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346-360-Thyroid Disorders in Polycystic Ovary Syndrome European Review for Medical and Pharmacological Sciences 2017; 21: 346-360 Thyroid disorders in polycystic ovary syndrome K. KOWALCZYK1, G. FRANIK1, D. KOWALCZYK2, D. PLUTA1, Ł. BLUKACZ1, P. MADEJ1 1Department of Gynaecological Endocrinology, Medical Faculty in Katowice, Medical University of Silesia, Katowice, Poland 2Department of Gynaecology and Obstetrics, Centre of Gynaecology, Obstetrics and Neonatology in Opole, Opole, Poland Abstract. – OBJECTIVE: Thyroid disorders, Introduction especially Hashimoto’s thyroiditis (HT), are ob- served significantly more often in patients with polycystic ovary syndrome (PCOS) than in the Polycystic ovary syndrome (PCOS) is the most general population – approximately 27% and common female endocrinopathy in women of re- 8%, respectively. This is extremely important in productive age. It is characterized by a wide range young women, because both disorders are con- of symptoms, which can occur in different com- nected with fertility problems. As HT and PCOS binations and with different intensity. First of all, occur together, fertility problems may become a they are: ovarian dysfunction, which can cause serious clinical issue in these patients. rare menstruation or absence of it, hyperandroge- MATERIALS AND METHODS: A systematic literature review in PubMed of PCOS- and HT-re- nism and/or hyperandrogenemia, polycystic ova- 1 lated articles in English, published until Decem- ry/ovaries on gynaecological ultrasound and, in ber 2015 was conducted. many cases, disorders such as insulin resistance, RESULTS: The reasons for joint prevalence hyperinsulinemia, obesity (especially the central still remain unclear. Genetic and autoimmune type of obesity), hypertension, nonalcoholic ste- backgrounds are recognized to be possible atohepatitis (NASH) and, finally, fully developed common etiological factors. Three genetic poly- morphisms have been described to play a role in metabolic syndrome. PCOS as well as in HT. They are polymorphism The prevalence of PCOS is noted in 8-12% of the gene for fibrillin 3 (FBN3) regulating the of women of reproductive age1; however, in the activity of transforming growth factor-b (TGF-b) most current Danish research2 from 2014, it was and regulatory T cell levels, gonadotropin-re- set at up to 16.6%. These numbers vary because leasing hormone receptor (GnRHR) polymor- of the different diagnostic criteria. Nowadays, the phism and CYP1B1 polymorphism standing for most widely accepted criteria are the Rotterdam estradiol hydroxylation. High estrogen-to-pro- 1 gesterone ratios owing to anovulatory cycles, as criteria from 2003 . According to them, the diag- well as high estrogen levels during prenatal life, nosis is set if any two out of three criteria are met, disrupt development of the thymus and its func- in the absence of other entities that might cause tion in maintaining immune tolerance, and are these findings: suspected to enhance autoimmune response 1) Oligoovulation and/or anovulation. in PCOS. Vitamin D deficiency could be also in- 2) Signs of androgen excess (clinical or biochem- volved in the pathogenesis of HT and PCOS. CONCLUSIONS: The above-mentioned com- ical). mon etiological factors associated with fertili- 3) Polycystic ovaries (one or two) on gynecolog- ty problems in HT and PCOS require further re- ical ultrasound. search. Following these criteria, four phenotypes of PCOS have been marked out: phenotype A, when Key Words: all three criteria are fulfilled and phenotypes with Hypothyroidism, Hashimoto’s disease, Polycystic ovary syndrome, Fertility disorders. two out of three fulfilled criteria: menstrual dis- orders and hyperandrogenism, hyperandrogenism 346 Corresponding Author: Karolina Kowalczyk, MD; e-mail: [email protected] Thyroid disorders in polycystic ovary syndrome and polycystic ovaries on ultrasound and finally companied by menstrual disorders, may suggest menstrual disorders and polycystic ovaries on ul- the symptoms of PCOS. trasound. The heterogeneity of these phenotypes The presence of receptors for signalling path- is the main cause of difficulties in determining ways (thyrotropin-releasing hormone – TRH, clear pathogenesis, as well as causal treatment TSH) and thyroid hormones has been demon- of PCOS. strated in animal studies in monkey uterus. More- Thyroid disorders may occur with thyroid hor- over, the impact of long-term estrogen and estro- mone deficiency (hypothyroidism), thyroid hor- gen-progestogen treatment on their expression mone excess (hyperthyroidism) or with thyroid has been evidenced5. The expression of TSH, hormones within the normal range (euthyreosis). TRα1 and TRβ1 receptors has been stated in the Hashimoto’s thyroiditis (HT) also called chronic human endometrium as well6. The highest TRα1 lymphocytic thyroiditis is the most frequent cause and TRβ1 receptor expression were found in of hypothyroidism and also the most frequent receptive endometrium before ovulation. Thy- autoimmune disorder. The diagnosis is made by roid hormones adjusted endometrial synthesis of detecting elevated levels of anti-thyroid peroxi- protein mRNA, among others leukemia inhibi- dase antibodies (anti-TPO) and/or antithyroglob- tory factor (LIF), which is important during the ulin (anti-Tg) in the serum and a characteristic implantation process, and glucose transporter 1 7 thyroid image on ultrasound – hypoechoic or het- (GLUT1) . Free triiodothyronine (fT3) has been erogeneous echotexture. The gold standard in the detected in follicular fluid8. TSH and its receptors’ diagnosis of HT is lymphocytic infiltration and transcripts have been revealed not only in ovarian fibrosis found on histological examination; how- structures such as oocytes, cumulus oophorus ever, nowadays it is not performed routinely. HT cells, granulosa cells and ovarian epithelium, but may occur with clinical hypothyroidism (most also in syncytiotrophoblast villi8. Moreover, in the often), euthyreosis or hyperthyroidism. placenta there are present membrane transport- According to the National Health and Nutrition ers for triiodothyronine (T3) and thyroxine (T4), Survey (NHANES) – the biggest epidemiological deiodinase enzymes type 2 and 3, which regulate research conducted in the USA on a group of thyroid hormone activity in the placenta, and tran- 17 000 subjects – the frequency of hypothyroid- sthyretin – a protein binding thyroid hormones ism with a thyroid-stimulating hormone (TSH) and retinol. In vitro research on bovine oocytes level above 4.5 mIU/L in women of reproductive and embryos suggests that thyroid hormones play age is approximately 4%3. In research on the a role in the implantation process. Oocytes and incidence of thyroid disorders, conducted in Col- embryos mentioned above, cultured in medium orado on 25 000 individuals, the percentage of enriched with thyroid hormones, presented better hypothyroidism increased with age4. Therefore, outcomes regarding blastocyst formation, implan- the most probable thyroid disorder among young tation capacity, decreased apoptosis rate and vital- women is HT with normal thyroid function and ity after cryopreservation9. elevated levels of anti-TPO and/or anti-Tg. The Overt hypothyroidism is accompanied with prevalence of anti-TPO and anti-Tg in the age TRH increase, which causes hyperprolactinemia, group of 20-29 years is 11.3% and 9.2% respec- luteinizing hormone (LH) pulsatile secretion dis- tively, while in the age group of 30-39 years it is ruption, sex hormone-binding globulin (SHBG) 14.2% and 14.5%, respectively. synthesis decrease, estrogen peripheral metabo- NHANES revealed that the prevalence of hy- lism disruption and increase of ovarian androgen perthyroidism in the eastern population is low3. production. In research on female pigs, hypothy- TSH below 0.4 mIU/L was observed in 3% of roidism resulted in increased gonadotropin re- subjects of reproductive age. ceptor sensitivity in the ovary, which finally pro- Hypothyroidism has an important impact on moted ovarian hypertrophy, as well as multiple women’s reproductive health. In the prepuber- ovarian cyst formation10. Hypothyroidism may tal period, it can lead to delayed puberty. In contribute to heavy, irregular menstrual bleeding, adult women hypothyroidism, as well as hy- spotting during the menstrual cycle, insufficient perthyroidism, is considered to be the cause of endometrial thickness, ovulation disorders and, menstrual disorders and decreased fertility as a in consequence, endometrial proliferative phase consequence. Women with undiagnosed PCOS disorders. are often referred for thyroid examination. On the Sex hormone imbalance has likewise been other hand, overt hypo- or hyperthyroidism, ac- described in hyperthyroidism. It covers: SHBG 347 K. Kowalczyk, G. Franik, D. Kowalczyk, D. Pluta, Ł. Blukacz, P. Madej synthesis increase, estrogen metabolism disrup- control group15. It is really interesting, consider- tion, increased estrogen to androgen conversion, ing the fact that analogical research conducted higher basal gonadotropin-releasing hormone on patients with autoimmune diseases such as (GnRH) concentration and stronger pituitary to rheumatoid arthritis, spondyloarthritis or Behçet GnRH response. Menstrual disorders have been disease revealed a decreased ovarian reserve16. also observed, while in women in euthyreosis Significantly, a lower fT3, but normal TSH, the ovulation remains regular. level was marked in infertile women with HT Taking into consideration the high prevalence treated with LT4 compared to fertile women with of both
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