{"paper_id":"4feebf0b-e8e3-479d-afb6-884b1605b675","body_text":"RESEARCH Open Access\n© The Author(s) 2025. Open Access  This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 \nInternational License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you \ngive appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the \nlicensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or \nother third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the \nmaterial. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or \nexceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit  h t t p  : / /  c r e a  t i  \nv e c  o m m  o n s .  o r  g / l  i c e  n s e s  / b  y - n c - n d / 4 . 0 /.\nLi et al. BMC Pregnancy and Childbirth          (2025) 25:727 \nhttps://doi.org/10.1186/s12884-025-07828-1\nBMC Pregnancy and Childbirth\n*Correspondence:\nTing Zhao\nzhaoting@fudan.edu.cn\nFull list of author information is available at the end of the article\nAbstract\nBackground Women diagnosed with adenomyosis often suffer from infertility and frequently seek assisted \nreproductive techniques (ART). It remains unclear whether certain patients possess the potential to achieve \nspontaneous pregnancy. This study aimed to investigate the role of uterine parameters, which indicate the \nprogression of adenomyosis, in predicting spontaneous pregnancy outcomes after controlling for other factors that \naffect natural infertility synergistically.\nMethods This retrospective study included 138 infertile women diagnosed with adenomyosis with uterine \ndiameters < 70 mm, who pursued natural conception. Laparoscopy and hysteroscopy were conducted to exclude \nother factors impacting natural fertility such as hydrosalpinx, and to diagnose and treat endometriosis. The clinical \npregnancy rate (CPR) and live birth rate (LBR) within 24 months were compared between patients with endometriosis \n(n = 98) and those without (n = 40). Logistic regression models were employed to identify predictors of the clinical \npregnancy and live birth in both groups, the entire cohort, and subgroups stratified based on age or anti-Müllerian \nhormone (AMH). Their predictive performance was assessed utilizing receiver operating characteristic (ROC) curves.\nResults Among the 138 patients, 81 (58.70%) achieved clinical pregnancies, comprising 75 live births (54.35%) and \n6 early miscarriages (4.35%). No significant difference was found in CPR or LBR between patients with and without \nendometriosis. The uterine anteroposterior diameter (AD) predicted pregnancy outcomes in each group and overall. \nIn patients under 35 years, uterine AD independently correlated with successful clinical pregnancy [odds ratio \n(OR) = 0.878, 95% confidence interval (CI) = 0.814–0.946] and live birth (OR = 0.884, 95% CI = 0.821–0.951). A uterine AD \nof < 41.5 mm predicts successful clinical pregnancy [sensitivity: 0.625, specificity: 0.652, area under the curve (AUC): \n0.690] and live birth (sensitivity: 0.623, specificity: 0.656, AUC: 0.688).\nConclusion Uterine AD predicted spontaneous pregnancy outcomes in patients under 35 years diagnosed with \nadenomyosis. Adenomyosis probably compromises fertility from the early stages of the condition. However, the \nUterine anteroposterior diameter predicts \nspontaneous pregnancy outcomes \nin women under 35 years with adenomyosis: \na retrospective study\nJiaye Li1, Meiling Sun2, Pengrong Lu1 and Ting Zhao1*\n\nPage 2 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \nIntroduction\nAdenomyosis is characterized as the invasion of endo -\nmetrial glands and stroma into the uterine myometrium \n[1]. This condition is associated with an increased risk \nof pregnancy loss [ 2, 3], predominantly occurring at the \nearly biochemical stage before fetal viability is achieved, \nthus contributing to infertility [ 4]. The presence of ade -\nnomyosis likely impairs implantation and reduces fertil -\nity potential through perturbed uterine peristalsis and \naltered endometrial receptivity [ 5]. Patients diagnosed \nwith adenomyosis frequently resort to assisted repro -\nductive techniques (ART), and contemporary research \non fertility issues associated with adenomyosis predomi -\nnantly centers on in vitro fertilization (IVF), with scant \nattention given to spontaneous pregnancies. However, \nduring the process of superovulation in IVF, the fol -\nlicles produce a substantial quantity of estrogen, which \nmay exacerbate the progression of adenomyosis. Con -\nsequently, for patients with adenomyosis pursuing IVF, \nthis situation presents a paradoxical challenge. Sponta -\nneous conception differs from IVF, wherein long-acting \ngonadotropin-releasing hormone agonists (GnRH-a) can \nbe used prior to each embryo transfer to optimize the \nuterine environment. It remains unknown whether all \npatients with adenomyosis are unsuitable for attempting \nnatural conception, or if certain individuals may still pos-\nsess the potential to achieve spontaneous pregnancy.\nEndometriosis (EM) is characterized by the growth of \nendometrial glands and stroma outside the uterus. EM \nand adenomyosis are closely related diseases and usu -\nally coexist. It has been reported that 79% of EM patients \nexhibited adenomyosis under magnetic resonance imag -\ning (MRI), and this ratio reached as high as 90% among \nEM patients with infertility [ 6]. EM can cause tubal fac -\ntor infertility through adhesions that block one or both \nfallopian tubes or impede tubal access to the Douglas \npouch where follicular fluid containing an oocyte is often \ndrained to [7]. EM may also adversely affect oocyte qual -\nity by inducing inflammatory and oxidative damage to \nthe oocytes [ 8]. A retrospective study revealed that in \npatients receiving surgical intervention for coexisting EM \nand adenomyosis, the endometriosis fertility index (EFI) \nand mean uterine diameter predicted live birth rate (LBR) \nafter surgery, reflecting the adverse effects of EM and \nadenomyosis on pregnancy, respectively [ 9]. However, in \nthat study merely a smaller cohort (26.23%, 48/183) opted \nfor spontaneous conception, whereas a significant major-\nity (73.77%, 135/183) underwent IVF. While the mean \nuterine diameter was identified as a predictive factor, \nthe inclusion of patients with leiomyoma compromised \nthe accuracy of uterine measurements. Furthermore, a \nsubset of the cohort (76 patients) underwent excision of \nadenomyotic lesions, which may improve the pregnancy \noutcomes for these individuals. Consequently, the spe -\ncific initial uterine diameter at which adenomyosis signif-\nicantly impairs the likelihood of spontaneous pregnancy \nremains undetermined.\nBeyond EM, infertile women diagnosed with adeno -\nmyosis may also have concurrent conditions such as \nhydrosalpinx due to pelvic inflammatory disease sequelae \nor uterine cavity abnormalities. These coexisting condi -\ntions could contribute to infertility in combination with \nadenomyosis. After excluding or addressing other factors \nthat could affect natural conception, the isolated effect of \nadenomyosis on fertility can be observed. The primary \nobjective of this study is to assess, after excluding or \naddressing other factors that could influence spontane -\nous conception and uterine measurements, the prognos -\ntic role of uterine parameters in predicting spontaneous \npregnancy outcomes among patients with adenomyosis. \nThis research contributes to our understanding of the \nspecific stage at which adenomyosis begins to compro -\nmise fertility. Furthermore, it provides valuable insights \nthat may assist in making therapeutic decisions.\nMethods\nParticipants\nThis retrospective study included patients diagnosed with \nfemale infertility, defined as at least 12 months of unpro -\ntected intercourse without achieving a pregnancy, who \nsought natural conception and presented to our clinical \nteam between July 2019 and December 2022. Only those \ndiagnosed with adenomyosis under transvaginal ultraso -\nnography (TVS, Voluson E8 General Electric, Milwaukee, \nWisconsin) and with a maximum uterine diameter of < 70 \nmm were included, as those with a uterine diameter ≥ 70 \nmm in the retrospective dataset typically underwent sur -\ngical resection, a procedure reported to improve fertility \nin patients with severe adenomyosis [ 10]. The diagnostic \ncriteria of adenomyosis adhered to the revised Morpho -\nlogical Uterus Sonographic Assessment (MUSA) state -\nment, which stipulates that the presence of at least one \ndirect sign, such as myometrial cysts, hyperechogenic \nislands, or echogenic subendometrial lines and buds, is \nrequired [11].\nThe exclusion criteria were: (1) malignant tumors; (2) \nabnormal male semen examinations; (3) male/female \nchromosome abnormality; (4) serum anti-Müllerian \nretrospective design, the potential presence of confounding factors and limited sample size of this study indicate the \nnecessity for large-scale prospective studies to validate these findings.\nKeywords Adenomyosis, Endometriosis, Hysteroscopy, Laparoscopy, Pregnancy outcome\n\nPage 3 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \nhormone (AMH) < 0.5 ng/mL; (5) > 45 years; (6) history \nof oophorectomy or oophorosalpingectomy; (7) his -\ntory of ectopic pregnancy; (8) use of hormone drugs or \nGnRH agonists or antagonists within the past 3 months; \n(9) hydrosalpinx or fallopian tubes obstruction under \nlaparoscopy and/or hysteroscopy; (10) cesarean section \nincision diverticulum detected by ultrasound or hyster -\noscopy; (11) intramural uterine fibroids; (12) intrauterine \nadhesions or uterine malformation detected by ultra -\nsound or hysteroscopy; (13) endometrial atypical hyper -\nplasia confirmed by pathology; (14) endocrine disease \nsuch as polycystic ovary syndrome and thyroid disease; \n(15) without intention of natural conception after surgery \n(Fig. 1). The study was approved by the ethics committee \nof the Obstetrics and Gynecology Hospital of Fudan Uni -\nversity, and verbal informed consent was obtained from \nall patients by telephone connection.\nStudy design and data collection\nUterine longitudinal diameter (LD) was defined as the \ndistance from the cervical internal os to the fundus in the \nsagittal plane; transversal diameter (TD) was measured \nas the maximum diameter from the left side of the uter -\nine corpus to the right side in the transverse plane; and \nanteroposterior diameter (AD) was measured from the \nanterior to the posterior serosa at the thickest point per -\npendicular to the endometrial line in the sagittal plane. \nUterine volume was calculated using the formula (3.14 \n* LD * TD * AD)/6 [ 12]. The visual analog scale (VAS) \nscore for dysmenorrhea over the past three months was \nrecorded through a face-to-face interview before surgery. \nAll patients underwent simultaneous laparoscopy and \nhysteroscopy performed by the same two gynecologists \nfrom our clinical team within three days following men -\nstruation. The diagnosis of EM was confirmed by lapa -\nroscopy and pathology. The revised American Society \nfor Reproductive Medicine (rASRM) and EFI scores were \nevaluated according to the definitions [ 13, 14]. During \nthe surgical procedure, peritoneal EM lesions underwent \nelectrocoagulation. The cyst wall of endometrioma was \nstripped and the ovary was sutured. Efforts were made \nto avoid damage to the normal ovarian tissue as much \nas possible. Pelvic adhesions were separated through \nboth blunt and sharp dissection. Intrauterine lesions or \nFig. 1 The scheme of the study\n \n\nPage 4 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \nadhesions were removed under hysteroscopy. Intubation \nwas conducted in the interstitial segments of both fallo -\npian tubes, followed by the injection of a diluted methy -\nlene blue solution to evaluate tubal patency. At the end \nof the operation, the pelvic cavity was washed repeatedly \nwith a large amount of saline until a clear washing fluid \nwas obtained.\nPatients received three doses of GnRH-a (3.75 mg Leu -\nprorelin Acetate Microspheres, Lizhu Pharmaceutical \nCompany Limited, China) every 28 days, starting from \nthe second day after surgery. The subsequent spontane -\nous pregnancy outcomes within 24 months after the last \ndose of GnRH-a were followed up on through face-to-\nface consultations, telephone calls, or by consulting our \nhospital’s medical record system. Confirmed pregnancies \nwere followed until termination. The conception interval \nwas defined as the time from the last dose of GnRH-a to \nthe calculated date of fertilization, assessed in months. \nClinical pregnancy was defined as the observation of \na gestational sac on early ultrasound including ectopic \npregnancies. Live birth was defined as the spontane -\nous delivery or cesarean section of a viable infant at ≥ 28 \ngestational weeks, with the newborns surviving at birth. \nMiscarriage was defined as pregnancy loss before 22 ges -\ntational weeks. These definitions are based on the Inter -\nnational Glossary on Infertility and Fertility Care [ 15]. \nThe primary and second endpoints were LBR and clinical \npregnancy rate (CPR), respectively.\nStatistical analysis\nSPSS software (version 26.0, IBM Corp., Armonk, NY, \nUSA) was used for statistical analysis. To determine the \ndistribution of the variables, the Kolmogorov-Smirnov \ntests were used for parameters with sample sizes greater \nthan 50, and the Shapiro-Wilk tests were used for param-\neters with sample sizes smaller than 50. Continuous \nvariables were expressed as mean ± standard deviation \n(SD) or median (interquartile range). The t-tests and \nMann-Whitney U tests were applied for normally and \nnon-normally distributed data, respectively. Categorical \nvariables were presented as numbers and percentages, \nwith the Chi-square test used for comparisons. Kaplan-\nMeier curve was performed to compare the cumulative \nCPR. Variables were initially assessed using univariable \nlogistic regression for their correlation with pregnancy \noutcomes. Those with p < 0.1 were then included in a \nmultivariate conditional logistic regression model with a \nforward procedure. A p-value < 0.05 was considered sta -\ntistically significant.\nResults\nCharacteristics of the study population\nDuring the study period, a total of 285 women suspected \nof female infertility and diagnosed with adenomyosis \nwith uterine diameters < 70 mm were presented to our \nclinical team for evaluation. According to the exclusion \ncriteria, 156 patients were initially deemed eligible for \nthe study. Of these, 12 patients ceased attempts at natural \nconception after trying for several months and resorted \nto IVF, and 6 patients were lost of follow-up. Ultimately, \nthe spontaneous pregnancy outcomes of 138 patients \nwere analyzed (Fig. 1).\nThere were 98 (71.01%) patients with laparoscopically \ndiagnosed and treated EM and 40 (28.99%) patients with-\nout EM. Among patients with EM, 29 (21.01%), 8 (5.80%), \n30 (21.74%), and 31 (22.46%) were diagnosed with stages \nI, II, III and IV, respectively. Patients with EM presented \nlower body mass index (BMI), shorter menstrual cycles, \nand higher VAS scores for menstrual pain compared to \nthose without EM (Table 1).\nSpontaneous pregnancy outcomes and the contributing \nfactors in patients with or without EM and throughout the \nentire cohort\nAmong 138 patients, there were 81 (58.70%) spontaneous \nclinical pregnancies, including 75 (54.35%) live births and \n6 (4.35%) early miscarriages in total. No ectopic preg -\nnancy has been observed. In the subgroup with EM, the \nCPR and LBR were 59.18% (58/98) and 54.08% (53/98), \nrespectively; the median time to conception was 8.37 \n[95% confidence interval (CI) = 4.64–12.10] months. In \nthe subgroup without EM, the CPR and LBR were 57.50% \n(23/40) and 55.00% (22/40), respectively. The median \ntime to conception was 7.83 months (95% CI = 4.96–\n10.70). There was no difference in CPR and LBR between \ntwo subgroups (Table  1). Similarly, the Kaplan-Meier \ncurve showed no difference in cumulative CPR between \nsubgroups (Fig. 2).\nThe correlation between age, preoperative AMH level, \nBMI, gravidity, parity, menstrual period and cycle, the \nVAS score for dysmenorrhea, uterine diameters, and \nuterine volume with clinical pregnancy or live birth was \nassessed using a logistic regression model. Additionally, \nfor the subgroup with EM, the association between the \nrASRM and EFI scores with pregnancy outcomes was \nalso analyzed.\nUterine AD independently correlated with clinical \npregnancy [OR (odds ratio) = 0.918, 95% CI = 0.856–\n0.985, p = 0.017] and live birth (OR = 0.909, 95% CI \n= 0.845–0.978, p = 0.011) in the subgroup with EM. The \nrASRM score or EFI did not correlate with the preg -\nnancy outcomes. Uterine AD also independently cor -\nrelated with clinical pregnancy (OR = 0.838, 95% CI \n= 0.731–0.960, p = 0.011) and live birth (OR = 0.871, 95% \nCI = 0.770–0.986, p = 0.029) in the subgroup without EM. \nSince the pregnancy outcomes and their predictive fac -\ntors were comparable between the two subgroups, they \nwere combined for analysis. Uterine AD was the only \n\nPage 5 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \nTable 1 General characteristics and reproductive outcomes of adenomyosis subgroups with and without endometriosis\nPatient characteristic With endometriosis (n = 98) Without endometriosis (n = 40) p\nAge (years) 30.00 (28.00, 32.00) 30.00 (29.25, 33.00) 0.099\nAMH (ng/mL) 3.07 (2.26, 4.14) 3.55 (1.92, 6.53) 0.337\nBMI (kg/m2) 20.32 (19.11, 22.51) 21.94 (19.75, 25.03) 0.005\nGravidity 0.00 (0.00, 1.00) 0.00 (0.00, 1.00) 0.910\nParity 0.00 (0.00, 0.00) 0.00 (0.00, 0.00) 0.400\nMenstruation period (days) 6.00 (5.00, 7.00) 7.00 (6.00, 7.00) 0.066\nMenstrual cycle (days) 29.00 (28.00, 30.00) 30.00 (28.25, 33.00) 0.018\nMenstrual phase during ultrasonography 0.179\n Proliferative 54 (55.10) 17 (42.50)\n secretory 44 (44.90) 23 (57.50)\nUterine longitudinal diameter (mm) 49.80 ± 5.67 50.30 ± 6.62 0.653\nUterine transverse diameter (mm) 49.08 ± 5.83 49.63 ± 6.96 0.640\nUterine anteroposterior diameter (mm) 41.00 (37.00, 46.00) 41.50 (37.00, 46.75) 0.860\nUterine volume (cm3) 52.97 (40.00, 64.29) 54.22 (39.45, 67.34) 0.864\nVAS score for menstrual pain 4.00 (2.00, 5.00) 2.00 (0.00, 4.00) 0.016\nClinical pregnancy, n (%) 58 (59.18) 23 (57.50) 0.855\nLive birth, n (%) 53 (54.08) 22 (55.00) 0.922\nMiscarriage, n (%) 5 (83.3) 1 (16.67) 0.669\nData were presented as mean ± standard deviation, median (interquartile range) or frequencies (percentages)\nAMH anti-Müllerian hormone, BMI body mass index, VAS the visual analog scale\nFig. 2 Cumulative spontaneous pregnancy rates of patients with and without endometriosis\n \n\nPage 6 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \nindependent factor correlated with successful clinical \npregnancy (OR = 0.897, 95% CI = 0.842–0.956, p = 0.001) \nand live birth (OR = 0.898, 95% CI = 0.843–0.957, p = \n0.001) in all patients (Table 2).\nComparison of features between patients with and without \nlive birth\nPatients with live births exhibited longer menstrual \ncycles, and smaller uterine diameters as well as volume \ncompared to those without live births. Additionally, the \nparity and VAS scores for menstrual pain in patients with \nlive births were marginally lower (Table 3).\nPregnancy outcomes and the contributing factors in \npatients stratified by age and AMH level\nPatients were categorized into three age groups: < 30 \nyears old (n = 56), 30–34 years old ( n = 61), and ≥ 35 years \nold ( n = 21). Additionally, patients were stratified into \nthree groups according to their AMH levels: < 1.1 ng/ml \n(n = 6), 1.1–3.5 ng/ml ( n = 51), and ≥ 3.5 ng/ml ( n = 44). \nNo significant differences were observed in CPR, LBR, or \nmiscarriage rate among these groups (Table 4).\nIn individuals under 30 years of age, uterine AD was \nthe sole factor significantly associated with clinical preg -\nnancy (OR = 0.884, 95% CI = 0.790–0.988, p = 0.029) and \nlive birth (OR = 0.869, 95% CI = 0.775–0.975, p = 0.017). \nAmong patients aged 30–34 years, uterine AD was \nalso the only variable linked to clinical pregnancy (OR \n= 0.874, 95% CI = 0.790–0.968, p = 0.009) and live birth \n(OR = 0.896, 95% CI = 0.814–0.986, p = 0.024). However, \nin patients aged 35 and above, no variables demonstrated \nan association with the pregnancy outcomes (Table  5). \nOverall, in patients under 35 years, uterine AD was con -\nsistently associated with clinical pregnancy (OR = 0.878, \n95% CI = 0.814–0.946, p = 0.001) and live birth (OR \n= 0.884, 95% CI = 0.821–0.951, p = 0.001).\nIn women with AMH levels of 1.1–3.5 ng/ml, uterine \nAD was significantly correlated with both clinical preg -\nnancy (OR = 0.847, 95% CI = 0.754–0.952, p = 0.005) and \nlive birth (OR = 0.857, 95% CI = 0.765–0.960, p = 0.008). \nSimilarly, among women with AMH levels ≥ 3.5 ng/ml, \nuterine AD showed significant association with clini -\ncal pregnancy (OR = 0.805, 95% CI = 0.693–0.935, p = \n0.005) and live birth (OR = 0.864, 95% CI = 0.758–0.984, \nTable 2 Contributing factors for clinical pregnancy and live birth in patients with or without endometriosis and throughout the entire \ncohort using logistic regression model\nFactors With endometriosis (n=98) Without endometriosis (n=40) All (n=138)\nUnivariate Multivariate Univariate Multivariate Univariate Multivariate\np OR (95% CI) p p OR (95% CI) p p OR (95% CI) p\nAge pregnancy 0.751 0.486 0.578\nlive birth 0.942 0.815 0.571\nAMH pregnancy 0.305 0.423 0.175\nlive birth 0.409 0.176 0.110\nBMI  pregnancy 0.103 0.563 0.104\nlive birth 0.314 0.835 0.951\nGravidity pregnancy 0.898 0.247 0.404\nlive birth 0.279 0.332 0.149\nParity pregnancy 0.688 0.135 0.125\nlive birth 0.189 0.153 0.038\nMenstruation \nperiod\npregnancy 0.292 0.654 0.262\nlive birth 0.455 0.587 0.375\nMenstrual \ncycle\npregnancy 0.803 0.500 0.547\nlive birth 0.419 0.861 0.504\nVAS score pregnancy 0.152 0.442 0.118\nlive birth 0.223 0.670 0.209\nUterine LD pregnancy 0.074 0.066 0.011\nlive birth 0.062 0.138 0.017\nUterine TD pregnancy 0.035 0.263 0.018\nlive birth 0.018 0.497 0.021\nUterine AD pregnancy 0.017 0.918 (0.856-0.985) 0.017 0.011 0.838 (0.731-0.960) 0.011 0.001 0.897 (0.842-0.956) 0.001\nlive birth 0.011 0.909 (0.845-0.978) 0.011 0.029 0.871 (0.770-0.986) 0.029 0.001 0.898 (0.843-0.957) 0.001\nUterine \nvolume\npregnancy 0.021 0.041 0.002\nlive birth 0.014 0.083 0.003\nrASRM score pregnancy 0.081\nlive birth 0.260\nEFI pregnancy 0.384\nlive birth 0.464\nOR odds ratio, CI confidence interval, AMH anti-Müllerian hormone, BMI body mass index, VAS the visual analog scale, LD longitudinal diameter, TD transverse diameter, AD anteroposterior \ndiameter, rASRM the revised American Society for Reproductive Medicine, EFI endometriosis fertility index\n\nPage 7 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \np = 0.014). In the 6 patients with AMH levels < 1.1 ng/ml, \nno variables exhibited an association with pregnancy out-\ncomes (Table 6).\nThe receiver operating characteristic (ROC) curves of \nuterine AD for predicting spontaneous pregnancy \noutcomes in patients with adenomyosis under 35 years\nThe ROC curves of uterine AD for predicting clinical \npregnancy and live birth in patients under 35 years are \npresented in Fig. 3. The optimal cutoff values were 41.5 \nmm for both clinical pregnancy (sensitivity: 0.625, speci -\nficity: 0.652) and live birth (sensitivity: 0.623, specific -\nity: 0.656). Among patients with uterine AD < 41.5 mm, \n71.43% (45/63) reached a clinical pregnancy, and 66.67% \n(42/63) had a successful live birth.\nDiscussion\nIt has been observed that in early stages, adenomyosis \nlesion shows preponderance in the sagittal midline of the \nmid-corporal and fundal part of the uterus under MRI \nand TVS. Pathologically, adenomyotic foci are generally \nlocalized in the posterior or anterior uterine walls, with \ninfrequent occurrence in the lateral walls. In a previous \nstudy, we demonstrated that uterine AD, rather than \nother dimensions or volume, independently correlated \nwith the diagnosis of adenomyosis under TVS [ 16]. A \nuterine AD of 38.5 mm (sensitivity: 0.723, specificity: \n0.667) and 39.5 mm (sensitivity: 0.703, specificity: 0.723) \npredicted the diagnosis of adenomyosis in patients with \nand without EM, respectively. Similar results were also \nreported by other researchers [ 17]. These results sug -\ngest that increased uterine AD is a crucial feature of \nadenomyosis.\nUterine AD also independently correlated with the \nVAS scores for menstrual pain regardless of the presence \nof EM. A uterine AD of 39.5 mm predicted dysmenor -\nrhea (VAS ≥ 4) in patients with (sensitivity: 0.806, speci -\nficity: 0.656) and without (sensitivity: 0.721, specificity: \n0.658) EM. In the present study, uterine AD was found to \nindependently correlate with the spontaneous pregnancy \nTable 3 General characteristics of patients with and without live birth\nPatient characteristic With live birth (n = 75) Without live birth (n = 63) p\nAge (years) 30.00 (28.00, 32.00) 30.00 (28.00, 33.00) 0.624\nAMH (ng/mL) (n = 101) 3.11 (1.99, 4.00) 3.20 (2.23, 5.91) 0.316\nBMI (kg/m2) 20.83 (19.20, 22.72) 21.23 (19.29, 23.05) 0.622\nGravidity 0.00 (0.00, 1.00) 0.00 (0.00, 1.00) 0.232\nParity 0.00 (0.00, 0.00) 0.00 (0.00, 0.00) 0.057\nMenstruation period (days) 6.00 (5.00, 7.00) 6.00 (6.00, 7.00) 0.414\nMenstrual cycle (days) 30.00 (28.00, 30.00) 29.00 (28.00, 30.00) 0.031\nMenstrual phase during ultrasonography 0.841\n Proliferative 38 (50.67) 33 (52.38)\n secretory 37 (49.33) 30 (47.62)\nUterine longitudinal diameter (mm) 48.81 ± 5.18 51.29 ± 6.53 0.014\nUterine transverse diameter (mm) 48.00 (44.00, 52.00) 50.00 (46.00, 54.00) 0.039\nUterine anteroposterior diameter (mm) 40.00 (36.00, 43.00) 43.00 (39.00, 48.00) 0.001\nUterine volume (cm3) 48.67 (38.59, 61.68) 60.41 (43.14, 73.43) 0.003\nVAS score for menstrual pain 3.00 (2.00, 4.00) 4.00 (2.00, 6.00) 0.091\nThe presence of EM 53 (70.67) 45 (71.43) 0.922\nrASRM score 26.00 (4.00, 40.00) 26.00 (3.50, 76.50) 0.635\nEFI 8.00 (6.00, 8.50) 7.00 (6.00, 9.00) 0.619\nData were presented as mean ± standard deviation, median (interquartile range) or frequencies (percentages)\n AMH anti-Müllerian hormone, BMI body mass index, VAS the visual analog scale, rASRM the revised American Society for Reproductive Medicine, EFI endometriosis \nfertility index\nTable 4 The pregnancy outcomes of patients classified according to age or anti-Müllerian hormone (AMH)\nAge (year) < 30 (n = 56) 30–34  (n = 61) ≥ 35  (n = 21) p\nPregnancy 35 (62.50) 34 (55.74) 12 (57.14) 0.776\nLive birth 32 (57.14) 32 (52.46) 11 (52.38) 0.870\nMiscarriage 3 (5.36) 2 (3.28) 1 (4.76) 1.000\nAMH (ng/ml) < 1.1 (n = 6) 1.1–3.5  (n = 51) ≥ 3.5  (n = 44) p\nPregnancy 4 (66.67) 28 (54.90) 24 (54.54) 0.900\nLive birth 3 (50.00) 27 (52.94) 22 (50.00) 0.948\nMiscarriage 1 (16.67) 1 (1.96) 2 (4.55) 0.249\nData were presented as frequencies (percentages)\n\nPage 8 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \nTable 5 Contributing factors for pregnancy outcomes in patients stratified by age using logistic regression model\nFactors < 30 (n = 56) 30–34  (n = 61) ≥ 35  (n = 21)\nUnivariate Multivariate Univariate Multivariate Univariate\np OR (95% CI) p p OR (95% CI) p  P\nAge pregnancy 0.917 0.755 0.745\nlive birth 0.838 0.696 0.606\nmiscarriage 0.655 0.105 0.808\nAMH pregnancy 0.596 0.147 0.774\nlive birth 0.359 0.159 0.774\nmiscarriage 0.341 0.801 -\nBMI pregnancy 0.116 0.929 0.259\nlive birth 0.398 0.946 0.483\nmiscarriage 0.116 0.654 0.392\nGravidity pregnancy 0.281 0.502 0.565\nlive birth 0.153 0.494 0.834\nmiscarriage 0.267 0.853 0.998\nParity pregnancy 0.204 0.094 0.205\nlive birth 0.060 0.126 0.469\nmiscarriage 0.068 0.999 0.999\nMenstruation period pregnancy 0.580 0.302 0.160\nlive birth 0.615 0.476 0.173\nmiscarriage 0.983 0.463 0.912\nMenstrual cycle pregnancy 0.314 0.310 0.219\nlive birth 0.231 0.265 0.103\nmiscarriage 0.378 0.591 0.994\nVAS score pregnancy 0.710 0.097 0.751\nlive birth 0.665 0.226 0.764\nmiscarriage 0.810 0.344 0.977\nUterine longitudinal diameter pregnancy 0.160 0.076 0.271\nlive birth 0.052 0.229 0.400\nmiscarriage 0.107 0.153 0.653\nUterine transverse diameter pregnancy 0.058 0.207 0.402\nlive birth 0.036 0.333 0.344\nmiscarriage 0.349 0.443 0.601\nUterine anteroposterior diameter pregnancy 0.029 0.884 (0.790–0.988) 0.029 0.009 0.874 (0.790–0.968) 0.009 0.437\nlive birth 0.017 0.869 (0.775–0.975) 0.017 0.024 0.896 (0.814–0.986) 0.024 0.351\nmiscarriage 0.056 0.386 0.494\nUterine volume pregnancy 0.056 0.028 0.256\nlive birth 0.019 0.070 0.268\nmiscarriage 0.100 0.249 0.791\nOR odds ratio, CI confidence interval, AMH anti-Müllerian hormone, BMI body mass index, VAS the visual analog scale, rASRM the revised American Society for Reproductive Medicine, EFI endometriosis fertility index\n\nPage 9 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \noutcomes in patients with adenomyosis under 35 years, \nregardless of whether EM was present. A uterine AD of \n< 41.5 mm forecasted a successful live birth (sensitivity: \n0.623, specificity: 0.656). We used to believe that an obvi-\nously enlarged uterus might compromise fertility; none -\ntheless, our results suggest that the detrimental effects \nof adenomyosis on fertility may occur much earlier than \npreviously assumed. Collectively, these findings under -\nscore uterine AD as a critical marker of adenomyosis \nprogression and its predictive potential for symptoms \nsuch as dysmenorrhea and fertility impairment.\nIt was noteworthy that in patients aged 35 years and \nolder with adenomyosis, uterine AD did not serve as \na predictor in pregnancy outcomes, which may be \nattributed to confounding factors that potentially obscure \nits predictive capacity in this older cohort. These find -\nings enhanced our understanding of the role of prognos -\ntic factors across different age groups. Regarding AMH, \nuterine AD correlated with pregnancy outcomes in \npatients with AMH levels ≥ 1.1 ng/ml or higher, whereas \nno correlation in patients with AMH levels below 1.1 ng/\nml. However, these results should be interpreted with \ncaution due to the limited sample size of only six patients \nin the subgroup with AMH levels below 1.1 ng/ml.\nAlthough surgical eradication of EM probably did \nnot confer benefits for IVF outcomes [ 18], it enhanced \nthe spontaneous pregnancy rate compared to patients \nreceiving only diagnostic-laparoscopy [ 19]. As a result, \nTable 6 Contributing factors for pregnancy outcomes in patients stratified by anti-Müllerian hormone (AMH) using logistic regression \nmodel\nFactors < 1.1 ng/ml (n=6) 1.1-3.5 ng/ml (n=51) ≥ 3.5 ng/ml (n=44)\nUnivariate Univariate Multivariate Univariate Multivariate\np p OR (95% CI) p p OR (95% CI) p\nAge pregnancy 0.998 0.626 0.151\nlive birth 0.305 0.781 0.220\nmiscarriage 0.617 0.557 0.770\nBMI pregnancy 0.285 0.365 0.126\nlive birth 0.602 0.382 0.235\nmiscarriage - 0.991 0.495\nGravidity pregnancy 0.407 0.182 0.259\nlive birth 0.999 0.162 0.414\nmiscarriage - 0.639 0.999\nParity pregnancy 0.366 0.134 0.133\nlive birth 0.999 0.172 0.185\nmiscarriage - 0.999 1.000\nMenstruation period pregnancy 0.403 0.338 0.806\nlive birth 0.390 0.661 0.505\nmiscarriage - 0.995 0.344\nMenstrual cycle pregnancy 1.000 0.294 0.727\nlive birth 1.000 0.283 0.429\nmiscarriage - 0.796 0.252\nVAS score pregnancy 1.000 0.136 0.034\nlive birth 1.000 0.255 0.106\nmiscarriage 1.000 0.996 0.230\nUterine longitudinal diameter pregnancy 0.490 0.013 0.025\nlive birth - 0.022 0.136\nmiscarriage - 0.534 0.138\nUterine transverse diameter pregnancy 0.997 0.040 0.028\nlive birth 0.998 0.070 0.070\nmiscarriage 0.999 0.411 0.478\nUterine anteroposterior diameter pregnancy 0.998 0.005 0.847 (0.754-0.952) 0.005 0.005 0.805 (0.693-0.935) 0.005\nlive birth 0.997 0.008 0.857 (0.765-0.960) 0.008 0.028 0.864 (0.758-0.984) 0.014\nmiscarriage 0.997 0.856 0.217\nUterine volume pregnancy 0.316 0.020 0.008\nlive birth - 0.030 0.037\nmiscarriage - 0.526 0.203\nOR odds ratio, CI confidence interval, AMH anti-Müllerian hormone, BMI body mass index, VAS the visual analog scale, LD longitudinal diameter, TD transverse \ndiameter, AD anteroposterior diameter, rASRM the revised American Society for Reproductive Medicine, EFI endometriosis fertility index\n\nPage 10 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \noperative laparoscopy can be offered as a treatment \noption for EM-associated infertility [ 20]. EFI has been \nproven to predict the conception rates following laparo -\nscopic eradication of EM [ 9, 14]. Nonetheless, our study \nrevealed that the EM group exhibited comparable spon -\ntaneous pregnancy outcomes to those without EM, while \nEFI did not predict pregnancy outcomes in this cohort. \nThe functional status of the tubes and fimbriae is one \nof the main focuses of the EFI scale [ 14]. EM can lead \nto the formation of adhesions and scarring, resulting in \ntubal obstruction [ 7], which may contribute to a low EFI \nscore. These patients were excluded from the cohort due \nto ineligibility for natural conception ascribed to tubal \nfactors. Consequently, the majority of the EM patients \nincluded in this study had an EFI score above 5 (80/98, \n81.63%), which may account for the lack of predictive \npower of EFI for pregnancy outcomes in our analysis.\nBy inducing a hypoestrogenic state, long-acting GnRH-\na inhibits the proliferation of ectopic endometrial cells \nand attenuates inflammatory responses, thus prob -\nably improving endometrial receptivity [ 21, 22]. In EM \npatients, post-surgical administration of GnRH-a, as \ncompared to no medical therapy or placebo, may confer \nbenefits in achieving pregnancy [ 23]. The scenario for \npatients with adenomyosis, however, is more complex. \nGnRH-a administration prior to frozen embryo trans -\nfer, rather than fresh embryo transfer, has been shown to \nenhance pregnancy rates [ 24]. In those receiving GnRH-\na pretreatment before frozen embryo transfer, a uterine \nvolume of < 98.81 cm³ was associated with improved \npregnancy outcomes [ 25], suggesting that a specific \nsubgroup of patients may derive greater benefit from \nGnRH-a therapy.\nWhile distinct from assisted reproduction, in which \nGnRH-a may be administered prior to each embryo \ntransfer, GnRH-a can be utilized solely for a single course \nbefore attempting natural conception. Evidence sup -\nporting the role of GnRH-a in enhancing spontaneous \npregnancy in patients with adenomyosis is limited. In a \nprospective study, Xie et al. administered Triptorelin 3.75 \nmg for 6 months to infertile patients diagnosed with ade -\nnomyosis. Of the 45 women, 12 (26.7%) became pregnant \nwhen menstruation was expected to resume. GnRH-a \nmay enhance spontaneous pregnancy by improving uter -\nine elasticity, despite the study’s lack of a control group \n[26]. However, the follow-up duration is not long enough \nto observe either the outcomes of the known pregnancy \nor the pregnancy after menstruation resumption. The \nhypoestrogenic efficacy of GnRH-a typically persists for \na few months, as evidenced by the resumption of men -\nstruation. However, several studies have observed that \nthe relief of pain symptoms lasted up to one year after \nthe final dose of the medication, suggesting a long-term \nbenefit of this treatment modality [ 27]. In the current \nstudy, a subset of infertile women with adenomyosis, yet \nwithout other apparent contributing factors to infertility \nsuch as EM, successfully achieved live births. This find -\ning seems to imply a possibility of potential long-term \nbenefits of GnRH-a in improving spontaneous pregnancy \noutcomes. However, the lack of a control group necessi -\ntates a cautious interpretation of these results. Further -\nmore, the absence of data regarding morphological or \nFig. 3 Receiver operating characteristic (ROC) curves for clinical pregnancy ( A) and live birth ( B) estimated by uterine anteroposterior diameter (AD) in \npatients under 35 years with adenomyosis\n \n\nPage 11 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \nelastic changes in the uterus following GnRH-a treat -\nment renders it uncertain whether differential responses \nto GnRH-a influence pregnancy outcomes.\nSymptomatic adenomyosis, characterized by condi -\ntions such as dysmenorrhea, was reported to have a \nsignificant adverse effect on IVF outcomes [ 28]. In our \nstudy, although the VAS score for menstrual pain showed \na marginal difference between patients with and without \na live birth, it did not serve as a predictor for spontane -\nous pregnancy outcomes according to the logistic regres -\nsion analysis. Similarly, another study also reported that \nneither the VAS score nor the duration of dysmenorrhea \ninfluenced the likelihood of achieving a live birth (includ-\ning both IVF and spontaneous pregnancies) in patients \nwith concurrent adenomyosis and EM [9].\nThe present study has several strengths. To our knowl -\nedge, this is the first study focusing on the predictor for \nspontaneous pregnancy outcomes in patients with ade -\nnomyosis. Through laparoscopy and hysteroscopy, we \nmeticulously excluded or eliminated other conditions \nthat could affect natural conception. Then, the isolated \nimpact of adenomyosis on spontaneous pregnancy rates \ncan be accurately assessed. We also excluded patients \nwith factors that could affect uterine measurements, \nthereby allowing the determination of the accurate cutoff  \nvalue of uterine AD in predicting pregnancy outcomes. \nOur results revealed that adenomyosis may exert a det -\nrimental effect on fertility at a very early stage. The selec -\ntion of optimal, evidence-based treatment strategies for \nadenomyosis in fertility clinics remains challenging due \nto the scant evidence linking fertility outcomes with the \nextent of adenomyosis [ 5]. Our findings may offer valu -\nable insights in guiding therapeutic choice.\nThis study is subject to several limitations. Firstly, it is a \nretrospective analysis with a relatively small sample size, a \nconstraint partially resulting from the rigorous exclusion \ncriteria, and lacks an external control group of infertile \nwomen without gynecological disease. Secondly, there is \na possibility of inter-operator variability in the ultrasound \nmeasurements. Thirdly, an internal control group of ade -\nnomyosis patients that did not utilize GnRH-a was absent \ndue to patient interest considerations. Additionally, data \non morphological or elastic changes in the uterus follow -\ning GnRH-a treatment, which could indicate differential \nresponses to the therapy, were absent. Consequently, \ndefinitive conclusions regarding the role of GnRH-a \ntreatment in enhancing spontaneous conception among \npatients with adenomyosis cannot be drawn. Fourthly, \nthe study was unable to reach a conclusion regarding the \nprognostic role of uterine AD in patients with preop -\nerative AMH levels below 1.1 ng/mL due to the limited \nsample size. Additionally, the study did not assess the \nassociation between postoperative AMH levels and preg -\nnancy outcomes because of incomplete data availability. \nThese limitations underscore the need for further pro -\nspective studies with larger sample sizes. Lastly, the study \ndid not evaluate the impact of adenomyosis location on \npregnancy outcomes owing to the limitations of ultra -\nsound images inherent in the retrospective study design. \nAlthough the position of adenomyosis on the posterior \nor anterior uterine wall may not significantly affect LBR \n[29], adenomyosis affecting the inner myometrium has \nbeen observed more frequently in patients experiencing \nrecurrent pregnancy loss [ 30]. The pathologic condition \nof the inner myometrium is characterized by increased \nthickness, a key indicator of adenomyosis on TVS and \nMRI, which probably contributes to increased uterine \ndiameters. Further large-scale prospective studies are \nrequired to determine whether the inner myometrium \nthickness can predict spontaneous pregnancy outcomes.\nConclusions\nThis research identified that uterine AD, which indicates \nthe progression of adenomyosis, is an independent pre -\ndictor for spontaneous pregnancy outcomes in affected \npatients under 35 years. A uterine AD of < 41.5 mm \n(sensitivity: 0.623, specificity: 0.656) predicts successful \nlive births. These findings illuminate the early detrimen -\ntal effects of adenomyosis on fertility and offer critical \ninsights that may assist in making therapeutic decisions.\nAbbreviations\nART  Assisted reproductive technique\nCPR  Clinical pregnancy rate \nLBR  Live birth rate\nAD   Anteroposterior diameter \nIVF  In vitro fertilization \nGnRH-a  Gonadotropin-releasing hormone agonist \nEM  Endometriosis\nMRI   Magnetic resonance imaging \nEFI  Endometriosis fertility index \nTVS   Transvaginal ultrasonography \nAMH  Anti-Müllerian hormone \nLD  Longitudinal diameter \nTD  Transversal diameter \nVAS  Visual analog scale\nrASRM  The revised American Society for Reproductive Medicine \nBMI  Body mass index \nAcknowledgements\nNot applicable.\nAuthors’ contributions\nJ. L. contributed to data collection, data analysis, follow-up, and manuscript \npreparation; M. S. contributed to data collection and follow-up; P . L. \nparticipated in the supervision of the study and performed surgeries; T. Z. \nconceived and designed the study, performed surgeries, analyzed data, \nand prepared the manuscript. All authors reviewed and approved the final \nmanuscript.\nFunding\nThe research is supported by the National Natural Science Foundation of \nChina (82301858) and the Shanghai Clinical Research Center for Gynecological \nDiseases (22MC1940200).\nData availability\nAll data supporting this study are included in this manuscript.\n\nPage 12 of 12\nLi et al. BMC Pregnancy and Childbirth           (2025) 25:727 \nDeclarations\nEthics approval and consent to participate\nThis study was conducted in accordance with the ethical principles outlined \nin the Declaration of Helsinki, and was approved by the ethics committee \nof the Obstetrics and Gynecology Hospital of Fudan University (Code: 2024 \n− 148). The verbal informed consent was obtained from all patients by \ntelephone connection.\nConsent for publication\nNot applicable.\nCompeting interests\nThe authors declare no competing interests.\nAuthor details\n1Department of Gynecology, Obstetrics and Gynecology Hospital of \nFudan University, 419 Fangxie Road, Shanghai 200011, China\n2Department of Gynecology, Affiliated Huaian Hospital of Xuzhou \nMedical University, 62 South Huaihai Road, Huaian,  \nJiangsu Province 223001, China\nReceived: 9 December 2024 / Accepted: 10 June 2025\nReferences\n1. Kho KA, Chen JS, Halvorson LM. Diagnosis, evaluation, and treatment of \nadenomyosis. JAMA. 2021;326(2):177–8.\n2. Bender Atik R, Christiansen OB, Elson J, et al. ESHRE guideline: recurrent preg-\nnancy loss: an update in 2022. Hum Reprod Open. 2023;2023(1):hoad002.\n3. Busnelli A, Barbaro G, Pozzati F, et al. 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