• 제목/요약/키워드: Maternal hypothyroidism

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Effects of Maternal Hypothyroidism on the Pubertal Development in Female Rat Offspring

  • Park, Jin-Soo;Lee, Sung-Ho
    • 한국발생생물학회지:발생과생식
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    • 제25권2호
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    • pp.83-91
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    • 2021
  • The present study was performed to investigate the effect of maternal hypothyroidism and puberty onset in female rat pups. To do this, we employed propylthiouracil (PTU) to prepare a hypothyroid rat model. Pregnant rats were treated with PTU (0.025%) in drinking water from gestational day 14 to postnatal day 21 of offspring. Comparison of general indices such as body and tissue weights and puberty indices such as vaginal opening (VO) and tissue histology between control and PTU-treated rats were conducted. There was no significant difference in the date of VO between control and PTU group. The body weights of the PTU group were significantly lower, only 36.8% of the control group (p<0.001). Although the absolute thyroid weight was not changed by PTU treatment, the relative weight increased significantly about 2.8 times (p<0.001), indicating that hypothyroidism was successfully induced. On the other hand, the absolute weights of the ovary and uterus were markedly decreased by PTU administration (p<0.001), and the relative weight was not significantly changed. The ovarian histology of PTU group revealed the advanced state of differentiation (i.e., presence of corpora lutea). Inversely, the uterine histology of PTU group showed underdeveloped structures compared those in control group. Taken together, the present study demonstrates that our maternal hypothyroidism model resulted in minimal effect on pubertal development symbolized by VO despite of huge retardation in somatic growth. More sophisticatedly designed hypothyroidism model will be helpful to achieve a better understanding of pubertal development and related disorders.

Adrenal and thyroid function in the fetus and preterm infant

  • Chung, Hye Rim
    • Clinical and Experimental Pediatrics
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    • 제57권10호
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    • pp.425-433
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    • 2014
  • Adrenal and thyroid hormones are essential for the regulation of intrauterine homeostasis, and for the timely differentiation and maturation of fetal organs. These hormones play complex roles during fetal life, and are believed to underlie the cellular communication that coordinates maternal-fetal interactions. They serve to modulate the functional adaptation for extrauterine life during the perinatal period. The pathophysiology of systemic vasopressor-resistant hypotension is associated with low levels of circulating cortisol, a result of immaturity of hypothalamic-pituitary-adrenal axis in preterm infants under stress. Over the past few decades, studies in preterm infants have shown abnormal clinical findings that suggest adrenal or thyroid dysfunction, yet the criteria used to diagnose adrenal insufficiency in preterm infants continue to be arbitrary. In addition, although hypothyroidism is frequently observed in extremely low gestational age infants, the benefits of thyroid hormone replacement therapy remain controversial. Screening methods for congenital hypothyroidism or congenital adrenal hyperplasia in the preterm neonate are inconclusive. Thus, further understanding of fetal and perinatal adrenal and thyroid function will provide an insight into the management of adrenal and thyroid function in the preterm infant.

Endocrine problems in children with Prader-Willi syndrome: special review on associated genetic aspects and early growth hormone treatment

  • Jin, Dong-Kyu
    • Clinical and Experimental Pediatrics
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    • 제55권7호
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    • pp.224-231
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    • 2012
  • Prader-Willi syndrome (PWS) is a complex multisystem genetic disorder characterized by hypothalamic-pituitary dysfunction. The main clinical features include neonatal hypotonia, distinctive facial features, overall developmental delay, and poor growth in infancy, followed by overeating with severe obesity, short stature, and hypogonadism later in development. This paper reviews recent updates regarding the genetic aspects of this disorder. Three mechanisms (paternal deletion, maternal disomy, and deficient imprinting) are recognized. Maternal disomy can arise because of 4 possible mechanisms: trisomy rescue (TR), gamete complementation (GC), monosomy rescue (MR), and postfertilization mitotic nondisjunction (Mit). Recently, TR/GC caused by nondisjunction at maternal meiosis 1 has been identified increasingly, as a result of advanced maternal childbearing age in Korea. We verified that the d3 allele increases the responsiveness of the growth hormone (GH) receptor to endogenous GH. This paper also provides an overview of endocrine dysfunctions in children with PWS, including GH deficiency, obesity, sexual development, hypothyroidism, and adrenal insufficiency, as well as the effects of GH treatment. GH treatment coupled with a strictly controlled diet during early childhood may help to reduce obesity, improve neurodevelopment, and increase muscle mass. A more active approach to correct these hormone deficiencies would benefit patients with PWS.

산모의 요오드섭취가 산후 갑상선염 발현에 미치는 영향 (The Effects of Dietary Iodine Intake on the Postpartum Thyroiditis(PPT) Manifestation)

  • 조여원
    • Journal of Nutrition and Health
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    • 제30권10호
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    • pp.1195-1202
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    • 1997
  • Iodine-rich seaweed soup has been traditionally supplied to postpartum women in Korea. This dietary habit might introduce over-intake of iodine above the recommended requirements, and might provoke postpartum thyroid dysfunction. Although the response to excess iodine intake is highly variable, goiter, hyperthyroidism, hypothyroidism, and thyroiditis could follow the daily intake of 1,500$\mu\textrm{g}$ of iodine. A few studies are available concerning iodine toxicity in Korea. The purpose of this study was to investigate the relationships between the dietary intake of iodine and thyroid function change as well as the incidence of postpartum thyroiditis. One hundred and thirty-seven postpartum women who had experienced normal deliveries were studied. Dietary intake of iodine and excretion concentration of iodine in breast milk and maternal urine were measured . Serum T$_3$, T$_4$, TSH, anti-thyroglobulin antibody, and anti-microsomal antibody were anlayzed 1 week before delivery and 1, 6, 12, and24 weeks after delivery. Iodine intake was analyzed by one-to-one interviews using 24-hr recall and a food frequncy questionnaire. The result showed that the intake of dietary iodine before delivery and 1 and24 weeks after delivery were 483$\mu\textrm{g}$/day, 3367$\mu\textrm{g}$/day, and 1069$\mu\textrm{g}$/day, respectively. The concentration of iodine in urine at the first week after delivery was 63$\mu\textrm{g}$/dL, and 23.9$\mu\textrm{g}$/dL in breast milk . The levels of serum T$_3$ and T$_4$ before delivery were 2.01ng/mL and 11.49$\mu\textrm{g}$U/dL, respectively, showing that the levels were gradually dropping to normal values after delivery. Positive serum anti-thyroglobulin antibody and anti-microsomal antibody appeared in 3 cases. After a 24 week follow-up period , 6 women(10.3%) experienced cases of postpartum thyroiditis, 5 of which were cases of hyperthyroidism and one of which was a case of hypothyroidism. These figures of postpartum thyroiditis are similar to those of other countries.

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자가면역성 갑상선질환에서 TSH 수용체 항체의 역활에 관한 연구 (The Roles of the TSH Receptor Antibodies in Autoimmune Thyroid Diseases)

  • 고창순
    • 대한핵의학회지
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    • 제20권2호
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    • pp.85-100
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    • 1986
  • To evaluate the clinical and pathogenetic roles of TSH receptor antibodies in autoimmune thyroid diseases, TBII were measured by TSH-radioreceptor assay methods in 352 patients with Graves' disease, 108 patients with other thyroid diseases and 69 normal persons. The normal range of TBII activity was less than 15%. The frequencies of detectable TBII in 169 patients with untreated Graves' disease, 31 patients with hyperthyroidism under treatment and 70 patients with euthyrodism under treatment were 92.4%, 87.1% and 54.3% respectively. However 12 (21.8%) out of 55 patients who have been in remission more than one year after discontinuation of antithyroid drugs treatment had detectable TBII activities in their sera. In 196 patients with untreated Graves' disease, the frequency of TBII increased by increasing size of goiter and the frequency of proptosis was significantly high in patients whose TBII activities were more than 60%. TBII activities were roughly correlated with total $T_3,\;T_4$ and free $T_4$ index but low $\gamma^2$ value(less than 0.1). In 67 patients with Graves' disease who were positive TBII before antithyroid drugs treatment, TBII activities began to decrease from the third months and it was converted to negative in 35.8% of patients at 12 months after treatment. There were no significant differences of the declining and disappearing rates of TBII activities between high dose and conventional dose groups. TBII activities were significantly increased initially (2-4 months) and then began to decrease from 5-9 months after $^{131}I$ treatment. There were two groups, one whose TBII activities decreased gradually and the other did not change untill 12 months after subtotal thyroidectomy. Although preoperative clinical and laboratory findings of both groups were not different, TBII activities of non-decreasing group were significantly higher than those of decreasing group$(74.6{\pm}18.6%\;vs\;39.2{\pm}15.2%;\;P<0.01)$. Thirty three(55.9%) out of 59 patients with Graves' disease relapsed within 1 year after discontinuation of antithyroid drugs. The positive rate of TBII at the end of antithyroid drug treatment in relapse group(n=33) was significantly higher than those in remission group (n=26) (63.6% vs 23.1%; P < 0.05). The mean value of TBII activities at the end of antithyroid drug treatment in relapse group was significantly elevated $(29.7{\pm}21.4%\;vs\;14.7{\pm}11.1%,\;P<0.05)$. Positive predictive value of TBII for relapse was 77.8%, which was not different from those of TRH nonresponsiveness(78.6%). The frequencies of detectable TBII in 68 patients with Hashimoto's thyroiditis, 10 patients with painless thyroiditis and 5 patients subacute thyroiditis were 14.7%, 20% and 0%, respectively. However in 25 patients with primary nongoitrous myxedema, 11 patients(44%) showed TBII activities in their sera. 9 out of 11 patients who had TBII activities in their sera showed high TBII activities(more than 70% binding inhibition) and their IgG concentrations showing 50% binding inhibition of $^{125}I-bTSH$ to the TSH receptor were ranges of 0.1-2.6 mg/dl. One patient who had high titer of TBII in her serum delivered a hypothyroid baby due to transplacental transfer of maternal TBII. These findings suggested that 1) TSH receptor antibodies are closely related to a pathogenetic factor of Graves' hyperthyroidism and of some patients with primary non-goitrous myxedema, 2) measurement of TSH receptor antibodies is helpful in evaluating the clinical outcome of patients with Graves' disease during antithyroid drug treatment and in predicting the neonatal transient hypothyroidism of baby delivered from primary myxedema patients. 3) there are 2 or more different types of TSH receptor antibodies in autoimmune thyroid diseases including one which stimulates thyroid by binding to the TSH receptor and another which blocks adenylate cyclase stimulation by TSH.

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