Fetal Loss Associated With Excess Thyroid Hormone Exposure—Reply

JAMA ◽  
2005 ◽  
Vol 293 (2) ◽  
pp. 160
JAMA ◽  
2004 ◽  
Vol 292 (6) ◽  
pp. 691 ◽  
Author(s):  
João Anselmo

2005 ◽  
Vol 60 (2) ◽  
pp. 82-83
Author(s):  
Jo??o Anselmo ◽  
Dingcai Cao ◽  
Theodore Karrison ◽  
Roy E. Weiss ◽  
Samuel Reetoff

2021 ◽  
Author(s):  
Anna Scholz ◽  
Laura Bloomfield ◽  
Mari Chambers ◽  
Raghav Bhargava ◽  
Peter Taylor ◽  
...  

1991 ◽  
Vol 131 (1) ◽  
pp. 39-48 ◽  
Author(s):  
R. J. Denver ◽  
S. Harvey

ABSTRACT Hypothyroidism reduces GH synthesis and release in several mammalian species, in which thyroid hormone directly stimulates GH gene transcription. In contrast, hypothyroidism stimulates GH secretion in birds, in which thyroid hormone directly inhibits pituitary GH release. We have, therefore, investigated the effects of thyroid status on the accumulation of newly synthesized GH in the pituitaries of 8- to 10-week-old Leghorn cockerels in vitro and in vivo. The incorporation of [35S]methionine into immunoprecipitable GH ([35S] GH) was increased, over a 4-h incubation period, in glands from birds made hypothyroid by injections of methimazole (50 mg/kg day for 10 days) in comparison with glands from vehicle-injected controls. Treatment with tri-iodothyronine (T3, 100 μg/kg per day for 10 days) in vivo did not significantly alter the accumulation of [35S]GH in vitro but did block the release of [35S]GH in response to a GH secretagogue (thyrotrophin-releasing hormone; exposure to 280 nmol/l for 30 min) and reduced immunoassayable pituitary GH content. Pretreatment of glands from euthyroid birds with T3 (100 nmol/l) in vitro (for 20 h) reduced the basal accumulation of [35S]GH as well as that induced by another GH secretagogue (GH-releasing factor; 100 nmol/l) during a 6-h labelling period. These results show that, unlike the generally stimulatory action of thyroid hormone in mammals, in birds, T3 exerts a direct inhibitory effect on the accumulation of newly synthesized pituitary GH. Journal of Endocrinology (1991) 131, 39–48


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Enoch Joseph Abbey ◽  
Eleanor M Simonsick ◽  
John McGready ◽  
Jennifer Sophie Mammen

Abstract Abstract: Introduction: Thyrotropin (TSH) levels on average are higher and vary more widely among older adults.1 Large meta-analyses and treatment trials for isolated elevated TSH in older adults did not demonstrate harm from no treatment or benefit from treatment in this population.2 Isolated, elevated TSH can result from adaptations to aging, rather than primary thyroid disease, suggesting that thyroid hormone treatment could actually cause harm.3 Objective:To determine if there is a survival effect from thyroid hormone treatment in adults aged 65+. Methodology:Thyroid functional status and thyroid hormone exposure were analyzed for 1,258 participants of the BLSA aged 65+ through death or end of follow up. We analyzed exposures by visit and also compared survival between individuals with consistently elevated, euthyroid or low TSH both on and off of therapy.Incident rate ratios (IRR) were calculated using time-dependent Poisson regression models. Covariates included age, sex, race, walking index (measure of physical function), self-rated health (SF-12), body mass index (BMI), smoking and comorbidity score. Results: Average follow-up was 9 years, with 169 deaths over the study period. The cohort comprised 49.5% women, with average age in the study being 78 years (SD ±8.2). Thyroid hormone use trended towards harm analyzed at each visit with an IRR=1.40 (95% CI 0.93–2.12) after adjusting for other covariates. Among ‘treated-to-target’versus euthyroid individuals, thyroid hormone use was associated with a significantly increased mortality rate with an IRR=1.80 (95% CI 1.09–2.96) in multivariable analysis. Conclusion: Thyroid hormone replacement among older adults,even when treated-to-target, is associated with a significantly increased mortality risk compared to euthyroid individuals with no history of thyroid hormone exposure. This suggests that treating isolated elevated TSH when changes are aging adaptations rather than primary thyroid disease could adversely affect health by altering key homeostatic adaptation. We recommend clinicians consider the underlying physiology of aging and employ age specific reference ranges when deciding on treatment for elevated TSH in older adults.4References 1. Surks et al., J Clin Endo. Met. 2007;92(12):4575–4582. 2. Stott et al., NEJM. 2017;376(26):2534–2544. 3. Mammen et al., Thyroid. 2017;27(11):1370–1377. 4. Surks et al., J Clin Endo. Met. 2010:95(2):496-502Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.


2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
James John Cray ◽  
Seth M Weinberg ◽  
Mohammed El-Salanty

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