom- and pathway-driven evaluation while avoiding both premature diagnostic closure and indiscriminate dual-pathology screening.
Materials and methods
Protocol Registration and Reporting
This systematic review was prospectively registered in the International Prospective Register of Systematic Reviews (PROSPERO; CRD420261304541) and was conducted and reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 (PRISMA 2020) statement.12 The protocol specified a GRADE assessment; however, this was not undertaken because the review did not generate a common summary estimate to which certainty could be assigned. The completed PRISMA 2020 checklist is provided as Supplementary file 1.
Eligibility Criteria
Original human studies were eligible if they enrolled women with adenomyosis and/or endometrial polyps and reported sufficient data to estimate at least one of the following outcomes: the prevalence of EPs among women with AM or the prevalence of AM among women with EPs. Studies were eligible when the relevant numerator and analytical denominator were reported directly or could be derived from the full text. Diagnosis of AM or EPs could be based on imaging, hysteroscopy, intraoperative assessment, histopathology, clinical records, or a combination of these methods, provided that direction-specific coexistence data were available.
We excluded: (1) non-original publications, including reviews, commentaries, editorials, case reports, and conference abstracts; (2) in vitro or animal studies; (3) studies that did not report the outcome of interest and from which a direction-specific prevalence estimate could not be calculated; (4) duplicate or overlapping reports, in which case the most complete report was retained; and (5) reports for which the full text could not be obtained.
Information Sources and Search Strategy
PubMed, Embase, the Cochrane Library, and Scopus were searched from the earliest date available in each database to February 10, 2026, with an updated search conducted on July 14, 2026. The search was restricted to human studies, with no restrictions on language, publication year, or geographical region. Controlled vocabulary and free-text terms relating to adenomyosis, endometrial polyps, and their synonyms were combined. The complete database-specific search strategies and numbers of records retrieved are provided in Supplementary file 2.
Study Selection
Two reviewers independently screened all retrieved records for eligibility. Duplicates were removed using EndNote, after which titles and abstracts were screened and potentially eligible reports underwent full-text assessment. Disagreements were resolved through discussion. No automated screening tools were used. The selection process is presented in the PRISMA 2020 flow diagram (Figure 1),13 and reasons for full-text exclusion are listed in Supplementary file 3.
Data Extraction
Two reviewers independently extracted data using a standardized form and cross-checked all entries. Disagreements were resolved through discussion. Extracted information included first author, publication year, country or region, study period, study design, source population, clinical entry pathway, sample size, age, methods used to ascertain AM and EPs, and the numerators and denominators required to calculate direction-specific prevalence estimates.14–16 When potentially eligible reports contained insufficient information to determine eligibility or calculate an estimate, the corresponding authors were contacted for clarification or supplementary data.
Outcomes and Effect Measures
The primary outcome was the prevalence of coexisting AM and EPs, evaluated in two directions. Panel A represented the prevalence of EPs among women with AM, whereas Panel B represented the prevalence of AM among women with EPs. Studies reporting both analytical denominators contributed separately to both panels.
For each study, prevalence was calculated as the number of women with coexisting AM and EPs divided by the number of women in the corresponding direction-specific analytical population and multiplied by 100. Study-specific Wilson score 95% confidence intervals were calculated from the extracted numerators and denominators. The two panels were interpreted separately because they used different analytical denominators and answered different clinical questions.
Methodological Appraisal
Two reviewers independently appraised the included studies using the Joanna Briggs Institute Critical Appraisal Checklist for Prevalence Studies.17 Each applicable domain was rated as “Yes”, “No”, “Unclear”, or “Not applicable”, and disagreements were resolved through discussion. The appraisal examined the appropriateness of the sampling frame and recruitment process, adequacy of sample size, description of participants and setting, validity and consistency of disease ascertainment, completeness of coverage, and appropriateness of statistical analysis. Study-specific concerns relating to selective source populations, incomplete reporting of case ascertainment, and limited representativeness are summarized in Supplementary file 4. Appraisal findings were not used to exclude studies or statistically weight their estimates.
Synthesis and Presentation
Before synthesis, the feasibility of quantitative pooling was assessed by comparing source population, clinical entry pathway, analytical denominator, procedural indication, and the methods and intensity of AM and EP ascertainment. Study-specific estimates arose from clinically distinct settings, including hysterectomy and other pathology-confirmed surgical cohorts, hysteroscopic polypectomy or resectoscopy populations, fertility-preserving surgery, imaging-based evaluation, intraoperative assessment, and mixed clinical records. These settings differed not only in participant characteristics but also in the opportunity to identify intracavitary and myometrial disease. The resulting estimates therefore represented clinically non-equivalent prevalence constructs rather than exchangeable estimates of a single common target parameter. A pooled prevalence was consequently not calculated; the study-level basis for this decision is documented in Supplementary file 5.
A structured narrative synthesis was performed separately for Panels A and B. Study-specific numerators, denominators, prevalence estimates, and Wilson score 95% confidence intervals were organized according to source population and diagnostic pathway, with particular attention to hysteroscopic, hysterectomy-based, fertility-preserving, and other surgically or pathologically enriched settings.
Among studies contributing to both panels, an exploratory descriptive comparison was undertaken to identify recurrent direction-specific patterns. No formal statistical comparison between panels was performed because the two estimates used different denominators and the sets of contributing studies were not identical. Because no common summary effect was estimated, formal tests for publication bias, small-study effects, and leave-one-out sensitivity analyses were not performed.
Results
Study Selection and Study Characteristics
The database searches identified 2839 records. After duplicate removal, 2510 records underwent title and abstract screening, and 74 reports were assessed in full text. Sixteen observational studies involving 14,917 women were included.18–33 Detailed reasons for full-text exclusion are provided in Supplementary file 3. Twelve studies contributed data on the prevalence of endometrial polyps among women with adenomyosis (Panel A), 11 contributed data on the prevalence of adenomyosis among women with endometrial polyps (Panel B), and seven informed both analytical directions.
The included studies were conducted across multiple countries and clinical settings. Most recruited surgically or pathologically selected populations, including hysterectomy specimens, hysteroscopic polypectomy cohorts, resectoscopy populations, fertility-preserving surgery, and other gynaecological procedural pathways. Methods used to ascertain AM and EPs ranged from dual histopathological confirmation to imaging, hysteroscopy, intraoperative findings, physical examination, and mixed clinical records. No study sampled an unselected general population. Detailed study characteristics are presented in Table 1.
|
Table 1 Characteristics of Included Studies |
Methodological Appraisal
Domain-level appraisal showed that analytical denominators and the data required to calculate direction-specific prevalence estimates were generally clearly reported. The principal concerns were selective sampling frames, limited representativeness, and incomplete or inconsistent reporting of disease ascertainment. Detailed domain-level assessments are presented in Table 2, and study-specific concerns are summarized in Supplementary file 4.
|
Table 2 Methodological Quality Assessment of Included Studies |
Endometrial Polyps Among Women with Adenomyosis (Panel A)
Across 12 studies, the prevalence of EPs among women with AM ranged from 4.3% to 34.6% (Table 3; Figure 2). Most pathology-based hysterectomy or surgical estimates fell between 4.3% and 22.9%. The highest estimate, 34.6%, was observed among asymptomatic postmenopausal women undergoing hysterectomy for uterovaginal prolapse. Estimates from other procedural pathways were 20.3% among women undergoing fertility-preserving laparoscopy and 24.9% among women undergoing resectoscopy.
|
Table 3 Prevalence of Endometrial Polyps Among Women with Adenomyosis |
Adenomyosis Among Women with Endometrial Polyps (Panel B)
Across 11 studies, the prevalence of AM among women with EPs ranged from 3.9% to 91.9% (Table 4; Figure 3). Estimates in hysteroscopic polypectomy cohorts were 3.9% and 14.5%, and the resectoscopy cohort yielded an estimate of 13.0%. Hysterectomy-based estimates were highly variable, ranging from 9.7% to 91.9%. The two highest study-specific estimates, 55.9% and 91.9%, arose from selected gynaecological surgical or pathology-enriched populations.
|
Table 4 Prevalence of Adenomyosis Among Women with Endometrial Polyps |
Directional and Pathway-Specific Patterns
Among the seven studies contributing data to both analytical directions, six reported a higher prevalence of AM among women with EPs than the corresponding prevalence of EPs among women with AM. Panel A estimates were comparatively more concentrated, whereas Panel B showed substantially greater dispersion across clinical pathways. This difference was characterized by relatively low Panel B estimates in hysteroscopic polypectomy cohorts and the concentration of its highest estimates in selected surgical or pathology-based populations.
Discussion
Principal Findings
This systematic review identified three principal findings. First, AM and EPs were repeatedly co-detected across diverse gynaecological pathways, indicating that coexistence is not confined to a single clinical scenario. Second, the two analytical directions showed an asymmetric pattern: AM prevalence among women with EPs was generally higher and substantially more dispersed than EP prevalence among women with AM, with six of seven bidirectional studies showing this pattern. Third, the observed magnitude of coexistence was closely related to clinical entry pathway and ascertainment intensity, particularly in Panel B, where estimates ranged from relatively low values in hysteroscopic polypectomy cohorts to markedly higher values in selected surgical or pathology-enriched populations.
The principal contribution of this review is therefore not a universal coexistence rate, but a direction- and pathway-specific interpretation of when the second lesion is more likely to be detected. The recurrently higher prevalence of AM among women with EPs suggests that clinicians should remain attentive to features of coexisting AM when evaluating women with EPs, particularly symptoms or myometrial findings suggestive of adenomyosis on routine ultrasonography. This should not be interpreted as a recommendation for additional systematic screening, because the observed estimates were strongly influenced by clinical selection and ascertainment intensity.
Directional Asymmetry and Pathway-Dependent Detection
The directional asymmetry should first be understood in relation to denominator structure. Within studies reporting both directions, the number of women with coexisting AM and EPs was the same, but the denominators were the total numbers of women with AM and women with EPs, respectively. A higher Panel B estimate therefore does not indicate that EPs cause AM or that the biological association is stronger in that direction; it indicates that the coexistence cases constituted a larger proportion of the EP denominator within that particular clinical population.
Ascertainment opportunities also differed between the two lesions. EPs are focal intracavitary abnormalities that may be identified by hysteroscopy, imaging, or histopathology, whereas AM detection depends more strongly on the intensity of myometrial assessment. Complete histopathological examination after hysterectomy may identify AM that was previously unrecognized, while routine hysteroscopic or polypectomy pathways may not systematically evaluate the myometrium. This difference likely contributed to the greater dispersion observed in Panel B.
Clinical selection further shaped the estimates. Hysterectomy cohorts included women selected for major surgery because of symptoms, prolapse, treatment failure, or coexisting uterine disease, whereas hysteroscopic cohorts generally represented women entering care through an intracavitary diagnostic or therapeutic pathway. These populations differed in age, menopausal status, symptom burden, disease severity, and pre-test probability of AM. Consequently, apparently similar denominators such as “women with EPs” represented clinically distinct patient groups.
These structural differences also meant that a single pooled prevalence would not have had a consistent clinical interpretation.
Relationship to Previous Evidence and Possible Shared Biological Context
Broader adenomyosis literature has similarly shown that AM is frequently identified alongside other uterine or pelvic disorders, particularly leiomyomas and endometriosis, and in some hysterectomy series with endometrial hyperplasia or malignant disease.34,35 Much of this evidence, however, has been derived from hysterectomy-based histopathological cohorts, in which comprehensive examination of the uterus increases the likelihood of detecting both clinically suspected and previously unrecognized lesions. These studies support viewing AM as part of a multi-pathology uterine phenotype in selected women, while also illustrating why coexistence observed in surgical specimens cannot be directly extrapolated to unselected outpatient populations.
The literature on EPs shows a parallel dependence on clinical setting. EPs are commonly investigated in women with abnormal uterine bleeding, during infertility work-up, and in peri- or postmenopausal or surgical populations.36 In abnormal-bleeding cohorts, hysteroscopy preferentially identifies intracavitary causes of bleeding; in infertility settings, uterine-cavity assessment may detect small or asymptomatic polyps; and in hysterectomy or postmenopausal cohorts, pathology provides more complete lesion ascertainment and a different spectrum of coexisting disease. Therefore, the clinical meaning of the denominator “women with EPs” differs according to why and how women entered evaluation.
Previous research has more frequently examined EPs in relation to endometriosis than to AM. A recent bidirectional systematic review and meta-analysis reported increased relative risks of EPs among women with endometriosis and of endometriosis among women with EPs, with particularly high pooled proportions in infertile and surgically confirmed populations.37 Although endometriosis and AM share certain hormone-responsive, inflammatory, and reproductive features, the comparative risk estimates reported for endometriosis cannot be transferred directly to AM.
At a biological level, AM and EPs may arise within overlapping hormone-responsive, inflammatory, and tissue-remodelling environments.38–42 AM has been associated with altered oestrogen signalling, inflammation, neuroangiogenesis, disruption of the endometrial–myometrial interface, and hormone-dependent myometrial remodelling,43,44 whereas EP formation has been linked to focal endometrial overgrowth, altered receptor expression, local inflammation, and dysregulated proliferation.36,45 These overlapping processes provide biological plausibility for coexistence but do not establish that either lesion causes the other.
Biological coexistence is also difficult to separate from shared clinical detection. Abnormal bleeding, infertility, pelvic pain, and peri- or postmenopausal symptoms may lead to imaging, hysteroscopy, or surgery, creating repeated opportunities to identify both lesions. The observed coexistence is therefore likely to reflect a combination of shared biological susceptibility and shared routes to investigation.
Clinical Implications
The findings are best translated into a directional clinical question: after one lesion has been identified, when should the other still be considered?
After identification of an EP, coexisting AM may warrant consideration when dysmenorrhoea or chronic pelvic pain is prominent, the uterus is enlarged or myometrial abnormalities are present on imaging, heavy bleeding persists after polypectomy, or infertility remains insufficiently explained by the intracavitary lesion. In these situations, targeted myometrial assessment using standardised transvaginal ultrasonography, with magnetic resonance imaging when clinically indicated, may be appropriate.
Conversely, after AM has been established, an EP should remain in the differential when intermenstrual or postmenopausal bleeding is present, imaging suggests a focal intracavitary abnormality, bleeding is disproportionate to the apparent myometrial disease or persists despite AM-directed treatment, or infertility remains multifactorial. Targeted uterine-cavity evaluation may then be considered according to age, symptoms, prior imaging, and reproductive goals.
This framework should not be interpreted as a recommendation for universal bidirectional screening. The included studies did not test whether routine investigation of the second lesion improves clinical or reproductive outcomes. Rather, the findings support avoiding premature diagnostic closure when the established diagnosis does not adequately explain bleeding, pain, uterine findings, infertility, or treatment response. Estimates from hysterectomy and pathology-enriched cohorts should not be transferred directly to routine outpatient populations.
Strengths and Limitations
This review has several strengths. It evaluated AM–EP coexistence in both clinical directions, preserved the appropriate direction-specific denominators, and reported study-level estimates with 95% confidence intervals. Estimates were linked to their source populations, clinical entry pathways, and ascertainment methods, allowing differences in clinical meaning to be distinguished rather than obscured. The review also identified a previously underemphasized directional pattern across studies contributing to both panels and assessed study-specific methodological concerns using the JBI prevalence checklist.
This review also has limitations. Most included studies were derived from surgically or pathologically selected populations, particularly hysterectomy- or hysteroscopy-based cohorts, which limits transportability to broader outpatient populations. Important clinical descriptors, including menopausal status, fertility setting, symptom profile and coexisting uterine pathology, were incompletely reported across studies. Methods used to ascertain adenomyosis were not uniform and were sometimes insufficiently described. In addition, grey literature was not systematically included; one report could not be retrieved despite attempts to obtain the full text and a formal statistical assessment of reporting bias was not undertaken. These limitations restrict generalization to unselected outpatient populations and prevent determination of whether detecting both lesions improves symptom control, fertility outcomes, treatment selection, or recurrence risk.
Implications for Future Research
Future studies should recruit consecutive women within clearly defined clinical scenarios, such as abnormal uterine bleeding, infertility evaluation, or peri- and postmenopausal assessment. Investigators should report explicit denominators, indications for evaluation, menopausal and fertility status, symptom profiles, coexisting uterine disease, and standardised criteria for diagnosing both AM and EPs. Prospective studies using reproducible imaging definitions with pathological verification, where appropriate, would improve comparability and help determine when identification of coexistence changes management or outcomes.
Future studies should move beyond prevalence alone and determine whether AM–EP coexistence defines a clinically distinct phenotype. Comparative prospective cohorts should evaluate symptom burden, infertility, treatment response, recurrence, and the incremental value of investigating the second lesion after one diagnosis has been established.
Conclusion
Adenomyosis and endometrial polyps are repeatedly identified together in selected gynaecological populations, but the observed coexistence pattern is directionally asymmetric and strongly shaped by clinical entry pathway and disease ascertainment. The evidence does not support a universal coexistence rate or routine dual-pathology screening; instead, it supports targeted consideration of coexisting AM in women with EPs, or coexisting EPs in women with AM, when bleeding, pain, imaging findings, infertility, or persistent symptoms after treatment remain incompletely explained. However, interpretation is limited by the predominance of surgically selected populations, heterogeneity in disease ascertainment, and the lack of prospective studies in unselected clinical populations.
Abbreviations
AM, adenomyosis; AUB, abnormal uterine bleeding; EPs, endometrial polyps; JBI, Joanna Briggs Institute; MRI, magnetic resonance imaging; PRISMA, Preferred Reporting Items for Systematic Reviews and Meta-Analyses; TVS, transvaginal ultrasonography; LNG-IUS, levonorgestrel-releasing intrauterine system.
Data Sharing Statement
All data generated or analysed during this study are included in this published article and its supplementary information files.
Ethics Approval and Informed Consent
Not applicable. This study was based exclusively on published literature and did not involve direct patient recruitment or the collection of identifiable personal data.
Author Contributions
All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.
Funding
This study received no external funding.
Disclosure
The authors report no conflicts of interest in this work.
References
1. Abbott JA. Adenomyosis and Abnormal Uterine Bleeding (AUB-A)-Pathogenesis, diagnosis, and management. Best Pract Res Clin Obstet Gynaecol. 2017;40:68–13.
2. Vannuccini S, Petraglia F. Recent advances in understanding and managing adenomyosis. F1000Research. 2019:8. doi:10.12688/f1000research.17242.1
3. Al Chami A, Saridogan E. Endometrial polyps and subfertility. J Obstet Gynaecol India. 2017;67(1):9–14. doi:10.1007/s13224-016-0929-4
4. Ferrazzi E, Zupi E, Leone FP, et al. How often are endometrial polyps malignant in asymptomatic postmenopausal women? A multicenter study. Am J Obstet Gynecol. 2009;200(3):
5. Lieng M, Istre O, Qvigstad E. Treatment of endometrial polyps: a systematic review. Acta obstetricia et gynecologica Scandinavica. 2010;89(8):992–1002. doi:10.3109/00016349.2010.493196
6. Moawad G, Fruscalzo A, Youssef Y, et al. Adenomyosis: an updated review on diagnosis and classification. J Clin Med. 2023;12(14):4828. doi:10.3390/jcm12144828
7. Santulli P, Vannuccini S, Bourdon M, Chapron C, Petraglia F. Adenomyosis: the missed disease. Reprod Biomed Online. 2025;50(4):104837. doi:10.1016/j.rbmo.2025.104837
8. Ghoubara A, Price MJ, Fahmy M-D, Ait-Allah AS, Ewies A. Prevalence of hyperplasia and cancer in endometrial polyps in women with postmenopausal bleeding: a systematic review and meta-analysis. Post Reprod Health. 2019;25(2):86–94. doi:10.1177/2053369119833583
9. Lim J-J, Simpson A, Shirreff L. Endometrial polyps. CMAJ. 2024;196(8):E265. doi:10.1503/cmaj.230716
10. Dason ES, Maxim M, Sanders A, et al. Guideline No. 437: diagnosis and management of adenomyosis. J Obstet Gynaecol Can. 2023;45(6):417–429.e411.
11. Vitale SG, Haimovich S, Laganà AS, Alonso L, Di Spiezio Sardo A, Carugno J. Endometrial polyps. An evidence-based diagnosis and management guide. Eur J Obstet Gyn R B. 2021;260:70–77. doi:10.1016/j.ejogrb.2021.03.017
12. Page MJ, Moher D, Bossuyt PM, et al. PRISMA, 2020 explanation and elaboration: updated guidance and exemplars for reporting systematic reviews. BMJ. 2021;372:n160.
13. Page MJ, McKenzie JE, Bossuyt PM, et al. The PRISMA, 2020 statement: an updated guideline for reporting systematic reviews. BMJ. 2021:n71. doi:10.1136/bmj.n71
14. Raffone A, Seracchioli R, Raimondo D, et al. Prevalence of adenomyosis in endometrial cancer patients: a systematic review and meta-analysis. Archives Gynecol Obstet. 2021;303:47–53.
15. Vitagliano A, Cialdella M, Cicinelli R, et al. Association between endometrial polyps and chronic endometritis: is it time for a paradigm shift in the pathophysiology of endometrial polyps in pre-menopausal women? Results of a systematic review and meta-analysis. Diagnostics. 2021;11(12):2182. doi:10.3390/diagnostics11122182
16. Wang M-H, Chen J-H, Qi X-Y, Li Z-X, Huang Y. Global prevalence of adenomyosis and endometriosis: a systematic review and meta-analysis. Reprod Biol Endocrinol. 2025;23:148.
17. Munn Z, Moola S, Riitano D, Lisy K. The development of a critical appraisal tool for use in systematic reviews addressing questions of prevalence. Int J Health Policy Manag. 2014;3(3):123–128. doi:10.15171/ijhpm.2014.71
18. Erkal N, Kaba M, Erdoğan K, Eryılmaz FEI, Sivri Z, Mayır YA. Factors associated with hysterectomy after failure of levonorgestrel-releasing intrauterine system treatment in women with abnormal uterine bleeding. BMC Women’s Health. 2026;26(1). doi:10.1186/s12905-026-04398-y
19. Fırtına Tuncer S, Sağnıç S, Tuncer HA. Comprehensive analysis of risk factors for recurrence in women of reproductive age undergoing hysteroscopic polypectomy. Med Sci Monit. 2025;31:e950098. doi:10.12659/MSM.950098
20. Goksever Celik H, Erkan IBO, Topcu EG, et al. Adenomyosis and coexisting gynecologic pathologies: how often do they coexist? Int J Gynaecol Obstet. 2025;171(2):728–735.
21. Huang J, Li Y, Chen P, Zhi Z. The risk factors and prognostic impact of different benign pathologic types of background endometrium surrounding endometrial polyps. Int J Gynaecol Obstet. 2025;169(1):247–257. doi:10.1002/ijgo.16067
22. Indraccolo U, Barbieri F. Relationship between adenomyosis and uterine polyps. Eur J Obstet,Gynecol Reprod Biol. 2011;157(2):185–189. doi:10.1016/j.ejogrb.2011.02.014
23. La Torre F, Hurni Y, Farsi E, et al. Adenomyosis is associated with proliferative endometrial disorders. Sci. 2026;7(3):260–264.
24. Matalliotakis M, Tsakiridis I, Matalliotaki C, et al. Coexistence of gynecological pathology with endometriosis and adenomyosis. Mol Clin Oncol. 2026;24(2):12.
25. Matalliotakis M, Zervou MI, Matalliotaki C, et al. There is no significant correlation of adenomyosis with benign, premalignant and malignant gynecological pathologies. Retrospective study on 647 specimens. Ginekol Pol. 2022;93(6):467–472.
26. Pervez SN, Javed K. Adenomyosis among samples from hysterectomy due to abnormal uterine bleeding. J Ayub Med Coll Abbottabad. 2013;25(1–2):68–70.
27. Preethi MR, Archana S, Eswari V. To estimate the prevalence of adenomyosis and its correlation with benign endometrial lesions in Tertiary Care Center. J Pharm Negat Results. 2022;13(3):859–864.
28. Ranaei M, Kohsari E, Galeshi M, Yazdani S. The correlation of adenomyosis with benign endometrial lesions in hysterectomy samples. J Obstet Gynecol Cancer Res. 2019;4(3):99–104. doi:10.30699/jogcr.4.3.99
29. Shi J, Wu Y, Li X, et al. Effects of localization of uterine adenomyosis on clinical features and pregnancy outcome. Sci Rep. 2023;13(1):14714.
30. Sidera A, Matalliotakis M, Tsakiridis I, et al. Coexistence of gynecological pathologies in women with cervical and endometrial polyps. Cureus. 2025;17(1):e77015. doi:10.7759/cureus.77015
31. Sordia-Hernández LH, Herrero J, Martínez AM, et al. Adenomyosis: pathologies associated in a set of patients underwent hysterectomy. Asian Pac J Reprod. 2012;1(4):283–286.
32. Topcu HO, Erkaya S, Guzel AI, et al. Risk factors for endometrial hyperplasia concomitant endometrial polyps in pre- and post-menopausal women. Asian Pac J Cancer Prev. 2014;15(13):5423–5425. doi:10.7314/APJCP.2014.15.13.5423
33. Weigel GM, Baison GN, Mihalov L, Mupombwa T. Prevalence of and risk factors for endometrial polyps among asymptomatic postmenopausal women with uterovaginal prolapse. Am J Obstet Gynecol. 2025;232(2):.
34. Naphatthalung W, Cheewadhanaraks S. Prevalence of endometriosis among patients with adenomyosis and/or myoma uteri scheduled for a hysterectomy. J Med Assoc Thai. 2012;95(9):1136–1140.
35. Tetikkurt S, Celik E, Tas H, Cay T, Isik S, Usta AT. Coexistence of adenomyosis, adenocarcinoma, endometrial and myometrial lesions in resected uterine specimens. Mol Clin Oncol. 2018;9(2):231–237.
36. Nijkang NP, Anderson L, Markham R, Manconi F. Endometrial polyps: pathogenesis, sequelae and treatment. Sage Open Med. 2019;7:2050312119848247. doi:10.1177/2050312119848247
37. Fiore A, Casalechi M, Somigliana E, Vigano P, Salmeri N. Association between endometriosis and endometrial polyps: a systematic review and meta-analysis. Reprod Biomed Online. 2026;52(1):105106. doi:10.1016/j.rbmo.2025.105106
38. Pinheiro A, Antunes A, Andrade L, De Brot L, Pinto-Neto AM, Costa-Paiva L. Expression of hormone receptors, Bcl-2, Cox-2 and Ki67 in benign endometrial polyps and their association with obesity. Mol Med Rep. 2014;9(6):2335–2341. doi:10.3892/mmr.2014.2125
39. Su Y, Feng W, Shi H. Treatment with progesterone attenuates proliferation of endometrial polyps (EP) via regulation of expression of miR-320b and its target gene, MCL1. Archives Med Sci. 2023;19(6):1934–1939. doi:10.5114/aoms/171308
40. Chiu CS, Yeh LY, Pan SH, Li SH. Transcriptomic analysis reveals intrinsic abnormalities in endometrial polyps. Int J Mol Sci. 2024;25(5):2557. doi:10.3390/ijms25052557
41. Prasnikar E, Kunej T, Gorenjak M, Potocnik U, Kovacic B, Knez J. Transcriptomics of receptive endometrium in women with sonographic features of adenomyosis. Reprod Biol Endocrinol. 2022;20(1):2. doi:10.1186/s12958-021-00871-5
42. Kobayashi H. Endometrial inflammation and impaired spontaneous decidualization: insights into the pathogenesis of adenomyosis. Int J Environ Res Public Health. 2023;20(4):3762. doi:10.3390/ijerph20043762
43. Rossi M, Vannuccini S, Capezzuoli T, et al. Mechanisms and pathogenesis of adenomyosis. Curr Obstet Gynecol Rep. 2022;11(2):95–102.
44. Zhai J, Vannuccini S, Petraglia F, Giudice LC. Adenomyosis: mechanisms and pathogenesis. Semin Reprod Med. 2020;38(2–03):129–143. doi:10.1055/s-0040-1716687
45. Indraccolo U, Di Iorio R, Matteo M, Corona G, Greco P, Indraccolo SR. The pathogenesis of endometrial polyps: a systematic semi-quantitative review. Eur J Gynaecol Oncol. 2013;34(1):5–22.
© 2026 The Author(s). This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms and incorporate the Creative Commons Attribution - Non Commercial (unported, 4.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.
Recommended articles
Prevalence, Clinical Manifestations, Treatment, and Clinical Course of Chronic Urticaria in Elderly: A Systematic Review
Kulthanan K, Rujitharanawong C, Munprom K, Trakanwittayarak S, Phumariyapong P, Prasertsook S, Ungprasert P
Journal of Asthma and Allergy 2022, 15:1455-1490
Published Date: 20 October 2022
A Systematic review on Prevalence, Serotypes and Antibiotic resistance of Salmonella in Ethiopia, 2010–2022
Kahsay AG, Dejene TA, Kassaye E
Infection and Drug Resistance 2023, 16:6703-6715
Published Date: 13 October 2023
Prevalence and Study-Level Predictors of Chronic Chemotherapy-Induced Peripheral Neuropathy: A Systematic Review and Meta-Analysis
D’Souza RS, Whitfield S, Hussain N, Bhatia A, Banks DW, Parmar J, Klasova J, Mizerak E, Prokop LJ, Her YF
Journal of Pain Research 2026, 19:643363
Published Date: 4 September 2026
Text is read by the "Ask this paper" AI Q&A widget below.
Extraction quality varies by source — PMC NXML preserves structure
cleanly, OA-HTML may include some navigation residue, and OA-PDF can
have broken hyphenation. The publisher copy
(via DOI)
is the canonical version.