The paradoxical association between endometrioma size and serum anti-Müllerian hormone levels in infertile women

Background: The impact of endometrioma size on ovarian reserve remains controversial. Although endometriomas are known to reduce anti-Müllerian hormone (AMH) levels, some studies suggest a paradoxical association between larger cysts and higher AMH.

This cross-sectional study enrolled 210 infertile women between January 2023 and March 2025: 150 with laparoscopy-confirmed untreated unilateral endometriomas and 60 controls with male-factor infertility and normal ovaries. Serum AMH, follicle-stimulating hormone, luteinizing hormone, and prolactin were measured on cycle day 3. Endometrioma diameter was measured by transvaginal ultrasound. AMH levels were compared across cyst size categories (≤30 mm, 31–50 mm, >50 mm) using one-way analysis of variance and multiple linear regression, adjusting for age and follicle-stimulating hormone.

Mean AMH levels did not differ significantly between the endometrioma and control groups (2.24 ± 1.90 vs. 2.38 ± 1.45 ng/mL; p = 0.30). Within the endometrioma cohort, AMH increased with cyst size (F = 4.98, p = 0.008): 1.72 ± 1.26 ng/mL (≤30 mm), 2.23 ± 1.78 ng/mL (31–50 mm), and 2.70 ± 1.69 ng/mL (>50 mm). Post hoc analysis showed significantly higher AMH in cysts >50 mm compared with ≤30 mm (p = 0.01). In multivariable regression analysis, cyst diameter independently predicted AMH levels (β = 0.031, p < 0.001). ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS

Larger endometriomas were paradoxically associated with higher AMH levels. Interpretation of AMH in women with endometriomas should be context-dependent, and clinical decisions regarding ovarian reserve should not rely solely on cyst size or AMH values. Key words: Endometrioma; Anti-Müllerian hormone (AMH); Ovarian reserve; Endometriosis

Endometriosis is a chronic, estrogen-dependent inflammatory disease affecting approximately 10-15% of women of reproductive age, with ovarian endometriomas occurring in 17-44% of cases (1). Endometriomas are well recognized to compromise fertility, largely through reduced ovarian reserve and altered follicular microenvironments. However, the relative contributions of intrinsic disease effects versus surgical damage remain incompletely understood (2). Anti-Müllerian hormone (AMH), produced by granulosa cells in preantral and small antral follicles, is a well-established biomarker of ovarian reserve, reflecting the quantity of remaining oocytes independent of menstrual cycle phase. Low AMH levels are predictive of poor response to assisted reproductive technologies (ART) and earlier menopause (3, 4). Surgical excision of endometriomas, while often necessary for symptom relief or to facilitate fertility treatments, carries risks of iatrogenic ovarian damage, including follicle loss and reduced postoperative AMH levels. However, the inherent impact of endometriomas themselves independent of surgery on ovarian reserve remains a subject of debate (5). A growing body of evidence suggests that endometriomas themselves exert a negative effect on ovarian reserve. Women with unoperated endometriomas often display lower AMH levels compared to those with healthy ovaries or ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS other benign cysts, with a mean reduction of approximately 0.84 ng/mL (6). Proposed mechanisms include chronic inflammation, oxidative stress, iron overload, and compromised cortical perfusion (2, 6, 7). Nevertheless, the relationship between the specific burden of disease particularly endometrioma size and the degree of ovarian reserve impairment remains highly controversial and is a subject of intense debate. The prevailing pathophysiological view would suggest a negative correlation, where larger cysts, through greater mechanical pressure or a more extensive inflammatory milieu, lead to a more significant reduction in AMH (7, 9, 10). However, this conventional paradigm has been challenged by several clinical studies. For instance, Marcellin et al. (8) reported a weak positive dose- response relationship between cyst volume and AMH after adjusting for confounders. Similarly, Roman et al. (9) found higher preoperative AMH levels in women with cysts larger than 6 cm. These paradoxical findings have raised concerns regarding potential selection bias, confounding, or AMH overestimation rather than a true physiological effect. Other investigations (3, 10) found no significant association, further highlighting methodological and population heterogeneity. This discordance creates a critical clinical dilemma: The potential for elevated AMH in the context of larger cysts to misleadingly suggest a robust ovarian reserve, potentially influencing decisions regarding the timing of cystectomy or ART protocols. To address this gap, we conducted a cross-sectional study of infertile women with untreated ovarian endometriomas to examine the association between cyst size and serum AMH levels. By focusing on women without prior ovarian surgery and applying standardized hormonal and ultrasonographic assessments, this study aims to clarify the paradoxical relationship between ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS endometrioma size and ovarian reserve markers and to provide evidence to guide fertility preservation strategies.

and Method: Study Design and Setting This cross-sectional study was conducted at the Fatemeh Zahra Infertility Center in Babol, Iran, between Jun 2023 and March 2025. The study population consisted of infertile women with untreated ovarian endometriomas confirmed by prior diagnostic laparoscopy and infertile controls with normal ovarian morphology. Due to the cross-sectional design, this study can identify associations but cannot establish causality or temporality between endometrioma size and serum AMH levels. The study protocol was approved by the Institutional Review Board of Babol University of Medical Sciences (approval number: IR.MUBABOL.HRI.REC.1402.009) and conducted in accordance with the Declaration of Helsinki. Written informed consent was obtained from all participants prior to enrollment. Participants and Eligibility Criteria The endometrioma group included women aged 20–38 years with a BMI < 28 kg/m², a history of diagnostic laparoscopy confirming endometrioma without any ovarian surgery (i.e., laparoscopy was diagnostic only, with no cystectomy, drainage, or ablation performed), and persistent ovarian cysts with typical ultrasonographic features (ground-glass echogenicity and vascularized cyst wall) at enrollment. All ultrasound assessments followed European Society of Human Reproduction and Embryology (ESHRE) diagnostic criteria. The control group consisted of infertile women with isolated male factor infertility, normal ovarian morphology on transvaginal ultrasonography (TVUS), and no history of endometriosis or other ovarian pathology. Exclusion criteria for both groups: ￿Polycystic ovary syndrome (per Rotterdam criteria) ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS ￿Pelvic malignancy ￿Recent pelvic infection (within 3 months) ￿Use of hormonal contraceptives, GnRH agonists, progestins, or any other hormonal therapy for endometriosis or contraception within 6 months prior to enrollment ￿Autoimmune disorders ￿Any previous ovarian surgery (including cystectomy, oophorectomy, ovarian drilling, or drainage/ablation of cysts), with the sole exception of diagnostic laparoscopy without ovarian manipulation ￿Prior chemotherapy or radiotherapy ￿Systemic or endocrine disorders known to affect ovarian reserve (e.g., thyroid dysfunction, hyperprolactinemia, adrenal disorders) ￿Current or recent (within 3 months) use of medications known to affect ovarian function or AMH levels (e.g., metformin, corticosteroids) ￿Known genetic disorders affecting ovarian reserve (e.g., Fragile X premutation, Turner mosaic) Sample Size Calculation. Sample size was calculated based on data from Ercan et al (4), which reported mean serum AMH levels of 1.62 ± 1.09 ng/mL in women with endometriomas and 2.0 ± 0.51 ng/mL in those with large endometriomas. Assuming an allocation ratio of 3:1, a two-sided α of 0.05, and 80% power (independent t- test), a minimum of 144 participants in the endometrioma group and 48 in the control group were required (calculated using G*Power version 3.1.9.2). To allow for potential attrition, 150 women with endometriomas and 60 controls were recruited. Clinical and Hormonal Assessment Demographic and clinical data were collected from medical records and the institutional endometriosis database, including age, BMI, duration of infertility, menstrual cycle regularity, and pain symptoms (dysmenorrhea and ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS dyspareunia). Dysmenorrhea severity was assessed using a 10-point visual analog scale (VAS). Hormonal assays were performed on day 3 of a spontaneous menstrual cycle. Serum levels of AMH, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin were measured. All samples were analyzed at the same laboratory using standardized protocols. Serum AMH was quantified using the Beckman Coulter Gen II ELISA kit (Brea, CA, USA). Intra-assay and inter-assay coefficients of variation were <5% and <7%, respectively, with a sensitivity of 0.08 ng/mL to eliminate inter-batch variability, all samples from each participant were processed in the same analytical run. FSH, LH, and prolactin were assayed via chemiluminescence immunoassay (Abbott Architect System, Abbott Park, IL, USA; intra-assay CV < 4%, inter-assay CV < 6%). Ultrasonographic Evaluation All participants underwent transvaginal ultrasonography using a Philips HD11 XE ultrasound system. Examinations were performed by a single experienced gynecologist blinded to the hormonal results, ensuring consistency and minimizing inter-observer variability. For each participant, cyst laterality classified as left-sided, right-sided, or bilateral was documented alongside cyst dimensions measured in centimeters. Cyst size was defined as the maximum diameter observed on transvaginal ultrasonography. In instances of bilateral involvement, both the cumulative maximum diameter and the aggregate volume of all identified cysts were computed and utilized for analytical purposes when indicated (8). Statistical Analysis ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS All statistical analyses were performed using SPSS version 24.0 (IBM Corp., Armonk, NY, USA). The normality of continuous variables was evaluated using the Kolmogorov–Smirnov test. Descriptive data are presented as mean ± standard deviation (SD) or median (interquartile range) for continuous variables, and as frequencies and percentages for categorical variables. Comparisons between the endometrioma and control groups were conducted using independent-samples t-tests for normally distributed variables and Mann–Whitney U tests for non-normally distributed variables, while categorical data were compared with the χ² test. To assess the relationship between endometrioma size and ovarian reserve, serum AMH levels were compared across three predefined cyst size categories (≤30 mm, 31–50 mm, >50 mm) using one-way analysis of variance (ANOVA) with Tukey’s post hoc test for pairwise comparisons. These size categories were selected a priori based on clinical thresholds reported in the literature, including ~3–4 cm as a potential cutoff for ovarian reserve or ART impact [18,19] and >5–6 cm for associations with higher AMH levels [8,9], rather than post-hoc data-driven cutoffs. Homogeneity of variances was confirmed by Levene’s test. Multiple linear regression analysis was then applied to determine the independent association between endometrioma size (entered as a continuous variable in mm) and AMH levels after adjusting for age and FSH. A two-tailed p-value < 0.05 was considered statistically significant.

Study Population and Baseline Characteristics A total of 210 women were included in this cross-sectional analysis, comprising 150 women with laparoscopy-confirmed untreated ovarian endometriomas and 60 infertile controls with isolated male-factor infertility and normal ovarian morphology on transvaginal ultrasonography. Demographic and clinical characteristics are summarized in Table 1. The ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS endometrioma and control groups were comparable in age, body mass index, and duration of infertility. Menstrual cycle regularity did not differ significantly between groups, with regular cycles reported by the majority of participants (87.1% overall). Hormonal Profiles and Symptomatology Baseline hormonal profiles are presented in Table 1. Mean serum AMH was slightly lower in the endometrioma group compared with controls (2.24 ± 1.90 vs. 2.38 ± 1.45 ng/mL), though not statistically significant (p = 0.30). No significant differences were observed in LH or prolactin levels. In contrast, FSH was higher in the endometrioma group (6.90 ± 3.23 vs. 6.14 ± 2.73 IU/L); this difference was not significant by the Mann–Whitney U test (p = 0.106). Endometriosis-related symptoms were more pronounced in women with endometriomas. Dyspareunia severity was significantly higher compared to controls (p = 0.007), and dysmenorrhea scores were also more severe and widely distributed in the case group (p <0.001). Endometrioma Characteristics and Staging Among the 150 women with endometriomas, bilateral involvement was present in 72 women (34.3%), unilateral left-sided in 45 women (21.4%), and unilateral right-sided in 33 women (15.7%). Staging according to the revised American Society for Reproductive Medicine (rASRM) classification revealed that 54.7% (n=82) of the women were classified as stage III and 44.7% (n=67) as stage IV. The mean cyst diameter was 37.0 ± 14.7 mm. Stage IV patients had significantly larger cysts than stage III patients (40.5 ± 16.2 vs. 34.2 ± 12.8 mm, p = 0.009); however, AMH levels did not differ between the two stages (2.17 ± 1.41 vs. 2.33 ± 2.38 ng/mL, p = 0.61). Association Between Endometrioma Size and Ovarian Reserve Stratification by endometrioma diameter revealed a paradoxical positive association between cyst size and serum AMH levels. Women with the ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS smallest cysts (≤30 mm; n=58) had the lowest mean AMH (1.72 ± 1.26 ng/mL), whereas those with the largest cysts (>50 mm; n=30) exhibited the highest mean AMH (2.70 ± 1.69 ng/mL). One-way analysis of variance (ANOVA) demonstrated a statistically significant difference in AMH across the three cyst size groups (≤30 mm, 31–50 mm, >50 mm) (F(2,147) = 4.98, p = 0.008), with a small-to-moderate effect size (partial η² = 0.064). Homogeneity of variances was confirmed by Levene’s test (p = 0.109). Post-hoc Tukey testing showed that women with cysts >50 mm had significantly higher AMH levels than those with cysts ≤30 mm (mean difference = 0.98 ng/mL, p = 0.01), corresponding to a medium effect size (Cohen’s d = 0.69). A multiple linear regression analysis was performed with serum AMH as the dependent variable and endometrioma size, age, FSH, BMI, and duration of infertility as predictors (Table 2). The overall model was statistically significant, F(5,143) = 4.75, p < 0.001, explaining 14.2% of the variance in AMH levels (R² = 0.142; adjusted R² = 0.113), indicating moderate explanatory power. Endometrioma size was independently and positively associated with AMH (B = 0.031, SE = 0.009; standardized β = 0.287, p < 0.001). Age was inversely associated with AMH (B = −0.062, SE = 0.025; standardized β = −0.204, p = 0.013). FSH showed a negative but non-significant association (B = −0.066, SE = 0.035; standardized β = −0.149, p = 0.060). Neither BMI (B = −0.012, SE = 0.045, p = 0.798) nor infertility duration (B = 0.011, SE = 0.041, p = 0.795) were significantly associated with AMH. Multicollinearity was not detected among the independent variables (VIF range 1.03–1.11).

ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS This cross-sectional study of 150 infertile women with unoperated ovarian endometriomas reveals a paradoxical positive association between endometrioma size and serum AMH levels, with larger cysts (>50 mm) linked to higher AMH compared to smaller cysts (≤30 mm). This finding, independent of age and FSH in multivariate analysis, challenges the conventional hypothesis that larger endometriomas exacerbate ovarian reserve impairment through mechanical pressure or inflammation. 1. Interpretation of Key Findings and Comparison with Existing Literature While our results align with a minority of studies reporting higher AMH in larger endometriomas (9) (8). this paradoxical finding contrasts with the majority of evidence, including meta-analyses showing reduced AMH in the presence of endometriomas. A meta-analysis by Muzii et al. (6) reported a mean AMH reduction of 0.84 ng/mL in women with unoperated endometriomas , supported by studies indicating ovarian reserve impairment due to inflammation or follicular damage (11-13). Other studies, however, found cyst size alone may not linearly correspond to functional ovarian damage (14) , with Akgul et al. (10) noting lower AMH but no size-related correlation. Studies in surgical cohorts often show that larger cyst size predicts a greater absolute decline in AMH postoperatively (2, 15). The association should be interpreted cautiously as it may reflect methodological heterogeneities, selection bias (e.g., women with severely diminished reserve and large cysts undergoing earlier surgery), or artifactual elevation rather than true physiological preservation of reserve and inadequate control for critical confounders such as bilateral disease and the underlying inflammatory burden. 2. Potential Mechanisms Underlying the Positive Association ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS The biological plausibility of a positive association between endometrioma size and AMH is not immediately apparent, but several non-mutually exclusive hypotheses warrant consideration. A contrasting hypothesis to explain the positive size-AMH correlation suggests that the inflammation and neoangiogenesis associated with larger endometriomas may increase local ovarian blood flow (8), This could enhance the clearance of AMH from the ovarian tissue into the systemic circulation, potentially leading to an overestimation of the true ovarian reserve based on serum AMH levels. This hypothesis requires further validation, as direct evidence linking specific mediators to AMH elevation is limited. Endometrioma cyst walls contain cells with histological similarities to ovarian granulosa cells, expressing steroidogenic markers such as aromatase, which may contribute to altered ovarian function (16, 17), Kitajima et al. demonstrated histological similarities between cyst wall cells and ovarian granulosa cells, though their AMH-secretory capacity remains unconfirmed (17). Transcriptomic studies are needed to validate this hypothesis. Ultrasonographic cyst size measurements may correlate with higher baseline AFC, reflecting greater follicular volume and AMH production. Additionally, women with large bilateral endometriomas and severely diminished ovarian reserve may undergo earlier surgical intervention, skewing our sample toward those with preserved AMH. This selection bias could explain the observed association, as noted in similar studies (9). Evidence suggests a threshold effect in the relationship between endometrioma size and ovarian reserve impairment, with cysts >3–4 cm linked to reduced ovarian responsiveness in assisted reproductive technology (ART) outcomes. Somigliana et al. identified a 4 cm threshold for impaired ovarian response (18). Orazov et al (19) and Esmaeilzadeh et al. (1) reported poorer oocyte and embryo quality with cysts >3 cm or advanced-stage endometriosis. The cumulative effect on ART outcomes is further highlighted ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS by Zeng et al. (20) who documented reduced antral follicle counts and oocyte yield in the presence of endometriomas >6 cm, as well as lower live birth rates associated with cysts ≥3 cm (3). Conversely, Akgul et al. observed lower AMH with endometriomas but no size-related differences, highlighting conflicting findings (10). Strengths and Limitations This study employs several methodological strengths that bolster its validity and clinical relevance. Firstly, the cross-sectional design deliberately excluded women with a history of ovarian surgery, thereby mitigating the confounding effects of iatrogenic ovarian damage prevalent in prior research. This approach enables a more precise evaluation of endometriomas' inherent impact on ovarian reserve. Diagnostic accuracy was enhanced by confirming endometriomas through both prior laparoscopy and current transvaginal ultrasonography. Additionally, the inclusion of a control group comprising infertile women with normal ovarian morphology strengthens the study's internal validity. Further, the study utilized standardized, high-sensitivity anti-Müllerian hormone (AMH) assays (Beckman Coulter ELISA, CV <7%) and transvaginal ultrasound assessments conducted by a single experienced gynecologist, minimizing measurement variability. Hormonal assays and ultrasonographic evaluations were performed using consistent, high-quality protocols by a single blinded operator, reducing inter-observer variability. Moreover, a multivariate regression model, adjusted for confounders such as age and follicle-stimulating hormone (FSH), identified cyst size as an independent predictor of AMH levels. Stratification of cysts into three size categories (≤30 mm, 31–50 mm, >50 mm) revealed a dose-response-like pattern, with larger cysts associated with significantly higher AMH levels, supporting a non-linear causal relationship. Despite these strengths, several limitations should be acknowledged. First, the cross-sectional design precludes determination of causality or temporal relationships between endometrioma size and serum AMH levels. Therefore, ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS our findings represent associations only and do not allow causal inference. We cannot conclude that larger cysts cause higher AMH, nor can we exclude reverse causality, residual confounding from unmeasured factors (e.g., inflammatory milieu, genetic predisposition, or baseline ovarian reserve prior to cyst development), or selection bias. Selection bias may be particularly relevant: women with large endometriomas and severely diminished ovarian reserve may undergo earlier surgical intervention and thus be underrepresented, potentially enriching the >50 mm subgroup with individuals who have higher baseline AMH. Second, the observed positive association between cyst size and AMH appears biologically counterintuitive given established mechanisms of endometrioma-related ovarian damage, including chronic inflammation, fibrosis, oxidative stress, and compromised follicular microenvironment. Accordingly, these results should be interpreted cautiously as hypothesis- generating rather than definitive evidence of a physiological effect. Third, although the overall sample size was calculated a priori, the subgroup with very large cysts (>50 mm) was relatively small, which may limit generalizability at the extremes of the cyst size spectrum. Additionally, we did not assess the relationship between AMH levels and assisted reproductive technology (ART) outcomes such as oocyte yield or quality; therefore, the clinical and prognostic significance of the paradoxical AMH elevation remains uncertain. Finally, while hormonal contraceptive use within the previous 6 months was excluded, residual effects of prior treatments or undiagnosed comorbidities (e.g., subtle thyroid dysfunction) cannot be entirely ruled out. Longitudinal studies tracking AMH changes in relation to endometrioma evolution are warranted to clarify causality and inform clinical relevance. Clinical Implications ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS This study identified a paradoxical positive association between endometrioma size and serum AMH levels. However, higher AMH in women with larger cysts does not indicate preserved ovarian reserve, improved follicular health, or any protective effect. Such elevations may reflect selection bias, artifactual factors, or unmeasured influences, and should not be interpreted as reassuring. Clinicians should exercise caution when assessing AMH in women with endometriomas, as serum levels may not accurately reflect underlying ovarian damage. Treatment decisions should not rely solely on cyst size or AMH; management must be individualized, taking into account age, symptoms, fertility goals, and comprehensive ovarian evaluation. In selected cases where fertility preservation is a priority, conservative (non- surgical) management with close monitoring may be considered, carefully balancing the risks of progressive disease against surgical intervention. These findings underscore the complexity of interpreting biomarkers in endometriosis-associated infertility and highlight the need for longitudinal studies to clarify the true impact of endometrioma size on ovarian reserve and reproductive outcomes. Final Conclusion In summary, this study provides new evidence that larger endometriomas are paradoxically associated with higher AMH levels, challenging traditional assumptions about the relationship between cyst burden and ovarian reserve. However, these findings should be interpreted within the context of the study's cross-sectional design and the absence of ART outcome data. AMH should not be interpreted in isolation when evaluating women with endometriomas; comprehensive clinical assessment remains essential to avoid misjudging ovarian function. Future longitudinal and mechanistic studies are warranted to clarify the biological basis of this paradox and its implications for reproductive outcomes. ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS Declarations Consent for publication: Written informed consent for publication of anonymized clinical data was obtained from all participants. No identifying information or images of individual patients are included in this manuscript. Availability of data and materials: The datasets during the current study available from the corresponding author on reasonable request.

We appreciate the Research and Technology Deputy of Babol University of Medical Sciences for the approval and funding. Competing interests: The authors declare that they have no competing interests. Authors contributions: PM conceived and designed the study, collected data, patient recruitment, and drafted the manuscript. SKH contributed to data collection. SE conceived the study, patient recruitment, and clinical assessments, HSH performed data analysis, interpretation of results, ZB patient recruitment, and clinical assessments, all authors reviewed and approved the final version of the manuscript and agree to be accountable for all aspects of the work. SE and SKH are co-first author. Ethics and Consent to Participate The study protocol was approved by the Institutional Review Board of Babol University of Medical Sciences (approval number: IR.MUBABOL.HRI.REC.1402.009) Funding: This research is funded by vice chancellor of Research and technology of Babol University of medical sciences.

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Somigliana E, Palomino MC, Castiglioni M, Mensi L, Benaglia L, Vercellini P, et al. The impact of endometrioma size on ovarian responsiveness. Reproductive biomedicine online. 2020;41(2):343-8. 19. Orazov MR, Radzinsky VY, Ivanov II, Khamoshina MB, Shustova VB. Oocyte quality in women with infertility associated endometriosis. Gynecological Endocrinology. 2019;35(sup1):24-6. 20. Zeng C, Lu R, Li X, Kuai Y, Wang S, Xue Q. The presence of ovarian endometrioma adversely affect ovarian reserve and response to stimulation but not oocyte quality or IVF/ICSI outcomes: a retrospective cohort study. Journal of Ovarian Research. 2022;15(1):116. ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS Table 1. Demographic and Clinical Characteristics of the Study Population Variable OMA Group (n=150) Control Group (n=60) P-value Age (years) 32.65 ± 4.74 33.28 ± 5.53 0.274* BMI (kg/m²) 23.92 ± 2.52 24.09 ± 2.92 0.615* Infertility Duration (years) 4.03 ± 2.85 4.29 ± 2.58 0.282* AMH (ng/mL) 2.24 ± 1.90 2.38 ± 1.45 0.295* LH (mIU/mL) 5.69 ± 2.90 5.79 ± 2.53 0.600* FSH (mIU/mL) 6.90 ± 3.23 6.14 ± 2.73 0.106* Prolactin (ng/mL) 17.95 ± 8.21 18.21 ± 7.44 0.826† Note: *Mann-Whitney U test; †Independent samples t-test. Data are mean ± SD. ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS Table 2. Multivariate Linear Regression Analysis of Predictors of Serum AMH Levels in Women with Endometriomas Predictor Unstandardized β SE Standardized β t P- value 95% CI Age (years) -0.062 0.025 -0.204 - 2.507 0.013 -0.11 to - 0.013 FSH (IU/L) -0.066 0.035 -0.149 - 1.892 0.060 -0.135 to 0.003 BMI (kg/m²) -0.012 0.045 -0.020 - 0.256 0.798 -0.101 to 0.077 Infertility duration (years) 0.011 0.041 0.021 0.261 0.795 -0.070 to 0.092 Cyst size (mm) 0.031 0.009 0.287 3.616 <0.001 0.014 to 0.048 Dependent variable: AMH (ng/mL). Model F(5,143) = 4.75, p < 0.001; R² = 0.142; Adjusted R² = 0.113.* *Standardized β coefficients are reported as measures of effect size for each predictor ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS Figure 1. Serum AMH levels (mean ± 95% CI) by endometrioma size: ≤30 mm (n = 58), 31–50 mm (n = 62), and >50 mm (n = 30). AMH was significantly higher in cysts >50 mm versus ≤30 mm (p = 0.01). ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS ACCEPTED MANUSCRIPT ARTICLE IN PRESSARTICLE IN PRESS