Effect of TSH on oocyte maturation of PCOS patients with normal thyroid function in IVF

Abstract

Background The serum TSH level of PCOS patients was higher than that of the general female population. For patients with thyroid dysfunction, the abnormal TSH level is negatively related to the outcomes of assisted reproductive technology, but for PCOS patients with normal thyroid function, the effect of TSH level on outcomes of in vitro fertilization has not been reported. In this study, PCOS patients with normal thyroid function were included in this study to evaluate the effect of TSH on the outcomes of IVF-ET. Methods A retrospective cohort study was conducted to analyze the clinical data of 3190 patients who underwent IVF-ET in the Department of Human Reproductive Center of Renmin Hospital Hubei University of Medicine from January 2017 to July 2021, including 594 PCOS patients and 2595 non PCOS patients. The IVF-ET outcomes between the two groups were compared; Multi-factor linear regression analysis was used to analyze the correlation between the related variables and the oocyte maturation of PCOS patients; The ROC curve of the effect of TSH on oocyte maturation in PCOS patients was drawn. The PCOS patients were divided into TSH < 2.98 group (n = 454) and TSH ≥ 2.98 group (n = 141) according to ROC threshold TSH 2.98, and the outcomes were compared. Results TSH level in PCOS group was significantly higher than that in non-PCOS group (2.42 ± 0.86 vs 2.00 ± 0.89 UU / ml, P < 0.01), and the oocyte maturation rate and 2PN fertilization rate in PCOS group were lower than those in non-PCOS group (90.9% vs 92.4%, P = 0.02) (84.57% vs 86.77%, P = 0.02). There was no significant difference in cleavage rate and high-quality embryo rate between the two groups (P > 0.05); There was no difference in clinical pregnancy rate, abortion rate, ectopic pregnancy rate and live birth rate between the two groups (P > 0.05). Multi-factor linear regression analysis showed that TSH was negatively correlated with oocyte maturation in PCOS patients [β = -0.124, P = 0.013,95%CI (-0.027 ~ -0.003)]; The oocyte maturation rate in TSH < 2.98 group was significantly higher than that in TSH ≥ 2.98 group (91.7% vs 88.2%, P = 0.001). Conclusion The TSH level of PCOS patients with normal thyroid function is higher than that of normal people, and it is negatively correlated with the oocyte maturation in in-vitro fertilization. The ROC curve showed that when TSH > 2.98uIU/ml, the possibility of immature oocytes was higher (specificity 28.9%, sensitivity 83.0%).

Polycystic ovary syndrome and thyroid disorder: a comprehensive narrative review of the literature

“…Further analysis of the data to only include studies in which a SCH diagnosis was ascertained using a TSH cutoff of ≥4 mUI/L, the SCH risk was 3.59 times higher in women with PCOS versus women without PCOS ( 18 ). Serum TSH concentration was higher in an infertile population of euthyroid women with PCOS versus euthyroid women without PCOS ( 36 ).…”

“…Based on this, it is possible to speculate that PCOS and AIT and/or SCH may represent a phenotype with a particularly poor reproductive prognosis during the IVF cycle. Initial indirect evidence can be extracted from studies investigating the independent impact of TSH level on IVF-related outcomes in women affected by PCOS ( 36 , 184 ). A small prospective cohort study on 32 AIT-negative patients with PCOS and a serum TSH level of 0.4−4.5 mIU/L ( 184 ), showed that both serum and follicular fluid TSH levels were negatively correlated with the rate of oocyte maturation and fertilization, whereas high-quality embryo production rate was negatively correlated with serum TSH concentration only ( 184 ).…”

“…Interestingly, the authors also observed an increased TSH receptor expression and cyclic adenosine monophosphate concentration in granulosa cells of patients with PCOS, suggesting a possible detrimental effect of TSH on the PCOS ovary mediated via TSH receptor/cyclic adenosine monophosphate ( 184 ) with a potential reduction of oocyte competence in women with PCOS ( 165 ). More recently, a multi-factor linear regression analysis was performed to identify variables that influence the maturation of oocytes in a cohort of 594 euthyroid women with PCOS selected for IVF ( 36 ). Serum TSH concentration was negatively correlated with oocyte maturation, and a TSH cutoff value of ≥2.98 uIU/ml was identified as a predictor of a poor oocyte maturation rate ( 36 ).…”

Using Machine Learning to Construct the Blood–Follicle Distribution Models of Various Trace Elements and Explore the Transport-Related Pathways with Multiomics Data

“…The inclusion criteria are 18 ≤ age ≤ 40; BMI ≤ 28 kg/m 2 ; and infertility duration ≥ 12 months. The exclusion criteria are hydrosalpinx, adenomyosis, thyroid dysfunction, hyperprolactinemia, serious cardiovascular disease, diabetes mellitus, polycystic ovarian syndrome (PCOS), endometrial polyps, endometriosis, and hormone therapy in the preceding 3 months due to their strong influence on the success rate of IVF-ET. − The treatment protocols of the original cohort have been described in detail in our previous study . A total of 340 participants were recruited in the original cohort after informed consent; 35 of them were lost to follow-up, resulting in 305 participants.…”

Hypothalamic-Ovarian axis and Adiposity Relationship in Polycystic Ovary Syndrome: Physiopathology and Therapeutic Options for the Management of Metabolic and Inflammatory Aspects

“…When the TSH level is abnormal, it can adversely affect the hypothalamus and the function of the hypothalamic-pituitary-thyroid axis, and, conversely, the imbalance of the gonadal axis in PCOS patients can affect the pituitary-thyroid axis. Many studies have found that PCOS patients with severe hyperandrogenism and insulin resistance also have abnormal thyroid function [ 83 ] Insulin Metabolic/Hormonal ↑ It is capable of increasing the frequency and amplitude of secretion of GnRH and LH pulses through upregulation of GnRH gene expression in hypothalamic GnRH neurons. Hyperinsulinemia, which may itself be caused by hyperandrogenism, potentiates the stimulatory effects of LH on androgen production in ovarian theca cells thus contributing to androgen-dependent anovulation, as well as inhibiting the production of SHBG [ 12 , 84 ].…”