The epidemiology of iodine-deficiency disorders in relation to goitrogenic factors and thyroid-stimulating-hormone regulation

Background Iodine deficiency disorders (lDD) are a significantpublic health problem globally. Iodine deficiency may causesubclinical hypothyroidism during pregnancy and early infancy.Neonatal thyroid screening of serum thyroid􀁊stimulating hormone(TSH) to detect hypothyroidism may also be used to determinethe prevalence of IDD in a population. Previous studies reportedmild ID D status in different parts of Indonesia.Objective To evaluate the iodine status of neonates born inMitra K eluarga Surabaya Hospital (MKSH) by TSH screeningover a 6􀁊year period.Methods T his is a cross􀁊sectional and hospital􀁊based studyconducted in MKSH from January 2005 to December 2010. Ofthe 5,619 infants born in MKSH during the study period, 3,349(59.6%) healthy infants took part in this study. Blood specimensfor TSH measurement were collected from subjects 2 to 6 daysafter birth, and sent to a reference laboraratory for evaluation.Using the neonatal TSH values, the iodine deficiency level ofthe group was determined according to the WHO/UNICEF/International Council for the Control of IDD criteria.Results A total of 3,349 newborn babies underwent neonatalTSH screening in MKSH. Subjects' mean TSH concentrationwas 5.14 mIU!L. A TSH concentration> SmIU!L was found in1270 (37.9%) subjects, 166 (27.6%) in 2005, 252 (44.0%) in 2006,331 (47.1 %) in 2007, 356 (57.7%) in 2008, 114 (20.7%) in 2009and 51 (16.8%) in 2010. On the basis of the WHO/UNICEF/International Council for the Control of Iodine DeficiencyDisorder criteria, this frequency corresponded to a moderate levelof IDD. Twenty􀁊two neonates had TSH > 20 mIU!L from which2 infants were confirmed positive for hypothyroidism.Conclusion A 6􀁊year study of 3,349 newborns screened for TSHrevealed that 37.9% of subjects had TSH concentration of morethan SmIU!L. This frequency indicates a moderate level of IDDin the study population. [Paediatr Indones. 2012;52:289,93].

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Genetic thyroid stimulating hormone regulation of atrial fibrillation risk is mediated through an effect on height

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/clinem/dgab272 ◽

2021 ◽

Author(s):

Mingjian Shi ◽

Ali M Manouchehri ◽

Christian M Shaffer ◽

Nataraja Sarma Vaitinadin ◽

Jacklyn N Hellwege ◽

...

Keyword(s):

Atrial Fibrillation ◽

Genetic Association ◽

Multiple Testing ◽

Mendelian Randomization ◽

Later Life ◽

Thyroid Stimulating Hormone ◽

Hormone Regulation ◽

Nucleotide Polymorphisms ◽

Free T4 ◽

Stimulating Hormone

Abstract Background A genetic predisposition to lower thyroid stimulating hormone (TSH) levels associates with increased atrial fibrillation (AF) risk through undefined mechanisms. Defining the genetic mediating mechanisms could lead to improved targeted therapies to mitigate AF risk. Methods We used two-sample Mendelian randomization (MR) to test associations between TSH-associated single nucleotide polymorphisms (SNPs) and 16 candidate mediators. We then performed multivariable Mendelian randomization (MVMR) to test for a significant attenuation of the genetic association between TSH and AF, after adjusting for each mediator significantly associated with TSH. Results Four candidate mediators (free T4, systolic blood pressure, heart rate, and height) were significantly inversely associated with genetically predicted TSH after adjusting for multiple testing. In MVMR analyses, adjusting for height significantly decreased the magnitude of the association between TSH and AF from -0.12 (s.e. 0.02) occurrences of AF per standard deviation change in height to -0.06 (0.02) (p=0.005). Adjusting for the other candidate mediators did not significantly attenuate the association. Conclusions The genetic association between TSH and increased AF risk is mediated, in part, by taller stature. Thus, some genetic mechanisms underlying TSH variability may contribute to AF risk through mechanisms determining height occurring early in life that differ from those driven by thyroid hormone level elevations in later life.

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Neonatal thyroid‐stimulating hormone concentrations in northern Sydney: further indications of mild iodine deficiency?

The Medical Journal of Australia ◽

10.5694/j.1326-5377.2002.tb04431.x ◽

2002 ◽

Vol 176 (7) ◽

pp. 317-320 ◽

Cited By ~ 36

Author(s):

Aidan McElduff ◽

Patrick McElduff ◽

Jenny E Gunton ◽

Graham Hams ◽

Veronica Wiley ◽

...

Keyword(s):

Iodine Deficiency ◽

Thyroid Stimulating Hormone ◽

Stimulating Hormone

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Role of Thyrotropin-Releasing Hormone in Thyroid-Stimulating Hormone and Growth Hormone Regulation during Postnatal Maturation in Female Wistar Rats

Neonatology ◽

10.1159/000242573 ◽

1986 ◽

Vol 50 (2) ◽

pp. 91-96 ◽

Cited By ~ 3

Author(s):

Vladimir Štrbák ◽

Robert Angyal ◽

Jana Jurčovičová ◽

Anna Randušková

Keyword(s):

Growth Hormone ◽

Wistar Rats ◽

Thyroid Stimulating Hormone ◽

Thyrotropin Releasing Hormone ◽

Hormone Regulation ◽

Postnatal Maturation ◽

Releasing Hormone ◽

Female Wistar Rats ◽

Stimulating Hormone

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Thyroid-Stimulating Hormone Regulation of Ornithine Decarboxylase Activity in the Thyroid

Endocrinology ◽

10.1210/endo-97-5-1089 ◽

1975 ◽

Vol 97 (5) ◽

pp. 1089-1095 ◽

Cited By ~ 18

Author(s):

DOUGLAS R. ZUSMAN ◽

GERARD N. BURROW

Keyword(s):

Ornithine Decarboxylase ◽

Thyroid Stimulating Hormone ◽

Decarboxylase Activity ◽

Hormone Regulation ◽

Ornithine Decarboxylase Activity ◽

Stimulating Hormone

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Neonatal Thyroid-Stimulating Hormone Concentrations in Belgium: A Useful Indicator for Detecting Mild Iodine Deficiency?

PLoS ONE ◽

10.1371/journal.pone.0047770 ◽

2012 ◽

Vol 7 (10) ◽

pp. e47770 ◽

Cited By ~ 29

Author(s):

Stefanie Vandevijvere ◽

Wim Coucke ◽

Jean Vanderpas ◽

Caroline Trumpff ◽

Maarten Fauvart ◽

...

Keyword(s):

Iodine Deficiency ◽

Thyroid Stimulating Hormone ◽

Stimulating Hormone

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Neonatal Thyroid-Stimulating Hormone Screening as an Indirect Method for the Assessment of Iodine Status in Central Siberia

International Journal of Diabetes & Metabolic Disorders ◽

10.33140/ijdmd/03/04/00003 ◽

2018 ◽

Vol 3 (4) ◽

Keyword(s):

Newborn Screening ◽

Congenital Hypothyroidism ◽

Iodine Deficiency ◽

Screening Program ◽

Thyroid Stimulating Hormone ◽

The Arctic ◽

Central Siberia ◽

Iodine Status ◽

The Republic ◽

Stimulating Hormone

Background: Iodine deficiency is associated with goiter and impaired brain function. Neonatal thyroid-stimulating hormone (TSH) screening for congenital hypothyroidism used as an indicator of the degree of iodine deficiency and of its control. An increased frequency of thyroid-stimulating hormone (TSH) measurements above 5 mIU/L in newborn screening corresponds to the impaired iodine status of the population. The aim: to estimate the iodine deficiency and the effectiveness of iodine prophylaxis in Krasnoyarsk territory, Republics of Tuva and Khakassia according the results of neonatal TSH_screening. Methods: An 18-year analysis was performed in 34,980 newborns participating in the national thyroid newborn screening program. The TSH concentration was measured in dry blood spots collected by heel stick on filter paper, 96 hours after birth, using DELFIA method. Results: According to the data of the congenital hypothyroidism screening the rate of TSH < 5 mU/1 was 11.8% in Krasnoyarsk territory (23.9% in 2000) and corresponded to mild iodine deficiency. In different regions of Krasnoyarsk territory the rate of TSH < 5 mU/1 in the newborn varied from 3.5% to 23.7%. The highest values were marked in the Arctic peninsula Taimyr, in cities Zheleznogorsk (nuclear facility) and Sosnovoborsk, in Irbeysky, Suchobuzimsky, Eniseysky, Tuchtetsky, Novoselovsky regions (20.9–23.7%). In the Republic of Khakasia the rate of TSH < 5 mU/1 was 12.5%. In the Republic of Tyva the rate of TSH < 5 mU/1 was – 6.6% (38.6% in 1997; 11.5% in 2000). These results indicate mild iodine deficiency. Conclusion: Our investigations show mild iodine deficiency in Central Siberia demanding continuous adequate iodine prevention. Additional assessment of the iodine intake in the regions with mild iodine deficiency is needed to prevent suboptimal cognitive and psychomotor outcomes.

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