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High anti-Müllerian hormone level as a predictor of poor pregnancy outcomes in women with polycystic ovary syndrome undergoing in vitro fertilization/intracytoplasmic sperm injection: a retrospective cohort study

Reproductive Biology and Endocrinology volume 23, Article number: 15 (2025) Cite this article

Abstract

Objective

To study the correlation between anti-Müllerian hormone levels and pregnancy outcomes after in vitro fertilization/intracytoplasmic sperm injection in women with polycystic ovary syndrome, which remains controversial.

Methods

This retrospective cohort study recruited 4,719 women with infertility and polycystic ovary syndrome aged 20–40 years who underwent treatment at the Reproductive Center of Peking University Third Hospital between February 2017 and June 2023. We divided the participants into three groups according to the 25th and 75th percentile cutoffs of serum anti-Müllerian hormone: low (≤ 4.98 ng/mL, n = 1,198), average (4.98 − 10.65 ng/mL, n = 2,346), and high (≥ 10.65 ng/mL, n = 1,175). Pregnancy outcomes included live birth rate, miscarriage rate, clinical pregnancy rate, and cumulative live birth rate.

Results

The live birth rate for fresh embryo transfer was 39.8%, 35.9%, and 30.4% in the low, average, and high anti-Müllerian hormone groups, respectively. The miscarriage rate was 11.3%, 17.1%, and 21.8% in the low, average, and high anti-Müllerian hormone groups, respectively. Significant intergroup differences were observed in the live birth rate (P = 0.017) and miscarriage rate (P = 0.018). No significant intergroup difference was observed in the clinical pregnancy rate (P = 0.204) or cumulative live birth rate (P = 0.423). After adjusting the confounders by multivariable logistic regression analysis, anti-Müllerian hormone was associated with decreased live birth rate in the high anti-Müllerian hormone group compared with that in the low anti-Müllerian hormone group (odds ratio: 0.629, 95% confidence interval: 0.460–0.860). Anti-Müllerian hormone was associated with increased miscarriage rate in the average and high anti-Müllerian hormone groups compared with that in the low anti-Müllerian hormone group (average vs. low: odds ratio: 1.592, 95% confidence interval: 1.017–2.490); high vs. low: odds ratio: 2.045, 95% confidence interval: 1.152–3.633).

Conclusion

High anti-Müllerian hormone is a prognostic factor for reduced live birth rate after fresh embryo transfer in women with polycystic ovary syndrome aged 20–40 years undergoing in vitro fertilization/intracytoplasmic sperm injection, and is associated with increased miscarriage rate in these patients.

Introduction

Anti-Müllerian hormone (AMH) is synthesized by pre-antral and small antral follicles in women and belongs to the members of the transforming growth factor β superfamily [1]. AMH counteracts the growth-promoting function of follicle-stimulating hormone (FSH) in granulosa cells (GCs) by reducing follicle sensitivity to FSH [2]. Therefore, a normal AMH concentration is essential for inhibiting primordial follicle recruitment, follicular development, and regulating dominant follicle selection [3]. AMH assesses ovarian reserve and predicts ovarian response to assisted reproductive technology in healthy women [4].

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder causing infertility in women of reproductive age, with a worldwide prevalence of 5%–18% [5]. PCOS phenotypes include oligo- or anovulation, hyperandrogenism, polycystic ovarian morphology, and metabolic disorders [6]. The pathological mechanisms underlying PCOS are complex. An ovarian follicular arrest is an important pathophysiological feature of PCOS, resulting from insufficient FSH secretion or FSH inhibition [7]. AMH levels in women with PCOS are 2- to-fourfold higher than those in healthy females. Excessive AMH inhibits the growth-promoting function of FSH, leading to follicular arrest in women with PCOS [8]. In addition, excessive AMH impairs aromatase catalytic activity stimulated by FSH, preventing the conversion of testosterone and androstenedione to estrogen in GCs [3]. Insufficient estradiol synthesis in the follicular microenvironment may lead to impaired follicular development in women with PCOS [9]. Therefore, excessive AMH may be associated with PCOS severity, contrary to its role in healthy females [10]. Recently, researchers have focused on the correlation between AMH levels and pregnancy outcomes in women with PCOS undergoing in vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI). High AMH levels may be beneficial for clinical pregnancy in women with PCOS [11]. However, AMH levels did not correlate with pregnancy outcomes in another study involving 418 women with PCOS [12]. In contrast, Tal et al. examined 184 women with PCOS and found a negative relationship between AMH levels and the live birth rate (LBR) [13]. These findings indicate that the correlation between AMH and pregnancy outcomes in women with PCOS undergoing IVF/ICSI remains controversial. Therefore, this study included large sample size representative of the nationwide population in China. We aimed to evaluate the correlation between AMH levels and pregnancy outcomes after IVF/ICSI in women with PCOS.

Materials and methods

Subjects

This retrospective cohort study included 5,844 women with PCOS who underwent IVF/ICSI at the Reproductive Center of Peking University Third Hospital between February 2017 and June 2023. The inclusion criteria were as follows: (i) women aged 20–40 years, (ii) male or tubal factor infertility, and (iii) complete clinical data. The exclusion criteria were as follows: (i) recurrent miscarriages or abnormal parental karyotyping; (ii) history of malignancies; (iii) endocrinological diseases, including endometriosis, hypothalamic tumors, and hyperprolactinemia; (iv) history of ovarian surgery; and (v) missing data regarding baseline characteristics. We included 4,719 women in the final analysis. This study was approved by the Medical Science Research Ethics Committee of Peking University Third Hospital (Reference Number M3032464). All participants provided written informed consent.

Ovarian stimulation and IVF/ICSI

A standardized controlled ovarian stimulation (COS) regimen was administered by clinicians. All patients were administered gonadotropin-releasing hormone antagonists or agonists. Ultrasonography indicated that ≥ 2 leading follicles had reached 18 mm in diameter. Clinicians administered recombinant human chorionic gonadotropin (HCG) (250 µg; Eiser, Serono, Germany), triptorelin (0.2 mg; Diphereline, Ipsen Pharma Biotech, France) combined with HCG, or triptorelin only to induce oocyte maturation on trigger day. Oocytes were retrieved 34–36 h after administration, followed by insemination via IVF or ICSI. Embryo cleavage or blastocyst transfer was performed on day 3 or 5 after oocyte retrieval. The criteria for converting to freeze-all embryos was performed as follows: The serum E2 levels ≥ 15,000 pmol/L on trigger day, oocytes retrieval numbers ≥ 20, an unsuitable endometrium, elevated progesterone levels > 6 nmol/L, and other personal reasons. These patients and patients without live births from fresh transfer subsequently received frozen-thawed embryo transfer (FET).

Laboratory tests

Serum AMH concentration was measured using a fully automatic chemiluminescence immunoassay analyzer (ADVIA Centaur XP, Siemens Healthcare Diagnostics) within 6 months before COS. Baseline serum hormone levels were measured on the second day of the menstrual cycle during the COS.

Study outcomes

A live birth refers to the delivery of ≥ 1 live fetus after 28 weeks of gestation. Miscarriage refers to pregnancy loss before 28 weeks of gestation. Clinical pregnancy refers to detecting the presence of gestational sacs in the uterus via ultrasonography. Cumulative live births resulting from a living fetus (or living fetus) occur in fresh and subsequent freeze–thaw transfers of one retrieval cycle. We analyzed cumulative live birth rates (CLBRs) of women involved between February 2017 and December 2021, considering that the pregnancy outcomes of embryos retrieved in 2022 were not completely obtained.

Statistical analysis

SPSS version 28.0 (SPSS Inc., Chicago, IL, USA) was used for all statistical analyses. Categorical data were presented as corresponding percentages and frequencies, continuous data with normal distribution as mean ± standard deviation, and continuous data with non-normal distribution as median (interquartile range). The chi-square test was used for categorical variables, one-way analysis of variance for continuous data with normal distribution (Bonferroni correction in the post hoc test), and the Kruskal‒Wallis test for continuous data with non-normal distribution. Multivariable logistic regression analysis was conducted to adjust for relevant confounders. The odds ratio (OR) and standard 95% confidence interval (CI) were calculated to evaluate differences. Statistical significance was set at a two-sided P-value of < 0.05.

Results

We recruited 5,844 women with infertility and PCOS. We screened 4,719 women with PCOS for the final analysis (Fig. 1). We divided all participants into three groups using the 25th and 75th percentile cutoffs for serum AMH concentrations. In the low AMH group, 1,198 women with PCOS had AMH levels of ≤ 4.98 ng/mL. In the average AMH group, 2,346 women with PCOS had AMH levels between 4.98 and 10.65 ng/mL. In the high AMH group, 1,175 women with PCOS had AMH levels of ≥ 10.65 ng/mL.

Fig. 1
figure 1

Flow chart of the study cohort population. AMH, anti-Müllerian hormone; ICSI, intracytoplasmic sperm injection; IVF, in vitro fertilization; PCOS, polycystic ovary syndrome

Full size image

We compared the baseline features of the three groups (Table 1). Age and body mass index (BMI) significantly decreased in women from the low to the high AMH groups. The baseline FSH level decreased, whereas the baseline luteinizing hormone level increased from the low to the high AMH group. The maximal estradiol (E2) concentration was 42,043 pmol/L, 58,601 pmol/L, and 68,250 pmol/L in the low, average, and high AMH group. A significant increase was observed in the number of antral follicles from the low to the high AMH group. The initial therapeutic dose, gonadotropin duration, and gonadotropin dose significantly decreased from the low to the high AMH group, indicating a positive correlation between AMH and ovarian response to COS in women with PCOS. In addition, the endometrium on the day of hCG administration in the high AMH group was slightly thinner than that in the low and average AMH groups. No significant difference was observed in infertility factors, infertility type, or infertility years among the groups.

Table 1 Baseline features of three groups
Full size table

We compared the characteristics and pregnancy outcomes among the three groups (Table 2). The ovarian stimulation syndrome (OHSS) rate was 0.9%, 0.8%, and 2.0% in the low, average, and high AMH group (P = 0.004). The number of oocytes retrieved and good-quality embryos per cycle significantly increased from the low to the high AMH group. No significant difference was observed in the fertilization rate, number, and embryo type transferred in fresh cycles among the groups. The fresh ET cycle rate significantly decreased from the low to the high AMH group (52.4%, 39.0%, and 27.1%, respectively; P < 0.001).

Table 2 Cycle characteristics and pregnancy outcomes of the three groups
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Importantly, the LBR of fresh ET was 39.8%, 35.9%, and 30.4% in the low, average, and high AMH groups, respectively. A significant intergroup difference was observed in LBR (P = 0.017). Post hoc tests indicated that the LBR in the high AMH group was lower than that in the low AMH group. The clinical pregnancy rate (CPR) for fresh ET was 44.9%, 43.3%, and 38.9% in the low, average, and high AMH groups, respectively. No significant difference was observed in the CPR of fresh ET among the groups (P = 0.204). The twin/multiple pregnancy rate for fresh ET was 17.0%, 16.5% and 13.6% in the low, average, and high AMH groups. There was no difference in the twin/multiple pregnancy rate for fresh ET among three groups (P = 0.432). The miscarriage rates of fresh ET were 11.3%, 17.1%, and 21.8% in the low, average, and high AMH groups, respectively. A significant intergroup difference was observed in miscarriage rate (P = 0.018). Post hoc tests indicated that the miscarriage rate in the average and the high AMH groups was higher than that in the low AMH group. CLBR was 55.2%, 57.1%, and 58.1% in the low, average, and high AMH groups, respectively. No significant difference was observed in CLBR among the groups (P = 0.423).

Subsequently, we conducted multivariable logistic regression analysis to analyze the correlation between AMH levels and pregnancy outcomes of fresh ET in women with PCOS. Table 3 presents the study results. Notably, the LBR for fresh ET was decreased in the high AMH group compared with that in the low AMH group (OR: 0.629, 95% CI: 0.460–0.860). The miscarriage rate for fresh ET was increased in the average and high AMH groups compared with that in the low AMH group (average vs. low: OR: 1.592, 95% CI: 1.017–2.490; high vs. low: OR: 2.045, 95% CI: 1.152–3.633). Finally, multivariable logistic regression analysis revealed no significant association between AMH levels and CLBR (Supplementary Table 1).

Table 3 Logistic regression analysis of factors that correlated with pregnancy outcomes of fresh ET
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Discussion

This retrospective study investigated whether AMH affects pregnancy outcomes among women with PCOS aged 20–40 years undergoing IVF/ICSI. Excessive AMH was correlated with a decreased LBR after fresh ET and was correlated with an increased miscarriage rate during fresh ET.

The correlation between AMH level and BMI has been explored in previous studies. AMH levels are reportedly inversely correlated with BMI in women with PCOS [14]. Lefebvre et al. reported that AMH was lower in women with PCOS with normal weight than in those with obesity [15]. This study indicated a negative correlation between AMH levels and BMI in women with PCOS, consistent with previous findings. However, the mechanisms underlying this correlation remain unclear. One possible explanation may be the unbalanced secretion of leptin in women with PCOS [16]. Leptin is secreted by adipocytes, which are the main components of adipose tissue [17]. Elevated leptin levels inhibit AMH expression in GCs [18]. Therefore, women with higher BMI and PCOS have more adipose tissue and secrete more leptin, leading to decreased AMH levels.

Previous study found the correlation between AMH and endometrium in PCOS. Su et al. reported that the endometrium on the transfer day was thinner in women with PCOS with AMH levels of ≥ 12 ng/mL than in those with AMH levels of < 12 ng/mL [19]. The mechanism underlying the relationship between AMH and the endometrium remains controversial. Recently, Paulson et al. reported the expression of AMH and AMH type II receptors in the endometria of women with PCOS [20]. AMH inhibits the growth of endometrial cancer cells by regulating several cell pathways and cellular factors [21, 22]. Besides, AMH expression in endometriotic tissues suppressed the viability and growth of endometriotic cells [23]. These studies provide a possible explanation that overexpressed AMH may inhibit endometrial cell viability and function in women with PCOS [24], leading to decreased endometrial thickness in women with high AMH levels. In this study, endometrial thickness on hCG day was slightly lower in the high AMH group than in the low and average AMH groups. This difference in thickness was small and clinically insignificance, which may be due to the large sample size.

In our study, no significant association was observed between AMH levels and CPR. Tal et al. reported that women with PCOS and with AMH levels of > 10 ng/mL had higher CPR than those with AMH levels of ≤ 10 ng/mL [11]. In another study, CPR was decreased in the high AMH group compared with in the low AMH group [25]. Nevertheless, Su et al. reported that no significant CPR differences were observed between women with AMH levels of ≥ 12 ng/mL and those with AMH levels of < 12 ng/mL [19]. In this study, we enrolled 4,719 women with PCOS in the analysis using 4.98 and 10.65 AMH levels as the 25th and 75th percentile cutoffs, respectively. In this study, no significant difference was observed in the CPR of fresh ET among the groups.

Whether AMH level affects the occurrence of miscarriage in women with PCOS remains debatable [26]. A study reported that AMH level of ≥ 3.99 ng/mL was a risk factor for early miscarriage in women undergoing IVF/ICSI [27]. In contrast, Liu et al. reported that women with AMH levels of ≥ 5.71 ng/mL had lower early miscarriage rates than women with AMH levels of ≤ 2.25 ng/mL [12]. Both studies included women with and without PCOS in their analysis. Therefore, the results did not reveal the condition of the women with PCOS. This study revealed that the miscarriage rate was higher in the high AMH group than in the low AMH group among women with PCOS undergoing IVF/ICSI. However, the mechanisms underlying this correlation remain unclear. Gleicher et al. reported that excessive AMH was correlated with spiking miscarriage rates across all ages [28]. They suggested that AMH may be an unknown “embryo quality factor.” In addition, premature delivery was twofold higher in women with PCOS than in healthy women [24]. Excessive AMH was significantly correlated with preterm birth [29]. All participants with AMH levels of > 20 ng/ML delivered preterm infants, while women who delivered at term showed AMH levels that were similar to those of healthy females [29]. AMH and its receptor have been detected in the endometrium, which could directly or indirectly affect endometrial function [20]. In addition, excessive AMH impairs myometrial maintenance, remodeling, and the inhibitory effect of contractility, preventing the fetus from developing in the uterus [29]. In addition, AMH is positively associated with the androgen concentration in women with PCOS [30]. Excessive androgen concentration in the endometrial environment impairs endometrial function and receptivity by altering the expression of factors and signals, including estrogen receptor, progesterone receptor, and proinflammatory NF-κB signaling [24, 31, 32]. Hyperandrogenism impairs trophoblast invasion and placental mitochondrial function, increasing the risk of miscarriage [33, 34]. Therefore, we considered that excessive AMH may lead to increased miscarriages in women with PCOS through the above possible mechanisms.

Importantly, we observed a negative correlation between AMH levels and LBR in patients with PCOS. However, no significant among-group difference was found in LBR using 4.91 and 10.88 as the 25th and 75th percentile cutoffs, respectively [12]. Tal et al. reported that excessive AMH was correlated with lower LBR using 3.32 and 8.27 as the 25th and 75th percentile cutoffs, respectively [13]. In addition, a negative relationship was observed between AMH levels and LBR in women with PCOS aged < 30 years, using 6.77 and 14.30 as the 25th and 75th percentile cutoffs, respectively [25]. In this study, we involved 4,719 women with PCOS aged 20–40 years in the analysis using 4.98 and 10.65 as the 25th and 75th percentile cutoffs, respectively. The live birth rate was significantly lower in the high AMH group than in the low AMH group. Accordingly, excessive AMH was an independent prognostic factor for reduced LBR after fresh ET in women with PCOS aged 20–40 years undergoing IVF/ICSI. This negative correlation may be owing to the pathogenic role of excessive AMH in women with PCOS. Excessive AMH correlates with hyperandrogenism, anovulation, inflammation, and metabolic abnormalities in women with PCOS [35, 36]. Women with PCOS and AMH level of ≥ 10.65 ng/mL are more prone to miscarriage, and less likely to delivery compared with those with PCOS and AMH level of ≤ 4.98 ng/mL (miscarriage rate, high vs. low, 21.8% vs. 11.3%; LBR, high vs. low, 30.4% vs. 39.8%). These findings prompted us to exercise greater caution when administering fresh ET in women with PCOS and AMH level of ≥ 10.65 ng/mL.

In our study, no significant intergroup difference was observed in CLBR. This study suggested a lower LBR in the high AMH group than in the low AMH group, whereas CLBR was comparable among the groups. Above results indicated that pregnancy outcomes in women with PCOS and high AMH levels benefited from FET. One explanation may be the increased number of good-quality embryos in the high AMH group. Overall, these findings indicate a guiding role for AMH levels in the clinical regimen of women with PCOS.

This study has some limitations. First, this was a single-center study, which may have resulted in bias. However, a single center can better control the quality of IVF-ET procedures and laboratory measurements. The second limitation is its retrospective and non-randomized design. Therefore, the findings of this study should be confirmed by large-scale, high-quality prospective cohort studies. Third, additional molecular biology experiments are essential to explore the role of AMH in PCOS pathogenesis.

Conclusions

The live birth rate for fresh ET was decreased in the high AMH group compared with that in the low AMH group, whereas the miscarriage rate for fresh ET was increased in the average and high AMH groups compared with that in the low AMH group. However, no significant differences were observed in CLBR among the groups. Therefore, high AMH level is associated with poor pregnancy outcomes of fresh ET in women with PCOS aged 20–40 years undergoing IVF/ICSI. These findings underscore the need for caution when administering fresh ET in women with PCOS and high AMH levels, providing useful medical insights into transplant strategies in this patient subgroup.

Data availability

No datasets were generated or analysed during the current study.

Abbreviations

AMH:

Anti-Müllerian hormone

ET:

Embryo transfer

CI:

Confidence interval

CLBR:

Cumulative live birth rates

COS:

Controlled ovarian stimulation

CPR:

Clinical pregnancy rate

FET:

Frozen-thawed embryo transfer

FSH:

Follicle-stimulating hormone

IVF/ICSI:

In vitro fertilization/intracytoplasmic sperm injection

LBR:

Live birth rate

BMI:

Body mass index

OR:

Odds ratio

References

  1. Pellatt L, Rice S, Mason HD. Anti-Mullerian hormone and polycystic ovary syndrome: a mountain too high? Reproduction. 2010;139:825–33.

    Article  PubMed  Google Scholar 

  2. Durlinger AL, Gruijters MJ, Kramer P, Karels B, Kumar TR, Matzuk MM, et al. Anti-Mullerian hormone attenuates the effects of FSH on follicle development in the mouse ovary. Endocrinology. 2001;142:4891–9.

    Article  PubMed  Google Scholar 

  3. Dewailly D, Andersen CY, Balen A, Broekmans F, Dilaver N, Fanchin R, et al. The physiology and clinical utility of anti-Mullerian hormone in women. Hum Reprod Update. 2014;20:370–85.

    Article  PubMed  Google Scholar 

  4. Broer SL, van Disseldorp J, Broeze KA, Dolleman M, Opmeer BC, Bossuyt P, et al. Added value of ovarian reserve testing on patient characteristics in the prediction of ovarian response and ongoing pregnancy: an individual patient data approach. Hum Reprod Update. 2013;19:26–36.

    Article  PubMed  Google Scholar 

  5. Joham AE, Norman RJ, Stener-Victorin E, Legro RS, Franks S, Moran LJ, et al. Polycystic ovary syndrome Lancet Diabetes Endocrinol. 2022;10:668–80.

    Article  PubMed  Google Scholar 

  6. Teede HJ, Tay CT, Laven JJE, Dokras A, Moran LJ, Piltonen TT, et al. Recommendations from the 2023 international evidence-based guideline for the assessment and management of polycystic ovary syndrome. J Clin Endocrinol Metab. 2023;108:2447–69.

    Article  PubMed  PubMed Central  Google Scholar 

  7. Azziz R, Carmina E, Chen Z, Dunaif A, Laven JSE, Legro RS, et al. Polycystic ovary syndrome. Nat Rev Dis Primers. 2016;2:16057.

    Article  PubMed  Google Scholar 

  8. Dewailly D, Robin G, Peigne M, Decanter C, Pigny P, Catteau-Jonard S. Interactions between androgens, FSH, anti-Mullerian hormone and estradiol during folliculogenesis in the human normal and polycystic ovary. Hum Reprod Update. 2016;22:709–24.

    Article  PubMed  Google Scholar 

  9. Grossman MP, Nakajima ST, Fallat ME, Siow Y. Mullerian-inhibiting substance inhibits cytochrome P450 aromatase activity in human granulosa lutein cell culture. Fertil Steril. 2008;89(5);Suppl:1364–70.

  10. Rudnicka E, Kunicki M, Calik-Ksepka A, Suchta K, Duszewska A, Smolarczyk K, et al. Anti-Mullerian hormone in pathogenesis, diagnostic and treatment of PCOS. Int J Mol Sci. 2021;22:12507.

    Article  PubMed  PubMed Central  Google Scholar 

  11. Tal R, Seifer DB, Khanimov M, Malter HE, Grazi RV, Leader B. Characterization of women with elevated antiMullerian hormone levels (AMH): correlation of AMH with polycystic ovarian syndrome phenotypes and assisted reproductive technology outcomes. Am J Obstet Gynecol. 2014;211(59):e1-8.

    Google Scholar 

  12. Liu S, Hong L, Mo M, Xiao S, Wang X, Fan X, et al. Association of antiMullerian hormone with polycystic ovarian syndrome phenotypes and pregnancy outcomes of in vitro fertilization cycles with fresh embryo transfer. BMC Pregnancy Childbirth. 2022;22:171.

    Article  PubMed  PubMed Central  Google Scholar 

  13. Tal R, Seifer CM, Khanimov M, Seifer DB, Tal O. High serum antiMullerian hormone levels are associated with lower live birth rates in women with polycystic ovarian syndrome undergoing assisted reproductive technology. Reprod Biol Endocrinol. 2020;18:20.

    Article  PubMed  PubMed Central  Google Scholar 

  14. Kriseman M, Mills C, Kovanci E, Sangi-Haghpeykar H, Gibbons W. AntiMullerian hormone levels are inversely associated with body mass index (BMI) in women with polycystic ovary syndrome. J Assist Reprod Genet. 2015;32:1313–6.

    Article  PubMed  PubMed Central  Google Scholar 

  15. Lefebvre T, Dumont A, Pigny P, Dewailly D. Effect of obesity and its related metabolic factors on serum anti-Mullerian hormone concentrations in women with and without polycystic ovaries. Reprod Biomed Online. 2017;35:325–30.

    Article  PubMed  Google Scholar 

  16. de Medeiros SF, Rodgers RJ, Norman RJ. Adipocyte and steroidogenic cell cross-talk in polycystic ovary syndrome. Hum Reprod Update. 2021;27:771–96.

    Article  PubMed  Google Scholar 

  17. Demirel F, Bideci A, Cinaz P, Camurdan MO, Biberoğlu G, Yesilkaya E, et al. Serum leptin, oxidized low density lipoprotein and plasma asymmetric dimethylarginine levels and their relationship with dyslipidaemia in adolescent girls with polycystic ovary syndrome. Clin Endocrinol (Oxf). 2007;67:129–34.

    Article  PubMed  Google Scholar 

  18. Merhi Z, Buyuk E, Berger DS, Zapantis A, Israel DD, Chua S, et al. Leptin suppresses anti-Mullerian hormone gene expression through the JAK2/STAT3 pathway in luteinized granulosa cells of women undergoing IVF. Hum Reprod. 2013;28:1661–9.

    Article  PubMed  Google Scholar 

  19. Su N, Zhan J, Xie M, Zhao Y, Huang C, Wang S, et al. High anti-Mullerian hormone level is adversely associated with cumulative live birth rates of two embryo transfers after the first initiated cycle in patients with polycystic ovary syndrome. Front Endocrinol (Lausanne). 2023;14:1123125.

    Article  PubMed  Google Scholar 

  20. Paulson M, Sahlin L, Hirschberg AL. Endometrial expression of anti-Mullerian hormone and its type II receptor in women with polycystic ovary syndrome. Reprod Biomed Online. 2020;41:128–37.

    Article  PubMed  Google Scholar 

  21. Renaud EJ, MacLaughlin DT, Oliva E, Rueda BR, Donahoe PK. Endometrial cancer is a receptor-mediated target for Mullerian inhibiting substance. Proc Natl Acad Sci U S A. 2005;102:111–6.

    Article  PubMed  Google Scholar 

  22. Kim SI, Yoon JH, Hur SY. Functional profiles of Mullerian inhibiting substance/anti-Mullerian hormone (MIS/AMH) in primarily cultured endometrial cancer cells. J Cancer. 2021;12:6289–300.

    Article  PubMed  PubMed Central  Google Scholar 

  23. Moon JW, Lee SK, Lee JO, Kim N, Lee YW, Kim SJ, et al. Identification of novel hypermethylated genes and demethylating effect of vincristine in colorectal cancer. J Exp Clin Cancer Res. 2014;33:4.

    Article  PubMed  PubMed Central  Google Scholar 

  24. Palomba S, Piltonen TT, Giudice LC. Endometrial function in women with polycystic ovary syndrome: a comprehensive review. Hum Reprod Update. 2021;27:584–618.

    Article  PubMed  Google Scholar 

  25. Guo Y, Liu S, Hu S, Li F, Jin L. High serum anti-Mullerian hormone concentrations are associated with poor pregnancy outcome in fresh IVF/ICSI cycle but not cumulative live birth rate in PCOS patients. Front Endocrinol (Lausanne). 2021;12:673284.

    Article  PubMed  Google Scholar 

  26. Palomba S, de Wilde MA, Falbo A, Koster MPH, La Sala GB, Fauser BCJM. Pregnancy complications in women with polycystic ovary syndrome. Hum Reprod Update. 2015;21:575–92.

    Article  PubMed  Google Scholar 

  27. Liu X, Han Y, Wang X, Zhang Y, Du A, Yao R, et al. Serum anti-Mullerian hormone levels are associated with early miscarriage in the IVF/ICSI fresh cycle. BMC Pregnancy Childbirth. 2022;22:279.

    Article  PubMed  PubMed Central  Google Scholar 

  28. Gleicher N, Kushnir VA, Sen A, Darmon SK, Weghofer A, Wu YG, et al. Definition by FSH, AMH and embryo numbers of good-, intermediate- and poor-prognosis patients suggests previously unknown IVF outcome-determining factor associated with AMH. J Transl Med. 2016;14:172.

    Article  PubMed  PubMed Central  Google Scholar 

  29. Hsu JY, James KE, Bormann CL, Donahoe PK, Pépin D, Sabatini ME. Mullerian-inhibiting substance/anti-Mullerian hormone as a predictor of preterm birth in polycystic ovary syndrome. J Clin Endocrinol Metab. 2018;103:4187–96.

    Article  PubMed  Google Scholar 

  30. Carlsen SM, Vanky E, Fleming R. Anti-Mullerian hormone concentrations in androgen-suppressed women with polycystic ovary syndrome. Hum Reprod. 2009;24:1732–8.

    Article  PubMed  Google Scholar 

  31. Simitsidellis I, Saunders PTK, Gibson DA. Androgens and endometrium: new insights and new targets. Mol Cell Endocrinol. 2018;465:48–60.

    Article  PubMed  Google Scholar 

  32. Hu M, Zhang Y, Li X, Cui P, Sferruzzi-Perri AN, Brännström M, et al. TLR4-associated IRF-7 and NFkappaB signaling act as a molecular link between androgen and metformin activities and cytokine synthesis in the PCOS endometrium. J Clin Endocrinol Metab. 2021;106:1022–40.

    Article  PubMed  Google Scholar 

  33. Hu M, Zhang Y, Guo X, Jia W, Liu G, Zhang J, et al. Hyperandrogenism and insulin resistance induce gravid uterine defects in association with mitochondrial dysfunction and aberrant reactive oxygen species production. Am J Physiol Endocrinol Metab. 2019;316:E794–809.

    Article  PubMed  Google Scholar 

  34. Hirschberg AL, Jakson I, Graells Brugalla C, Salamon D, Ujvari D. Interaction between insulin and androgen signalling in decidualization, cell migration and trophoblast invasion in vitro. J Cell Mol Med. 2021;25:9523–32.

    Article  PubMed  PubMed Central  Google Scholar 

  35. Lin YH, Chiu WC, Wu CH, Tzeng CR, Hsu CS, Hsu MI. AntiMullerian hormone and polycystic ovary syndrome. Fertil Steril. 2011;96:230–5.

    Article  PubMed  Google Scholar 

  36. Ou M, Xu P, Lin H, Ma K, Liu M. AMH is a good predictor of metabolic risk in women with PCOS: A cross-sectional study. Int J Endocrinol. 2021;2021:9511772.

    Article  PubMed  PubMed Central  Google Scholar 

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Acknowledgements

We thank Dr. Fatima Nasrallah for English language editing.

Funding

This study was supported by National Key R&D Program of China [grant number 2023YFC2705504], the second Tibetan Plateau Scientific Expedition and Research Program (STEP) [grant number 2019QZKK0606], and the National Natural Science Foundation of China [grant number 82171626].

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Authors and Affiliations

  1. Department of Obstetrics and Gynecology, Center for Reproductive Medicine, Peking University Third Hospital, Beijing, 100191, China

    Fei Zhao, Duo Wen, Ruiqi Wang, Dingran Wang, Huiyu Xu, Rong Li & Hongbin Chi

  2. National Clinical Research Center for Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China

    Fei Zhao, Duo Wen, Ruiqi Wang, Dingran Wang, Huiyu Xu, Rong Li & Hongbin Chi

  3. Department of Obstetrics and Gynecology, State Key Laboratory of Female Fertility Promotion, Peking University Third Hospital, Beijing, 100191, China

    Fei Zhao, Duo Wen, Ruiqi Wang, Dingran Wang, Huiyu Xu, Rong Li & Hongbin Chi

  4. Key Laboratory of Assisted Reproduction (Peking University), Ministry of Education, Beijing, China

    Fei Zhao, Duo Wen, Ruiqi Wang, Dingran Wang, Huiyu Xu, Rong Li & Hongbin Chi

  5. Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Beijing, 100191, China

    Fei Zhao, Duo Wen, Ruiqi Wang, Dingran Wang, Huiyu Xu, Rong Li & Hongbin Chi

  6. Research Center of Clinical Epidemiology, Peking University Third Hospital, Beijing, 100191, China

    Lin Zeng

Authors
  1. Fei Zhao
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  2. Duo Wen
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  3. Lin Zeng
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  4. Ruiqi Wang
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  5. Dingran Wang
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  6. Huiyu Xu
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  7. Rong Li
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  8. Hongbin Chi
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Contributions

Fei Zhao completed data curation and wrote the original draft. Duo Wen, Ruiqi Wang and Dingran Wang participated in data curation. Lin Zeng and Huiyu Xu participated in designing methodology. Rong Li participated in project administration. Hongbin Chi designed, supervised, and review this paper.

Corresponding author

Correspondence to Hongbin Chi.

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Ethics approval and consent to participate

This study was approved by the Medical Science Research Ethics Committee of Peking University Third Hospital (Reference Number M3032464) and was conducted according to the Declaration of Helsinki for Medical Research involving Human Subjects. All participants provided written informed consent.

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Not applicable.

Competing interests

The authors declare no competing interests.

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Zhao, F., Wen, D., Zeng, L. et al. High anti-Müllerian hormone level as a predictor of poor pregnancy outcomes in women with polycystic ovary syndrome undergoing in vitro fertilization/intracytoplasmic sperm injection: a retrospective cohort study. Reprod Biol Endocrinol 23, 15 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12958-025-01347-6

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  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12958-025-01347-6

Keywords

Reproductive Biology and Endocrinology

ISSN: 1477-7827

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