Thyroid disease and female reproduction

Krassas, Gerasimos E

doi:10.1016/s0015-0282(00)01589-2

Cited by 271 publications

(223 citation statements)

References 36 publications

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“…Além disso, na mulher, a deficiência dos hormônios tireoidianos causa irregularidade do ciclo menstrual, ciclos anovulatórios e polimenorréia (Krassas, 2000) ou amenorréia (Tamura et al, 1998). Em fêmeas gestantes, pode induzir ao aborto (Johnson, 1994) ou originar neonatos prematuros de baixo peso e com anomalias congênitas (Thomas e Reid, 1987;Krassas, 2000).…”

Section: Introductionunclassified

Histomorfometria e histoquímica dos ovários, tubas e útero de ratas hipotireóideas em metaestro-diestro

Silva

Serákides

Oliveira

et al. 2004

Arq. Bras. Med. Vet. Zootec.

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RESUMOA foliculogênese ovariana foi estudada em ratas adultas Wistar, hipotireóideas na fase de metaestrodiestro. O hipotireoidismo foi induzido pela administração oral e diária de propiltiouracil (1mg/animal). As ratas eutireóideas receberam placebo. Após 120 dias de tratamento, foi colhido o plasma para dosagem de tiroxina livre, progesterona e estradiol após o que foram sacrificadas para colheita dos ovários, tubas e útero, para avaliação histomorfométrica e histoquímica. O hipotireoidismo reduziu significativamente o peso dos ovários e o número de folículos secundários e terciários e de corpos lúteos sem, no entanto, alterar a porcentagem de folículos atrésicos e o número de folículos primários e pré-ovulatórios. As células da granulosa dos folículos secundários das ratas hipotireóideas apresentavam núcleo pequeno com significativa redução do número de regiões organizadoras de nucléolo (NORs). Essas mudanças não alteraram os valores periféricos de estradiol e de progesterona. Houve redução significativa da espessura do endométrio, do número de glândulas endometriais e da altura do epitélio do infundíbulo.Palavras-chave: rata, hipotireoidismo, ovário, tuba, útero, NORs ABSTRACT Ovarian folicullogenesis was studied in adult

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Section: Introductionunclassified

Histomorfometria e histoquímica dos ovários, tubas e útero de ratas hipotireóideas em metaestro-diestro

Silva

Serákides

Oliveira

et al. 2004

Arq. Bras. Med. Vet. Zootec.

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“…Alteration in thyroid function, particularly hypothyroidism, can cause ovulatory dysfunction, the latter being the leading cause of impaired female fertility 1–3. Although the underlying causes of hypothyroidism and polycystic ovary syndrome (PCOS) are completely different, these two entities have many features in common, including oligo- or anovulation; decreased serum sex hormone–binding globulin; increased serum free testosterone, luteinizing hormone (LH) and cholesterol concentrations 4–7.…”

mentioning

confidence: 99%

Effect of thyroid hormone replacement therapy on ovarian volume and androgen hormones in patients with untreated primary hypothyroidism

Müderris

Boztosun

Öner

et al. 2011

Annals of Saudi Medicine

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BACKGROUND AND OBJECTIVES:Primary hypothyroidism may be associated with ovarian enlargement and/ or cyst formation. We evaluated the effect of thyroid hormone replacement therapy on hormonal changes, ovarian volume and sonographic appearance.DESIGN AND SETTING:Open, prospective study of women admitted to university gynecology clinic.PATIENTS AND METHODS:The study included 26 patients with untreated hypothyroidism who had polycystic (n=10) or normal-appearing (n=16) ovaries and 20 euthyroidic controls. Basal serum total testosterone, free testosterone, androstenedione, dehydroepiandosterone-sulfate, prolactin, estradiol, luteinizing hormone, follicle-stimulating hormone, free T3, free T4 and thyroid-stimulating horone, together with ovarian volumes, were determined and repeated after euthyroidism was achieved.RESULTS:Ovarian volumes of patients with hypothyroidism were significantly greater compared with controls, and their magnitudes diminished significantly during thyroid hormone replacement therapy. Hypothyroidic patients with polycystic ovaries had significantly higher serum free testosterone and dehydroepiandosterone-sulfate, but lower androstenodione levels compared with those who had normal-appearing ovaries. Serum total testosterone concentrations were significantly higher in hypothyroidic patients without polycystic ovaries, and thyroid hormone replacement therapy achieved a significant reduction in total as well as free testosterone.CONCLUSION:Severe longstanding hypothyroidism leads to increased ovarian volume and/or cyst formation. A decrease in ovarian volume, resolution of ovarian cysts and reversal of the polycystic ovary syndrome-like appearance, together with improvement in serum hormone levels, occurred after euthyroidism was achieved.

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“…Overgrowth seen in the T-grt/grt and T-grt/+ mice after 7 weeks of age is a side effect related to the excessive feeding of thyroid powder. In humans, menstrual disturbances in thyrotoxicosis are 2.5 times more frequent than in the normal population, and hyperthyroidism in women has been linked to reduced fertility [21]. This may account for the decreased rates of copulation and parturition in both T-grt/grt and Tgrt/+ mice.…”

Section: Discussionmentioning

confidence: 99%

“…Several reports have indicated that the deficiency of LHR or FSHR signal cascades causes female infertility, which is characterized by follicular arrest beyond the Graafian follicle and disturbed ovulation [1,23,38,42]. Hypothyroidism, however, is associated with a broad spectrum of reproductive disorders ranging from abnormal sexual development through menstrual irregularities to anovulation in mice [14,16], rat [3,15,17], dog [32] and humans [9,21]. In rare cases, it has been reported that infertility in Pax8 null mice was due to the direct morphogenic function of Pax8 on both the thyroid and Müllerian duct.…”

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confidence: 99%

Female Infertility in grt Mice is Caused by Thyroid Hormone Deficiency, not by Insufficient TPST2 Activity in the Reproductive Organs

Hosoda

Sasaki

Agui

2008

The Journal of Veterinary Medical Science

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ABSTRACT. The growth-retarded (grt) mouse has an autosomal recessive hypothyroidism and the female shows lifelong infertility. We previously reported that these mutant phenotypes are caused by a deficiency in the enzymatic activity of tyrosylprotein sulfotransferase-2 (TPST2), and severe thyroid hypogenesis and consequent dwarfism are mainly due to the impairment of the tyrosine sulfation of thyroid-stimulating hormone receptor (TSHR) by TPST2. Although TPST2 is ubiquitously expressed and many proteins are predicted to be tyrosine sulfated and involved in many biological processes, the functional roles of tyrosine sulfation in the reproductive organs remain unclear. These findings tempted us to hypothesize two possible mechanisms underlying the infertility; a deficiency in TPST2 activity in the reproductive organs might cause the infertility in grt mice, or a significant decrease in serum thyroid hormones might impair the normal development of reproductive organs. When mutant female mice were fed a diet supplemented with sufficient thyroid powder to correct their growth retardation, the rate of copulation, pregnancy, and parturition was completely restored. Therefore, we concluded that the infertility in grt female is due to a thyroid hormone deficiency. The growth-retarded (grt) mouse has an autosomal recessive, fetal-onset, severe thyroid dysgenesis related to thyroid-stimulating hormone (TSH) hyporesponsiveness [20,41]. We identified that the grt phenotype is caused by a single misssense mutation in the tyrosylprotein sulfotransferase 2 (TPST2) gene with a C-to-G transition at nucleotide 798, leading to the replacement of a highly conserved histidine with glutamine at codon 266 in the sulfotransferase domain by positional cloning [36].TPST catalyzes the transfer of a sulfuryl group from the universal sulfation substrate, 3'-phosphoadenosine 5'-phosphosulfate, to a tyrosyl residue within the acidic motifs of proteins that transit the Golgi apparatus [28]. In mammals, two isozymes, TPST1 and 2, catalyze the tyrosine sulfation of proteins. Although TPST1 and 2 in mammals have 65~67% identical amino acid sequences [28], they seem to have different acceptor preferences [31,37]. Evidence indicates that the posttranslational modification by tyrosine sulfation regulates many important protein-protein interactions and modulates binding affinity and specificity [8,10,11,18,24,26,29,[33][34][35][36]. We previously showed that the sulfation of the tyrosine 385 of TSHR by TPST2 is indispensable for the activation of TSH signaling, and grt mice develop hypothyroidism and dwarfism since they are unable to fully respond to TSH. However, since many proteins besides TSHR are likely to be the substrates of TPST2, severe growth retardation of grt mice might conceal a defect in other proteins that act as substrates of TPST2 [36].

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Thyroid disease and female reproduction

Cited by 271 publications

References 36 publications

Histomorfometria e histoquímica dos ovários, tubas e útero de ratas hipotireóideas em metaestro-diestro

Histomorfometria e histoquímica dos ovários, tubas e útero de ratas hipotireóideas em metaestro-diestro

Effect of thyroid hormone replacement therapy on ovarian volume and androgen hormones in patients with untreated primary hypothyroidism

Female Infertility in grt Mice is Caused by Thyroid Hormone Deficiency, not by Insufficient TPST2 Activity in the Reproductive Organs

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