# Association between body mass index and anti-Müllerian hormone in women with ovarian endometrioma and dermoid cyst

## TL;DR

Higher BMI is weakly linked to lower AMH levels in women with ovarian cysts, but the effect is small and similar for both endometrioma and dermoid cysts.

## Contribution

This study investigates the relationship between BMI and AMH in endometrioma and dermoid cysts, revealing minimal differences between the groups.

## Key findings

- Each 1 kg/m² increase in BMI was associated with a 2.3% decrease in AMH levels.
- The association between BMI and AMH was similar for endometrioma and dermoid cysts.
- BMI explained only 1% of the variance in AMH levels, suggesting other factors are more influential.

## Abstract

Adiposity influences reproductive function via endocrine and immune pathways. The association between body mass index (BMI) and anti−Müllerian hormone (AMH) in endometriosis is uncertain, and BMI may not fully capture adiposity−related biology relevant to ovarian reserve. We assessed whether BMI is associated with AMH in untreated ovarian endometrioma and whether this differs from dermoid cysts.

Retrospective single−center cohort of 951 newly diagnosed, reproductive−age women from January 1, 2020 to December 31, 2023 (717 endometrioma; 234 dermoid). AMH was measured on one platform; imaging included transvaginal ultrasonography with MRI or contrast−enhanced abdominopelvic CT as needed. Multivariable linear regression modeled log−AMH versus BMI, adjusting for age, diagnosis, cyst size and laterality, parity, smoking, alcohol use, cycle regularity, and cycle length. Nonlinearity was screened with restricted cubic splines; piecewise models explored age breakpoints. An interaction term tested whether the BMI effect differed by diagnosis. Effects are reported as percent change in AMH per 1 kg/m².

Women with endometrioma were older (31.9 vs 29.9 years; P<.001) and had lower BMI (21.1 vs 22.4 kg/m²; P<.001) than those with dermoid. Median AMH was 2.52 vs 2.70 ng/mL; age−adjusted geometric means did not differ (P = .245). Piecewise modeling identified earlier age breakpoints in endometrioma (35.7 years) than dermoid (40.4 years). In fully adjusted models, each 1 kg/m² higher BMI was associated with 2.3% lower AMH (P = .003). Group−specific estimates were −1.9% per kg/m² in endometrioma (P = .060) and −2.8% per kg/m² in dermoid (P = .009); the BMI×diagnosis interaction was not significant (P = .538). Model fit was modest (adjusted R²=0.22), and BMI explained 1% of AMH variance (partial R²=0.01). Sensitivity analyses restricting the BMI range yielded consistent directions of effect with attenuation at lower BMI.

Across endometrioma and dermoid cysts, BMI shows a weak inverse association with AMH without evidence of between−group differences. Given BMI’s minimal explanatory value, local ovarian factors may more strongly determine ovarian reserve in endometrioma. Limited numbers of obese participants constrain inference at higher BMI; studies with broader BMI distributions and integrated metabolic profiling are warranted.