In our study, patients were categorized based on their Anti-Müllerian Hormone (AMH) levels to assess serum AMH levels and various factors related to polycystic ovary syndrome (PCOS). Notably, our findings revealed a generally positive correlation between PCOS laboratory findings and AMH levels. These results align with a previously published study, supporting the notion that elevated AMH levels are indicative of the severity of PCOS, which is consistent with our own observations [13].
Consistent with our findings, existing literature also indicates a positive association between AMH levels and total testosterone as well as androstenedione levels. Moreover, publications in the literature have reported an increase in AMH levels correlating with a decrease in the number of menstrual cycles per year [14, 15]. These concurrences emphasize the robustness of our results in the context of established knowledge in the field.
In our study, there was no significant relationship found between age at menarche and AMH levels, a finding consistent with data from another large-scale study in the literature [10]. However, a positive correlation was observed between DHEAS and 17-OHP levels with AMH levels. Conversely, no correlation was identified between SHBG levels and AMH levels. These observations align with the results of another extensive study in the literature, where no significant relationship was reported between AMH levels and DHEAS, 17-OH progesterone, and SHBG levels [10].
In previous studies, a negative correlation was observed between serum AMH levels and BMI [16]. However, in our study, although no significant difference was identified between BMI and AMH levels, this may be attributed to the exclusion of patients with a BMI exceeding 35 from the study. While the exclusion of patients with morbid obesity (BMI > 35) helped avoid potential statistical distortion from extreme metabolic values, it may have also limited the generalizability of our findings to the broader PCOS population, where obesity is a common clinical feature. Although a weak positive correlation was observed between AMH levels and HOMA-IR (r = 0.079), this finding was not statistically significant and should be interpreted cautiously. It may reflect a tendency that warrants further investigation in larger, prospective studies. Recent evidence has increasingly supported AMH’s utility not only as a diagnostic marker in PCOS but also as a surrogate for disease severity and metabolic burden. A large meta-analysis including 22 studies showed a weak correlation between AMH and HOMAIR, suggesting variability across populations but underlining potential metabolic associations [17]. Additionally, recent phenotype-based studies found that while AMH is highest in phenotype A, HOMAIR did not significantly differ across phenotypes, suggesting AMH may reflect ovarian rather than insulin resistance characteristics [18].
Analysis of various phenotypes showed that phenotype A and C are more associated with elevated AMH values. Previous in vitro studies have hypothesized that LH may contribute to silencing granulosa cells, leading them to enter a resting state and potentially disrupting their relationship with theca cells, thus creating a hyperandrogenic environment [19, 20]. Studies have shown that elevated AMH correlates with impaired ovulation induction success—even with clomiphene treatment—indicating AMH’s role as a biomarker for ovarian responsiveness. Mechanistically, increased AMH is associated with higher LH levels, which may exacerbate anovulation in PCOS [13, 21]. Our analyses of phenotypes aling with previous studies where additon of hyperandrogenism makes the difference in AMH values. The elevated AMH levels observed in phenotypes A and C can be attributed to the presence of hyperandrogenism in both phenotypes. According to the Rotterdam criteria, phenotype A is defined by the presence of PCOM, hyperandrogenism, and ovulatory dysfunction, while phenotype C includes PCOM and hyperandrogenism without ovulatory dysfunction. The shared feature of hyperandrogenism in these subgroups likely contributes to increased AMH levels, supporting the proposed link between androgen excess and early follicular growth arrest. Consistent with findings in the literature, our study revealed a significant positive relationship between AMH levels and both the FAI and the total number of antral follicles [22]. This further supports the notion that AMH levels are associated with the number of antral follicles and hormonal imbalances, emphasizing the interconnected nature of these variables in women with PCOS.
In our study, utilizing a population with already elevated AMH levels and a diagnosis of PCOS for comparison against non-PCOS individuals will create a deficiency in the comparison. However, considering the variations within the PCOS patient group, changes in AMH levels will aid in understanding their significance. While acknowledging that AMH alone may not serve as a definitive tool for the differential diagnosis of hyperandrogenic conditions, we believe it can provide valuable insights. Elevated AMH levels may also indicate a greater need for intensive treatment of hyperandrogenism symptoms.
Strengths and limitations
This study benefits from a relatively large and well-characterized PCOS cohort, standardized laboratory assessments, and the use of established diagnostic criteria. However, several limitations must be acknowledged. The retrospective design introduces the possibility of selection and measurement biases. The absence of a non-PCOS control group limits external comparison. Additionally, the exclusion of morbidly obese individuals and patients without definitive PCOM findings (including phenotype B) reduces generalizability to all PCOS populations. These factors should be considered when interpreting the results. Prospective studies with broader inclusion criteria and matched controls are needed to confirm and expand upon these findings.
In our experience, AMH measurements emerge as a highly valuable objective and numerical indicator, not only aiding in the diagnosis of PCOS but also offering indications of the severity of the disease. The use of AMH in conjunction with other clinical and laboratory parameters may contribute to a more comprehensive understanding and characterization of PCOS.