BMC endocrine disorders · 2026
Investigating the impact of phthalate exposure on endocrine function in women with polycystic ovary syndrome.
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Patel Jalpa, Chaudhary Hiral, Panchal Sonal, Rajput Kiransinh, Joshi Rushikesh
Аннотация
BACKGROUND: Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder influenced by genetic, hormonal, and environmental factors. In the environmental context, phthalate esters, specifically Mono-2-ethylhexyl phthalate (MEHP) and Di-2-ethylhexyl phthalate (DEHP), have emerged as potential endocrine disruptors, demanding a mysterious role in PCOS.
OBJECTIVE: The study aimed to compare demographic, biochemical parameters, and levels of phthalate esters, specifically MEHP and DEHP, in women with and without PCOS. The association between these phthalate esters and different biochemical markers was also of interest for investigation.
METHODS: The study included 160 participants, 90 in the PCOS group and 70 in the control group. Demographic and biochemical parameters were measured and compared for both groups. The levels of MEHP and DEHP in serum were determined using High-Performance Liquid Chromatography (HPLC).
RESULTS: The PCOS group had a significantly higher average age and Body Mass Index (BMI) compared to the control group (p < 0.0001). Testosterone and luteinizing hormone (LH) levels were significantly elevated in the PCOS group (p < 0.05). In contrast, estradiol, follicle-stimulating hormone (FSH), prolactin, LH/FSH ratio, dehydroepiandrosterone sulfate, and thyroid-stimulating hormone (TSH) levels showed no significant difference. Notably, MEHP and DEHP levels were significantly higher in the PCOS group compared to the control group (47.33 ± 27.67 vs. 31.09 ± 18.74, p < 0.0001 and 31.03 ± 25.76 vs. 22.98 ± 19.65, p = 0.03 respectively). DEHP levels in the PCOS group demonstrated significant positive correlations with LH levels, LH/FSH ratio, and estradiol levels. In contrast, MEHP levels showed no significant correlations with the evaluated biochemical parameters. Neither MEHP nor DEHP displayed significant correlations with any examined parameters in the control group.
CONCLUSION: This study underscores the elevated levels of MEHP and DEHP in women with PCOS, highlighting the potential influence of these environmental toxins in PCOS pathogenesis.
CLINICAL TRIAL NUMBER: Not applicable.
OBJECTIVE: The study aimed to compare demographic, biochemical parameters, and levels of phthalate esters, specifically MEHP and DEHP, in women with and without PCOS. The association between these phthalate esters and different biochemical markers was also of interest for investigation.
METHODS: The study included 160 participants, 90 in the PCOS group and 70 in the control group. Demographic and biochemical parameters were measured and compared for both groups. The levels of MEHP and DEHP in serum were determined using High-Performance Liquid Chromatography (HPLC).
RESULTS: The PCOS group had a significantly higher average age and Body Mass Index (BMI) compared to the control group (p < 0.0001). Testosterone and luteinizing hormone (LH) levels were significantly elevated in the PCOS group (p < 0.05). In contrast, estradiol, follicle-stimulating hormone (FSH), prolactin, LH/FSH ratio, dehydroepiandrosterone sulfate, and thyroid-stimulating hormone (TSH) levels showed no significant difference. Notably, MEHP and DEHP levels were significantly higher in the PCOS group compared to the control group (47.33 ± 27.67 vs. 31.09 ± 18.74, p < 0.0001 and 31.03 ± 25.76 vs. 22.98 ± 19.65, p = 0.03 respectively). DEHP levels in the PCOS group demonstrated significant positive correlations with LH levels, LH/FSH ratio, and estradiol levels. In contrast, MEHP levels showed no significant correlations with the evaluated biochemical parameters. Neither MEHP nor DEHP displayed significant correlations with any examined parameters in the control group.
CONCLUSION: This study underscores the elevated levels of MEHP and DEHP in women with PCOS, highlighting the potential influence of these environmental toxins in PCOS pathogenesis.
CLINICAL TRIAL NUMBER: Not applicable.