Skip to main content
Download PDF

Correlation between thyroid hormone sensitivity and the risk of polycystic ovary syndrome

BMC Endocrine Disorders volume 24, Article number: 76 (2024) Cite this article

Abstract

Objective

There has been some confusion in earlier research on the connection between thyroid function and polycystic ovary syndrome (PCOS). This research is aimed to probe into the correlation between thyroid condition and the risk of PCOS from a new standpoint of thyroid hormone sensitivity.

Methods

This research comprised 415 females with PCOS from Drum Tower Hospital Affiliated with the Medical School of Nanjing University, and 137 non-PCOS individuals were selected as the normal control. Based on free thyroxine (FT4), free triiodothyronine (FT3), and thyroid-stimulating hormone (TSH), we calculated the thyroid hormone sensitivity indices, which consist of Thyroid Feedback Quantile-based Index (TFQI), Thyroid-stimulating Hormone Index (TSHI), Thyrotroph Thyroxine Resistance Index (TT4RI) and Free Triiodothyronine /Free thyroxine (FT3/FT4). The binary logistic regression model was adopted to investigate the correlation between thyroid hormone sensitivity indices with the risk of PCOS. Pearson or Spearman correlation analysis was employed to explore the association among thyroid-related measures with metabolic parameters in PCOS.

Results

Results of this research showed that females with PCOS had rising TFQI, TSHI, TT4RI, and FT3/FT4 levels compared with the control group. After adjustment for the impact of various covariates, there was no significant correlation between FT3/FT4 and the risk of PCOS; However, the odds ratio of the third and fourth vs. the first quartile of TFQI were 3.57(95% confidence interval [CI]:1.08,11.87) and 4.90(95% CI:1.38,17.38) respectively; The odds ratio of the fourth vs. the first quartile of TSHI was 5.35(95% CI:1.48,19.37); The odds ratio of the second vs. the first quartile of TT4RI was 0.27(95%CI 0.09,0.82). In addition, no significant correlation was observed between thyroid-related measures and metabolic measures in females with PCOS.

Conclusions

A reduction in the sensitivity of central thyroid hormone is closely correlated with a higher risk of PCOS. Further research is necessary to corroborate our findings and the supporting mechanisms.

Peer Review reports

Introduction

As one of the most prevalent endocrine illnesses, polycystic ovary syndrome (PCOS) influences almost 5–10% of females of child-bearing age [1,2,3]. Menstrual disorders, anovulation infertility, androgen excess, and polycystic changes in ovaries are all symptoms of PCOS. In addition, it is also in connection with an added accident of obesity, insulin resistance (IR), Type 2 diabetes (T2D), metabolic syndrome (MS), cardiovascular disease, and cancer of the endometrium [1, 4,5,6].

Thyroid hormones are closely related to PCOS [7]. Multiple studies demonstrated that the prevalence of thyroid diseases was substantially greater in females with PCOS in comparison to age-matched controls [8,9,10]. For the past few years, a rising quantity of scholars has taken notice of the correlation between metabolic disorders and thyroid hormone sensitivity indexes which have been proven to be credible predictors of IR, T2D, hyperuricemia, cardiometabolic risk, and disturbances of lipid metabolism [11,12,13,14]. As a metabolic disease, however, PCOS has not been investigated concerning sensitivity to thyroid hormones. Therefore, we adopt four thyroid hormone sensitivity indices, including FT3/FT4, thyrotropin T4 resistance index (TT4RI), TSH index (TSHI), and thyroid feedback Quantile index (TFQI) [13,14,15,16], to look into the connection between thyroid conditions and PCOS.

Patients and methods

Study population

The study group consists of 415 females with PCOS who visited the PCOS Special Clinic of our hospital from May 2016 to February 2019 (Fig. 1). Inclusion criteria: (1) Definite diagnosis of PCOS, all patients were diagnosed by an experienced endocrinologist or gynecologist with expertise in the field and underwent our re-evaluation before enrollment; (2) Age 18–40 years old; (3) Has not been treated for PCOS. Exclusion criteria: (1) Use of hormones or added medications in the last three months that could exert an impact on endocrine metabolism; (2) The existence of significant thyroid dysfunction; (3) Pregnancy or lactation; (4) Severe cardiopulmonary dysfunction and liver and kidney insufficiency. Another 137 cases of concurrent health check-up females were chosen as the control group. Inclusion criteria: (1) Females aged 18–40 years; (2) Clinical information and examination indicators are complete. Exclusion criteria: Individuals with PCOS, obesity, hypertension, hyperlipidemia, and other metabolic diseases are excluded.

Fig. 1
figure 1

Flowchart of the inclusion and exclusion of participants

Full size image

Diagnostic criteria

The 2003 Rotterdam criteria revisions were used to diagnose PCOS [17]: (1). Oligo-ovulation and/or anovulation; (2). Hyperandrogenemia and/or clinical hyperandrogenic manifestations; (3). Polycystic changes in the ovaries; and exclusion of other diseases that may cause androgen excess such as Cushing’s syndrome.

Data collection

General clinical information such as age, height, weight, and blood pressure levels was recorded. And calculate body mass index (BMI). Approximately 5 ml of venous blood was drawn from each subject in the morning, on days 2–5 of the menstrual cycle, following a 12-hour overnight fast. Calculate thyroid hormone sensitivity indices: FT3/FT4 ratio = FT3/FT4, which indicates that peripheral thyroid hormone sensitivity is elevated when FT3/FT4 is higher. TT4RI = FT4∗TSH, TSHI = lnTSH + 0.1345∗FT4, the central thyroid hormone sensitivity is inversely linked to the TT4RI and TSHI values. TFQI = cdfFT4-(1-cdfTSH), the coefficient of TFQI is achieved by applying the medical examination population. TFQI is superior because it does not generate extremes even under the circumstance of thyroid dysfunction when compared to TT4RI and TSHI. TFQI takes the amount from − 1 to 1. A positive TFQI implies regular insensitivity, while a negative TFQI shows that the HPT axis is more responsive to variation in FT4, and 0 indicates normal sensitivity.

Laboratory tests

All laboratory parameters were measured at our hospital’s clinical laboratory, adhering to the ISO15189 international quality standard. The enzymatic auto-analyzer (Kyowa Medex Co., Ltd., Tokyo, Japan) was used to measure concentrations of Fasting Plasma Glucose (FPG), Triglyceride (TG), Total Cholesterol (TC), High-Density Lipoprotein Cholesterol (HDL-C), and Low-Density Lipoprotein Cholesterol (LDL-C), following the manufacturer’s instructions. Electrochemiluminescence (Roche Diagnostics, Basel, Switzerland) was used to measure serum levels of TSH, FT3, and FT4, according to standardized methods and rigorous quality control protocols. The reference ranges for each parameter are as follows. FPG, 3.9-6.1mmol/L; TG, ≤ 1.7mmol/L; TC, 2.9-5.72mmol/L; HDL-C, 0.94-2mmol/L; LDL-C, 1.89–3.1 mmol/L; TSH, 0.27–4.2 mIU/L; FT3, 3.1–6.8 pmol/L; FT4, 12–22 pmol/L.

Statistical analyze

The data were examined by adopting the program SPSS 27.0. Normally distributed variables were expressed as means ± SD, otherwise, they are expressed as quartiles. T-test and Mann-Whitney test were adopted to compare the differences between groups, separately. The binary logistic regression analysis was used to examine the overall PCOS risk at the thyroid hormone sensitivity index quartile. For finding the correlation, Pearson’s correlation was applied to continuous variables with normal distribution, while Spearman’s correlation was applied to skewed distributed ones. Statistics were deemed significant when P < 0.05.

Results

This research contained 552 participants, and their average age was 28 (SD 3.51 years); 415 were patients with PCOS, and 137 were from the healthy check-up population, with clinical characteristics shown in Table 1. Compared to the healthy check-up population, patients with PCOS had higher weight, BMI, blood pressure, FPG, TG, TC, LDL levels, lower HDL, and higher TSH, FT3, FT4, FT3/FT4, TT4RI, TSHI, TFQI levels (P<0.05).

Table 1 Baseline characteristics
Full size table

After age adjustment, in comparison to the first quartile of the TFQI (Q1), women in the third and fourth quartiles (Q3 and Q4) had a remarkably increased risk of PCOS by 130% (OR, 2.30;95% CI:1.32,4.00) and 240% (OR, 3.40;95% CI:1.87,6.18) separately (Table 2). Similarly, compared with the TSHI Q1 group, women in the Q3 and Q4 groups had a markedly increased risk of PCOS by 75% (OR, 1.75;95% CI:1.04,2.96) and 352% (OR, 4.52;95% CI:2.04,2.96) separately. Meanwhile, compared with the TT4RI Q1 group, the risk of PCOS was increased by 322% (OR, 4.22;95% CI:2.15,8.31) in the Q4 group. The FT3/FT4 quartiles have progressively increased PCOS risk (OR, 2.48 to 6.01).

Table 2 Associations between thyroid hormone sensitivity and PCOS
Full size table

After further adjustment for BMI, compared to the Q1 of TFQI, women in Q3 and Q4 still had a significantly increased risk of PCOS (OR 4.47,5.49, respectively); Compared with the Q1 group of TSHI, the risk of PCOS increased in Q4 (OR = 6.24); Compared with the Q1 group in TT4RI, the risk of PCOS decreased in Q2 (OR = 0.24); No difference was observed in the risk of PCOS between FT3/FT4 groups.

After further adjustment for hypertension, FPG ≥ 7.0, and dyslipidemia, compared with Q1 of TFQI, women in Q3 and Q4 remained considerably more likely to have PCOS. (OR 3.57,4.90, respectively); Q4 in TSHI showed a higher incidence of PCOS compared to Q1 (OR = 5.35); Q2 in TT4RI showed a decreased risk of PCOS compared to Q1 (OR = 0.27); No difference was observed among FT3/FT4 groups.

While finding the correlation of thyroid-related parameters with clinical, metabolic, and hormonal measures, our results revealed no significant relationship (r = 0.100∼0.166) (Table 3).

Table 3 Correlation analysis between thyroid hormone-related parameters and metabolic parameters in patients with PCOS
Full size table

Discussion

In this research, we probed into the correlation among thyroid hormone sensitivity with PCOS. We found that elevated peripheral thyroid hormone sensitivity (elevated FT3/FT4) was linked to an increased PCOS risk, but there was no noticeable correlation after accounting for numerous covariates. However, diminished central thyroid hormone sensitivity (elevated TFQI, TSHI) was in connection to an elevated risk of PCOS and remained significantly associated after controlling for a few confounding factors.

Our study elucidates important associations between thyroid hormone resistance and the occurrence of PCOS. This finding provides clinicians with a deeper understanding of the underlying mechanisms involved in PCOS. Furthermore, our study sheds light on thyroid hormone sensitivity served as a potential risk indicator that can aid in early identification and early intervention of PCOS patients, thereby improving patient outcomes. More importantly, addressing thyroid hormone resistance in PCOS patients may hold therapeutic potential for improving their symptoms and overall prognosis. By improving thyroid hormone sensitivity or optimizing thyroid hormone levels, clinicians may be able to mitigate the metabolic and reproductive disturbances associated with PCOS. This could potentially lead to better outcomes, such as improved menstrual regularity, ovulation, and fertility, as well as a reduction in insulin resistance, and other metabolic abnormalities.

PCOS and thyroid diseases are both common endocrine diseases, and even though they are completely different diseases, they share quantities of clinical features, including irregular menstruation, infertility, obesity, and abnormal glucose and lipid metabolism [3, 18,19,20]. Although the correlation between PCOS and thyroid diseases has not been clear, several studies have confirmed that dyslipidemia and IR are more severe among sufferers with combined thyroid diseases like subclinical hypothyroidism and thyroid nodules than those with PCOS alone [21,22,23,24], implying that thyroid diseases may exacerbate metabolic disorders in PCOS patients. Nevertheless, there is still insufficient proof to say if thyroid conditions impact the onset and progression of PCOS. A population-based investigation reported that Danish PCOS females showed a considerably greater prevalence of thyroid diseases than the control group (2.5% vs. 0.7%) before the diagnosis of PCOS [25]. Two studies showed that PCOS was substantially more common in females with autoimmune thyroid illness by 39% (OR, 1.39; 95% CI:1.07,1.71) and 137% (OR, 2.37; 95% CI:1.22,4.62), separately [26, 27]. However, another study indicated that there was no difference in PCOS prevalence between euthyroid women and subclinical hypothyroidism (SCH) women, and SCH was not a standalone PCOS risk factor (OR = 0.743,95% CI 0.423–1.305) [28]. The inconsistent findings of the research may be associated with the diverse criteria used to determine thyroid status and different participating members.

Furthermore, the hypothalamus influences the pituitary gland by releasing the thyrotropin-releasing hormone (TRH), and the pituitary directs the thyroid by the release of TSH. Once there are enough thyroid hormones in the blood, they will be coupled back to the pituitary and hypothalamus through negative feedback, reducing the production and secretion of TSH and TRH. In consideration of the HPT axis’ intricate interplay, it may be insufficient for individual parameters to reflect the thyroid status. We started to inquire into the unresolved debate on the correlation between thyroid and PCOS from the aspect of thyroid hormone sensitivity adopting composed indices.

Initially, some studies proposed TSHI and TT4RI to evaluate thyroid hormone sensitivity [15, 16]. Afterwards, Laclaustra et al. [14] put forward a novel index, TFQI, which has greater stability in comparison to TSHI and TT4RI. They found that TFQI is in connection to obesity, diabetes, and MS in euthyroid people and suggested we can use this new index to detect decreased sensitivity to thyroid hormones. Several cross-sectional investigations have discovered that impaired thyroid hormone sensitivity is linked to coronary artery disease, non-alcoholic fatty liver disease, renal insufficiency, along with osteoarthritis [12, 29,30,31]. Similarly, our findings imply that a higher TFQI is in connection to an elevated risk of PCOS, and this correlation remains statistically meaningful when other confounding factors are taken into account. Accordingly, we hypothesize that the occurrence of PCOS may be in connection with the central sensitivity to thyroid hormones.

Previous studies have examined the potential mechanisms by which thyroid hormones affect PCOS, mainly through the following: (1) Although currently an accepted genotypic milieu has not been set up, gene polymorphisms such as FBN3 gene variants cause the pathogenesis of PCOS and HT by affecting TGFb’s activity [32, 33]. (2) Thyroid function antibodies (stimulatory or inhibitory) may interact with functional ovarian antibodies (stimulatory or inhibitory) [34]. (3) Through their impacts on FSH, LH, and GnRH levels, thyroid hormones have the power to regulate the growth of germ cells and even to disrupt the HPT axis’s ability to operate [35]. (4) In experiments involving animals, all thyroid axis receptors, such as TRH, TSH, and thyroid hormones, existed in the monkey uterus [36], and even TSH receptors, TRα1 receptors, and TRβ1 receptors were expressed in the human endometrium [37]. Of course, it cannot be excluded that the comparative deficiency of thyroid hormones due to reduced sensitivity may also influence PCOS by means of the above-mentioned mechanisms.

For all we know, this research marks the first to investigate the connection among thyroid hormone sensitivity with PCOS. Although this study is relatively novel and achieved significant results, there exist a few limitations as well. The first and foremost is data missing: gonadal hormones and insulin concentrations are not routinely measured in healthy check-up populations, so the possibility of residual confounding factors cannot be eliminated. Secondly, epidemiological surveys are subject to challenges such as genetic, environmental, as well as other variables which could affect clinical outcomes, and consequently, we should view the results with a cautious eye. Furthermore, as an inventory survey, this investigation has not been capable of identifying the fundamental causes of the phenomenon. Further prospective studies are needed to confirm the potential benefits of improving thyroid hormone resistance in PCOS patients, including symptom, reproductive function, and prognostic assessment, to provide strong evidence of its effectiveness. In addition, mechanistic studies can reveal the molecular pathways between improvement of thyroid hormone resistance and improvement of PCOS symptoms, which can enhance the understanding of PCOS pathophysiology and investigate therapeutic targets.

Conclusion

Our research elucidates the linkage among PCOS risk in euthyroid people with diminished central sensitivity to thyroid hormones. Compared to individual parameters such as TSH and FT4, composed indices such as TFQI exhibit a stronger association with PCOS. Therefore, TFQI is expected to be a novel potential risk indicator to help clinicians early identify patients with high risk of PCOS.

Continuous variables are presented as mean ± standard deviation (SD) or median (interquartile range).

Abbreviations: BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; FPG, fasting plasma glucose level; TG, triglycerides; TC, total cholesterol; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TSH, thyroid stimulating hormone; FT3, free triiodothyronine; FT4, free thyroxine; TT4RI, Thyrotropin T4 resistance index; TSHI, TSH index; TFQI, thyroid feedback quantile-based index.

Data availability

Data and materials are available from the corresponding author on reasonable request.

References

  1. Nandi A, Chen Z, Patel R, Poretsky L. Polycystic ovary syndrome. Endocrinol Metab Clin North Am. 2014;43(1):123–47. https://doi.org/10.1016/j.ecl.2013.10.003

    Article  PubMed  Google Scholar 

  2. Escobar-Morreale HF. Polycystic ovary syndrome: treatment strategies and management. Expert Opin Pharmacother. 2008;9(17):2995–3008. https://doi.org/10.1517/14656560802559932

    Article  PubMed  Google Scholar 

  3. Fauser BC, Tarlatzis BC, Rebar RW, et al. Consensus on women’s health aspects of polycystic ovary syndrome (PCOS): the Amsterdam ESHRE/ASRM-Sponsored 3rd PCOS consensus workshop group. Fertil Steril. 2012;97(1):28–e3825. https://doi.org/10.1016/j.fertnstert.2011.09.024

    Article  PubMed  Google Scholar 

  4. Moran LJ, Misso ML, Wild RA, Norman RJ. Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review and meta-analysis. Hum Reprod Update. 2010;16(4):347–63. https://doi.org/10.1093/humupd/dmq001

    Article  CAS  PubMed  Google Scholar 

  5. Chen L, Xu WM, Zhang D. Association of abdominal obesity, insulin resistance, and oxidative stress in adipose tissue in women with polycystic ovary syndrome [published correction appears in Fertil Steril. 2014;102(5):1499]. Fertil Steril. 2014;102(4):1167–1174.e4. https://doi.org/10.1016/j.fertnstert.2014.06.027

  6. Setji TL, Brown AJ. Polycystic ovary syndrome: update on diagnosis and treatment. Am J Med. 2014;127(10):912–9. https://doi.org/10.1016/j.amjmed.2014.04.017

    Article  PubMed  Google Scholar 

  7. Gaberšček S, Zaletel K, Schwetz V, Pieber T, Obermayer-Pietsch B, Lerchbaum E. Mechanisms in endocrinology: thyroid and polycystic ovary syndrome. Eur J Endocrinol. 2015;172(1):R9–21. https://doi.org/10.1530/EJE-14-0295

    Article  CAS  PubMed  Google Scholar 

  8. Kachuei M, Jafari F, Kachuei A, Keshteli AH. Prevalence of autoimmune thyroiditis in patients with polycystic ovary syndrome. Arch Gynecol Obstet. 2012;285(3):853–6. https://doi.org/10.1007/s00404-011-2040-5

    Article  CAS  PubMed  Google Scholar 

  9. Romitti M, Fabris VC, Ziegelmann PK, Maia AL, Spritzer PM. Association between PCOS and autoimmune thyroid disease: a systematic review and meta-analysis. Endocr Connect. 2018;7(11):1158–67. https://doi.org/10.1530/EC-18-0309. Published 2018 Oct 26.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Glintborg D, Rubin KH, Nybo M, Abrahamsen B, Andersen M. Increased risk of thyroid disease in Danish women with polycystic ovary syndrome: a cohort study. Endocr Connect. 2019;8(10):1405–15. https://doi.org/10.1530/EC-19-0377

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Sun Y, Teng D, Zhao L, et al. Impaired sensitivity to thyroid hormones is associated with hyperuricemia, obesity, and cardiovascular disease risk in subjects with subclinical hypothyroidism. Thyroid. 2022;32(4):376–84. https://doi.org/10.1089/thy.2021.0500

    Article  CAS  PubMed  Google Scholar 

  12. Lai S, Li J, Wang Z, Wang W, Guan H. Sensitivity to thyroid hormone indices are closely associated with NAFLD. Front Endocrinol (Lausanne). 2021;12:766419. https://doi.org/10.3389/fendo.2021.766419. Published 2021 Nov 5.

    Article  PubMed  Google Scholar 

  13. Štěpánek L, Horáková D, Štěpánek L, et al. Free triiodothyronine/free thyroxine (FT3/FT4) ratio is strongly associated with insulin resistance in euthyroid and hypothyroid adults: a cross-sectional study. Endokrynol Pol. 2021;72(1):8–13. https://doi.org/10.5603/EP.a2020.0066

    Article  PubMed  Google Scholar 

  14. Laclaustra M, Moreno-Franco B, Lou-Bonafonte JM, et al. Impaired sensitivity to thyroid hormones is associated with diabetes and metabolic syndrome. Diabetes Care. 2019;42(2):303–10. https://doi.org/10.2337/dc18-1410

    Article  CAS  PubMed  Google Scholar 

  15. Yagi H, Pohlenz J, Hayashi Y, Sakurai A, Refetoff S. Resistance to thyroid hormone caused by two mutant thyroid hormone receptors beta, R243Q and R243W, with marked impairment of function that cannot be explained by altered in vitro 3,5,3’-triiodothyroinine binding affinity. J Clin Endocrinol Metab. 1997;82(5):1608–14. https://doi.org/10.1210/jcem.82.5.3945

    Article  CAS  PubMed  Google Scholar 

  16. Jostel A, Ryder WD, Shalet SM. The use of thyroid function tests in the diagnosis of hypopituitarism: definition and evaluation of the TSH Index. Clin Endocrinol (Oxf). 2009;71(4):529–34. https://doi.org/10.1111/j.1365-2265.2009.03534.x

    Article  CAS  PubMed  Google Scholar 

  17. Rotterdam ESHRE, ASRM-Sponsored PCOS consensus workshop group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod. 2004;19(1):41–7. https://doi.org/10.1093/humrep/deh098

    Article  Google Scholar 

  18. Singla R, Gupta Y, Khemani M, Aggarwal S. Thyroid disorders and polycystic ovary syndrome: an emerging relationship. Indian J Endocrinol Metab. 2015;19(1):25–9. https://doi.org/10.4103/2230-8210.146860

    Article  PubMed  PubMed Central  Google Scholar 

  19. Peddemul A, Tejovath S, Hassan D, et al. Influence of subclinical hypothyroidism on women with polycystic ovary syndrome: a Literature Review. Cureus. 2022;14(8):e28468. https://doi.org/10.7759/cureus.28468. Published 2022 Aug 27.

    Article  PubMed  PubMed Central  Google Scholar 

  20. Han C, He X, Xia X, et al. Subclinical hypothyroidism and type 2 diabetes: a systematic review and meta-analysis. PLoS ONE. 2015;10(8):e0135233. https://doi.org/10.1371/journal.pone.0135233. Published 2015 Aug 13.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Mueller A, Schöfl C, Dittrich R, et al. Thyroid-stimulating hormone is associated with insulin resistance independently of body mass index and age in women with polycystic ovary syndrome. Hum Reprod. 2009;24(11):2924–30. https://doi.org/10.1093/humrep/dep285

    Article  CAS  PubMed  Google Scholar 

  22. Yu Q, Wang JB. Subclinical hypothyroidism in PCOS: impact on presentation, insulin resistance, and cardiovascular risk. Biomed Res Int. 2016;2016:2067087. https://doi.org/10.1155/2016/2067087

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  23. Benetti-Pinto CL, Berini Piccolo VR, Garmes HM, Teatin Juliato CR. Subclinical hypothyroidism in young women with polycystic ovary syndrome: an analysis of clinical, hormonal, and metabolic parameters. Fertil Steril. 2013;99(2):588–92. https://doi.org/10.1016/j.fertnstert.2012.10.006

    Article  CAS  PubMed  Google Scholar 

  24. Karaköse M, Hepsen S, Çakal E, et al. Frequency of nodular goiter and autoimmune thyroid disease and association of these disorders with insulin resistance in polycystic ovary syndrome. J Turk Ger Gynecol Assoc. 2017;18(2):85–9. https://doi.org/10.4274/jtgga.2016.0217

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Glintborg D, Hass Rubin K, Nybo M, Abrahamsen B, Andersen M. Morbidity and medicine prescriptions in a nationwide Danish population of patients diagnosed with polycystic ovary syndrome. Eur J Endocrinol. 2015;172(5):627–38. https://doi.org/10.1530/EJE-14-1108

    Article  CAS  PubMed  Google Scholar 

  26. Ho CW, Chen HH, Hsieh MC, et al. Increased risk of polycystic ovary syndrome and it’s comorbidities in women with autoimmune thyroid disease. Int J Environ Res Public Health. 2020;17(7):2422. https://doi.org/10.3390/ijerph17072422. Published 2020 Apr 2.

    Article  PubMed  PubMed Central  Google Scholar 

  27. Ho CW, Chen HH, Hsieh MC, et al. Hashimoto’s thyroiditis might increase polycystic ovary syndrome and associated comorbidities risks in Asia. Ann Transl Med. 2020;8(11):684. https://doi.org/10.21037/atm-19-4763

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Zhang B, Wang J, Shen S, et al. Subclinical hypothyroidism is not a risk factor for polycystic ovary syndrome in obese women of reproductive age. Gynecol Endocrinol. 2018;34(10):875–9. https://doi.org/10.1080/09513590.2018.1462319

    Article  CAS  PubMed  Google Scholar 

  29. Yu N, Wang L, Zeng Y, et al. The association of thyroid hormones with coronary atherosclerotic severity in euthyroid patients. Horm Metab Res. 2022;54(1):12–9. https://doi.org/10.1055/a-1718-6283

    Article  CAS  PubMed  Google Scholar 

  30. Yang S, Lai S, Wang Z, Liu A, Wang W, Guan H. Thyroid feedback quantile-based index correlates strongly to renal function in euthyroid individuals. Ann Med. 2021;53(1):1945–55. https://doi.org/10.1080/07853890.2021.1993324

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Chen S, Sun X, Zhou G, Jin J, Li Z. Association between sensitivity to thyroid hormone indices and the risk of osteoarthritis: an NHANES study. Eur J Med Res. 2022;27(1):114. https://doi.org/10.1186/s40001-022-00749-1. Published 2022 Jul 11.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Akinci B, Comlekci A, Yener S, et al. Hashimoto’s thyroiditis, but not treatment of hypothyroidism, is associated with altered TGF-beta1 levels. Arch Med Res. 2008;39(4):397–401. https://doi.org/10.1016/j.arcmed.2007.12.001

    Article  CAS  PubMed  Google Scholar 

  33. Raja-Khan N, Urbanek M, Rodgers RJ, Legro RS. The role of TGF-β in polycystic ovary syndrome. Reprod Sci. 2014;21(1):20–31. https://doi.org/10.1177/1933719113485294

    Article  CAS  PubMed  Google Scholar 

  34. Gleicher N, Barad D, Weghofer A. Functional autoantibodies, a new paradigm in autoimmunity? Autoimmun Rev. 2007;7(1):42–5. https://doi.org/10.1016/j.autrev.2007.06.001

    Article  CAS  PubMed  Google Scholar 

  35. Ren B, Zhu Y. A new perspective on thyroid hormones: crosstalk with reproductive hormones in females. Int J Mol Sci. 2022;23(5):2708. https://doi.org/10.3390/ijms23052708. Published 2022 Feb 28.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Hulchiy M, Zhang H, Cline JM, Hirschberg AL, Sahlin L. Receptors for thyrotropin-releasing hormone, thyroid-stimulating hormone, and thyroid hormones in the macaque uterus: effects of long-term sex hormone treatment. Menopause. 2012;19(11):1253–9. https://doi.org/10.1097/gme.0b013e318252e450

    Article  PubMed  Google Scholar 

  37. Catalano RD, Critchley HO, Heikinheimo O, et al. Mifepristone induced progesterone withdrawal reveals novel regulatory pathways in human endometrium. Mol Hum Reprod. 2007;13(9):641–54. https://doi.org/10.1093/molehr/gam021

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

Not applicable.

Funding

This project was supported by the National Nature Science Funds of China (Grant No.81800752), the grant from Jiangsu Research Hospital Association for Precision Medication (JY202041), and Fundings for Clinical Trials from the Affiliated Drum Tower Hospital, Medical School of Nanjing University (Grant No.2022-YXZX-NFM-02).

Author information

Authors and Affiliations

  1. Department of Endocrinology, Endocrine and Metabolic Disease Medical Center, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China

    Qian Wang, Zeyu Huang, Yan Bi, Xiaowen Zhang & Shanmei Shen

  2. Branch of National Clinical Research Centre for Metabolic Diseases, Nanjing, China

    Qian Wang, Ru Zhao, Chen Han, Zeyu Huang, Yan Bi, Xiaowen Zhang & Shanmei Shen

  3. Department of Endocrinology, Endocrine and Metabolic Disease Medical Center, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, China

    Ru Zhao

  4. Department of Endocrinology and Metabolism, Drum Tower Clinical Medical College, Southeast University, Nanjing, China

    Chen Han

Authors
  1. Qian Wang
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Ru Zhao
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Chen Han
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Zeyu Huang
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Yan Bi
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Xiaowen Zhang
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Shanmei Shen
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

Qian Wang analyzed the data and wrote the article. Ru Zhao assisted in statistical analysis. Chen Han and Zeyu Huang collected the data together. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Yan Bi, Xiaowen Zhang or Shanmei Shen.

Ethics declarations

Ethics approval and consent to participate

All experiments and methods were performed in accordance with the Declaration of Helsinki. This research approved by the Ethics Committee of Drum Tower Hospital Affiliated to School of Medicine of Nanjing University. Informed consent was obtained from all participants.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Wang, Q., Zhao, R., Han, C. et al. Correlation between thyroid hormone sensitivity and the risk of polycystic ovary syndrome. BMC Endocr Disord 24, 76 (2024). https://doi.org/10.1186/s12902-024-01607-3

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12902-024-01607-3

Keywords

BMC Endocrine Disorders

ISSN: 1472-6823

Contact us