scholarly journals Spectrum of thyroid dysfunction and dementia: a dose–response meta-analysis of 344,248 individuals from cohort studies

2021 ◽  
Vol 10 (4) ◽  
pp. 410-421
Author(s):  
Xingyao Tang ◽  
Zhi-Hui Song ◽  
Dawei Wang ◽  
Jinkui Yang ◽  
Marly Augusto Cardoso ◽  
...  

Thyroid hormone, as a modifiable risk factor for dementia, promotes neurocognitive function and regulates metabolic processes. Various studies have defined different thyroid-stimulating hormone cutoffs, but the safest thyroid-stimulating hormone concentration was absent. A dose–response meta-analysis describing the overall functional relation and identifying exposure intervals associated with a higher or lower disease risk is thus desirable. Therefore, our current analysis was conducted to understand the influence of thyroid dysfunction on dementia risk. We searched PubMed, Embase, and Web of Science before May 1, 2020 for human studies published in English. Studies were considered for inclusion if they used a cohort study design to measure the risk of dementia in different thyroid function status groups, diagnosed thyroid functional status and all-cause dementia, included participants aged >18 years, and provided quantitative measures of data. The analysis contained 17 articles with 344,248 individuals with a 7.8-year mean follow-up. Ten studies with 329,287 participants indicated that only subclinical hyperthyroidism was associated with an increased risk of dementia. In contrast, subclinical hypothyroidism, clinical hyperthyroidism, and clinical hypothyroidism did not affect dementia. In the dose–response meta-analysis with 46,417 samples from 11 studies, the association of thyroid-stimulating hormone with the risk of dementia exhibited a U-shaped curve. Our study indicated that subclinical hyperthyroidism was associated with the risk of dementia and the thyroid-stimulating hormone concentration at around 1.55–1.60 mU/L as the optimum range for the risk of dementia.

Lupus ◽  
2018 ◽  
Vol 27 (13) ◽  
pp. 2120-2128 ◽  
Author(s):  
W Luo ◽  
P Mao ◽  
L Zhang ◽  
Z Yang

Introduction Systemic lupus erythematosus (SLE) is a chronic autoimmune disease, the pathogenesis of which remains elusive. The deficiency or excess of thyroid hormone is defined as thyroid dysfunction, including (subclinical) hypothyroidism and (subclinical) hyperthyroidism. Autoimmune factors are likely to be relevant to the development of SLE and thyroid dysfunction. Recently, many studies have indicated that the prevalence of thyroid dysfunction is higher in SLE patients than in the general population. The objective of our study was to perform a systematic review and meta-analysis to find out the relationship between SLE and thyroid dysfunction. Methods Literature databases were searched, including PubMed, Embase, Web of science, Cochrane, CNKI, CHINESE WANFANG, China Science and Technology Database (VIP). Studies comparing presence of thyroid dysfunction in SLE patients to healthy controls were extracted. All the statistical analyses were performed with STATA 12.0 software. Results Ten studies with 10,500 SLE patients and 44,170 healthy controls were included in this study. The meta-analysis results showed that the prevalence of (subclinical) hypothyroidism in SLE patients was higher than in the healthy controls (hypothyroidism: OR = 2.93, 95% CI = 1.81–4.75; subclinical hypothyroidism: OR = 5.67, 95% CI = 3.50–9.18). No statistical difference of (subclinical) hyperthyroidism was found between SLE patients and controls. Conclusion Our meta-analysis suggests that SLE is significantly associated with increased risk of (subclinical) hypothyroidism, but it has little influence on (subclinical) hyperthyroidism.


2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Jing Sun ◽  
Liang Yao ◽  
Yuan Fang ◽  
Ruifei Yang ◽  
Yaolong Chen ◽  
...  

Background. Evidence on the association between subclinical thyroid dysfunction and the risk of cardiovascular outcomes are conflicting. Methods and Results. PubMed, EMbase, Web of Science, Cochrane Library, and China Biology Medicine (CBM) databases were searched from inception to July 10, 2016. A total of 16 studies were included for meta-analysis. We found that subclinical hypothyroidism was not correlated with coronary heart disease (CHD) (RR = 1.17; 95% CI, 0.91–1.52), total mortality (RR = 1.02; 95% CI, 0.93–1.13), cardiovascular mortality (RR = 1.06; 95% CI, 0.77–1.45), heart failure (RR = 1.17; 95% CI, 0.87–1.57), and atrial fibrillation (RR = 1.05; 95% CI, 0.91–1.21), except CHD mortality (RR = 1.37; 95% CI, 1.03–1.84). Subgroup analysis indicated a higher estimation risk in CHD (RR = 1.54; 95% CI, 1.00–2.39), cardiovascular mortality (RR = 2.14; 95% CI, 1.43–3.22), and CHD mortality (RR = 1.54; 95% CI, 1.11–2.15) among participants < 65 years. Furthermore, subclinical hyperthyroidism was found to be associated with CHD (RR = 1.20; 95% CI, 1.02–1.42), total mortality (RR = 1.27; 95% CI, 1.07–1.51), and CHD mortality (RR = 1.45; 95% CI, 1.12–1.86). Conclusions. Subclinical hypothyroidism is likely associated with an increased risk of CHD mortality, and subclinical hyperthyroidism is likely associated with increased risk of CHD, CHD mortality, and total mortality.


1972 ◽  
Vol 55 (3) ◽  
pp. 479-487 ◽  
Author(s):  
D. EMRICH ◽  
A. von zur MÜHLEN ◽  
J. LINDNER ◽  
H. D. ZIMMERMANN ◽  
R. BECKMANN

SUMMARY In order to investigate the influence of thyroid-stimulating hormone (TSH) on the ratio of newly synthesized thyroxine( T4):tri-iodothyronine (T3), hemithyroidectomy was performed on rats maintained on an iodinerich diet. One and two weeks after the operation the concentration of TSH increased in the plasma. As a result, the weight of the residual lobes and their thyroidal uptake of 131I/mg increased and significant histological signs of increased function in the remaining lobes were observed. The most prominent effect was a significant alteration of the ratio of newly synthesized T4:T3 in favour of T3, both in the thyroid and plasma. Four weeks after the operation, when the residual lobes weighed 57% more than those in the controls, the alterations decreased or returned to normal. The total hormone concentration in the plasma (measured as protein-bound 127I) and the oxygen consumption of the animals remained unchanged during the entire study. These findings support the hypothesis that alteration of the production and secretion ratio of T4:T3 induced by TSH might act as another regulatory factor, if a hormone deficiency originates in the peripheral cells. The results show also that changes of the T4:T3 ratio induced by TSH occur in animals on an iodine-rich diet.


2016 ◽  
Vol 9 (3) ◽  
pp. 126-129 ◽  
Author(s):  
Helen Robinson ◽  
Philip Robinson ◽  
Michael D’Emden ◽  
Kassam Mahomed

Background First-trimester care of maternal thyroid dysfunction has previously been shown to be poor. This study evaluates early management of thyroid dysfunction in pregnancy in Australia. Methods Patients reviewed by the Obstetric Medicine team for thyroid dysfunction from 1 January 2012 to 30 June 2013 were included. Data were collected on gestation at referral from the patient’s general practitioner to the antenatal clinic, information provided in the referral letter, thyroid function tests and thyroid medications. Results Eighty-five women were included in the study. At the time of general practitioner referral to antenatal services, 19% of women with preexisting thyroid disease had no thyroid function tested. Forty-three percent had an abnormal thyroid-stimulating hormone defined as being outside the laboratory-specific pregnancy reference range if available, or outside the level of 0.1–2.5 mIu/L in the first trimester, 0.2–3.0 mIu/L in the second trimester and 0.3–3.0 mIu/L in the third trimester. Only 21% of women increased their thyroxine dose prior to their first antenatal clinic review. Conclusion This study highlights that a significant proportion of women with known thyroid disease either have untested thyroid function in the first trimester or a thyroid-stimulating hormone outside of levels recommended by guidelines.


1970 ◽  
Vol 26 (2) ◽  
pp. 91-96
Author(s):  
Satya Ranjan Sutradhar

Subclinical thyroid dysfunction is defined as an abnormal serum thyroid-stimulating hormone level and free thyroxine and triiodothyronine levels within their reference ranges. The prevalence of subclinical hyperthyroidism is about 2 percent. Subclinical hypothyroidism is found in approximately 4 to 8.5 percent of the population. Most national organizations recommend against routine screening of asymptomatic patients, but screening is recommended for high risk populations. The management of subclinical thyroid dysfunction is controversial. There is good evidence that subclinical hypothyroidism is associated with progression to overt disease. Patients with a serum thyroid-stimulating hormone level greater than 10 mIU/L have a higher incidence of elevated serum low density lipoprotein cholesterol concentrations; however, evidence is lacking for other associations. There is insufficient evidence that treatment of subclinical hypothyroidism is beneficial. A serum thyroid stimulating hormone level of less than 0.1 mIU/L is associated with progression to overt hyperthyroidism, atrial fibrillation, reduced bone mineral density, and cardiac dysfunction. There is little evidence that early treatment alters the clinical course. DOI: 10.3329/jbcps.v26i2.4187 J Bangladesh Coll Phys Surg 2008; 26: 91-96


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