Objective: To evaluate the prevalence and impact of impaired thyroid-stimulating hormone (TSH) levels on the reproductive outcomes of in vitro fertilization patients diagnosed with endometriosis and compared to controls without endometriosis. Design: Retrospective cohort study on prospectively collected data Setting: Tertiary care University Hospital Participants: Infertile women with histopathological diagnosis of endometriosis. Methods: for 12 months (January 2018 to January 2019), women were deemed suitable and subsequently divided according to serum thyroid-stimulating hormone levels above or below 2.5 mIU/L and compared to patients without endometriosis. Needed sample size was at least 41 patients for each cohort of women. Co-primary outcomes were the live birth rate (LBR), clinical pregnancy rate (CPR) and pregnancy loss rate (PLR). Results: 226 women (45 with endometriosis and 181 controls without endometriosis) were included. Diagnoses of Hashimoto thyroiditis were significantly more frequent in women with rather than without endometriosis (14/45 (31.1%) vs 27/181 (14.9%); p=0.012). Similarly, in women with endometriosis, Hashimoto diagnosis rates were higher with TSH ≥2.5 mIU/L compared to TSH <2.5 mIU/L (9/15 (60%) vs 5/30 (16.6%); p=0.001), so were the Hashimoto diagnosis rates in control group (women without endometriosis) with TSH ≥2.5 mIU/L compared to TSH <2.5 mIU/L (17/48 (35.4%) vs 10/133 (7.5%), respectively; p=0.001). Effect size analysis confirmed an increased risk of Hashimoto thyroiditis in women with endometriosis and TSH ≥2.5 mIU/L compared to women with endometriosis and TSH <2.5 mIU/L ((risk ratio (RR) 3.60 (95% CI 1.46 to 8.86)) and in women with endometriosis and TSH ≥2.5 mIU/L compared to non-endometriotic euthyroid patients (RR 7.98 (95% CI 3.86 to 16.48)). Dysmenorrhea risk was higher in endometriotic euthyroid women compared to euthyroid patients with no endometriosis (RR 1.87 (95% CI 1.21 to 2.87)). The risk was still increased in euthyroid women with endometriosis relative to dysthyroid women with no endometriosis (RR 1.97 (95% CI 1.11 to 3.50)). There were no significant differences between the four groups for CPR, LBR, PLR and retrieved oocytes, immature oocytes, degenerated and unfertilized oocytes, cultured blastocysts, embryos and transferred embryos. Limitations: Retrospective design, limited sample size and use of different ovarian stimulation protocol. Conclusions: Thyroid autoimmunity seems more common in women with endometriosis and thyroid-stimulating hormone over 2.5 mIU/L. However, there was no significant impact on in vitro fertilization and reproductive outcomes related to the coexistence of endometriosis, Hashimoto disease and higher thyroid-stimulating hormone levels. Due to limitations of the study, additional evidence is required to validate the abovementioned findings.
Korošec, S., Riemma, G., Šalamun, V., Franko Rutar, A., Laganà, A.S., Chiantera, V., et al. (2024). Coexistence of endometriosis and thyroid autoimmunity in infertile women: impact on in-vitro fertilization and reproductive outcomes. GYNECOLOGIC AND OBSTETRIC INVESTIGATION [10.1159/000539265].
Coexistence of endometriosis and thyroid autoimmunity in infertile women: impact on in-vitro fertilization and reproductive outcomes
Laganà, Antonio Simone;Chiantera, Vito;
2024-05-08
Abstract
Objective: To evaluate the prevalence and impact of impaired thyroid-stimulating hormone (TSH) levels on the reproductive outcomes of in vitro fertilization patients diagnosed with endometriosis and compared to controls without endometriosis. Design: Retrospective cohort study on prospectively collected data Setting: Tertiary care University Hospital Participants: Infertile women with histopathological diagnosis of endometriosis. Methods: for 12 months (January 2018 to January 2019), women were deemed suitable and subsequently divided according to serum thyroid-stimulating hormone levels above or below 2.5 mIU/L and compared to patients without endometriosis. Needed sample size was at least 41 patients for each cohort of women. Co-primary outcomes were the live birth rate (LBR), clinical pregnancy rate (CPR) and pregnancy loss rate (PLR). Results: 226 women (45 with endometriosis and 181 controls without endometriosis) were included. Diagnoses of Hashimoto thyroiditis were significantly more frequent in women with rather than without endometriosis (14/45 (31.1%) vs 27/181 (14.9%); p=0.012). Similarly, in women with endometriosis, Hashimoto diagnosis rates were higher with TSH ≥2.5 mIU/L compared to TSH <2.5 mIU/L (9/15 (60%) vs 5/30 (16.6%); p=0.001), so were the Hashimoto diagnosis rates in control group (women without endometriosis) with TSH ≥2.5 mIU/L compared to TSH <2.5 mIU/L (17/48 (35.4%) vs 10/133 (7.5%), respectively; p=0.001). Effect size analysis confirmed an increased risk of Hashimoto thyroiditis in women with endometriosis and TSH ≥2.5 mIU/L compared to women with endometriosis and TSH <2.5 mIU/L ((risk ratio (RR) 3.60 (95% CI 1.46 to 8.86)) and in women with endometriosis and TSH ≥2.5 mIU/L compared to non-endometriotic euthyroid patients (RR 7.98 (95% CI 3.86 to 16.48)). Dysmenorrhea risk was higher in endometriotic euthyroid women compared to euthyroid patients with no endometriosis (RR 1.87 (95% CI 1.21 to 2.87)). The risk was still increased in euthyroid women with endometriosis relative to dysthyroid women with no endometriosis (RR 1.97 (95% CI 1.11 to 3.50)). There were no significant differences between the four groups for CPR, LBR, PLR and retrieved oocytes, immature oocytes, degenerated and unfertilized oocytes, cultured blastocysts, embryos and transferred embryos. Limitations: Retrospective design, limited sample size and use of different ovarian stimulation protocol. Conclusions: Thyroid autoimmunity seems more common in women with endometriosis and thyroid-stimulating hormone over 2.5 mIU/L. However, there was no significant impact on in vitro fertilization and reproductive outcomes related to the coexistence of endometriosis, Hashimoto disease and higher thyroid-stimulating hormone levels. Due to limitations of the study, additional evidence is required to validate the abovementioned findings.File | Dimensione | Formato | |
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