Relationship between thyroid hormones and metabolic syndrome in a normal thyroid function population in Western China

Abstract BackgroundRecently, the relationship between thyroid hormones (THs) across the euthyroid ranges and metabolic syndrome (MetS) has been widely discussed. This study aimed to present specific cutoff values of THs to assess the association between THs and MetS in a euthyroid cohort.MethodsData of 2694 subjects, aged 18-80 years, who attended health examination in Xi’an Electric Power Central Hospital from April 2011 to December 2015 were collected and analyzed. The basic cohort enrolled 929 participants (followed up by 2221 person-years totally) to assess correlations between serum thyrotropin (TSH), triiodothyronine (T3), thyroxine (T4) levels and MetS. The second cohort included 698 participants (followed up by 1709 person-years totally) to evaluate relationships between serum free triiodothyronine (FT3), free thyroxine (FT4) levels and MetS. MetS was defined according to the criteria of the American Heart Association/National Heart, Lung, and Blood Institute (AHA/NHLBI) scientific statements of 2009. Euthyroidism was defined as serum TSH, FT3 and FT4 levels within the reference ranges without taking any thyroid medication.ResultsThe cutoff values for TSH, T3, T4, FT3 and FT4 were 2.0mIU/L, 1.9nmol/L, 117nmol/L, 4.3pmol/L and 16pmol/L, respectively. Participants were categorized into two groups according to cutoff values: the lower-THs group and the higher-THs group. There was no significant difference in the risk of MetS between two groups in TSH, T3, T4 and FT3. The incidence of MetS was significantly higher in lower-FT4 group than higher-FT4 group (1.00 vs 0.622 (0.458, 0.846), P=0.002). The lower-FT4/higher-TSH group had the highest hazard ratios of MetS. (2.131vs 1.0 (1.380,3.291), P=0.006)ConclusionsLower normal FT4 (FT4≤16.0 pmol/L) is an independent risk factor for MetS, and lower normal thyroid function (TSH>2.0 mIU/L and FT4≤16.0 pmol/L) is associated with a higher risk of developing MetS.

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Radioiodine treatment of feline hyperthyroidism in Germany

Nuklearmedizin ◽

10.1055/s-0038-1625296 ◽

2002 ◽

Vol 41 (06) ◽

pp. 245-251 ◽

Cited By ~ 3

Author(s):

M. Knietsch ◽

T. Spillmann ◽

E.-G. Grünbaum ◽

R. Bauer ◽

M. Puille

Keyword(s):

Radiation Exposure ◽

Radiation Protection ◽

Thyroid Function ◽

Radioiodine Therapy ◽

Whole Body ◽

Radioiodine Treatment ◽

Normal Thyroid ◽

Normal Thyroid Function ◽

Body Activity ◽

Thyroid Uptake

SummaryAim: Establishment of radioiodine treatment of feline hyperthyroidism in veterinary routine in accordance with German radiation protection regulations. Patients and methods: 35 cats with proven hyperthyroidism were treated with 131I in a special ward. Thyroid uptake and effective halflife were determined using gammacamera dosimetry. Patients were released when measured whole body activity was below the limit defined in the German “Strahlenschutzverordnung”. Results: 17/20 cats treated with 150 MBq radioiodine and 15/15 cats treated with 250 MBq had normal thyroid function after therapy, normal values for FT3 and FT4 were reached after two and normal TSH levels after three weeks. In 14 cats normal thyroid function was confirmed by controls 3-6 months later. Thyroidal iodine uptake was 24 ± 10%, effective halflife 2.5 ± 0.7 days. Whole body activity <1 MBq was reached 13 ± 4 days after application of 131I. Radiation exposure of cat owners was estimated as 1.97 Sv/MBq for adults. Conclusion: Radioiodine therapy of feline hyper-thyroidism is highly effective and safe. It can easily be performed in accordance with German radiation protection regulations, although this requires hospitalisation for approximately two weeks. Practical considerations on radiation exposure of cat owners do not justify this long interval. Regulations for the veterinary use of radioactive substances similar to existing regulations for medical use in humans are higly desirable.

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Thyroid dysfunction is associated with the loss of hepatitis B surface antigen in patients with chronic hepatitis B undergoing treatment with α-interferon

Journal of International Medical Research ◽

10.1177/03000605211025139 ◽

2021 ◽

Vol 49 (6) ◽

pp. 030006052110251

Author(s):

Wenfan Luo ◽

Shuai Wu ◽

Hongjie Chen ◽

Yin Wu ◽

Jie Peng

Keyword(s):

Chronic Hepatitis ◽

Hepatitis B ◽

Thyroid Function ◽

Thyroid Dysfunction ◽

Hepatitis B Surface Antigen ◽

Hbv Dna ◽

Interferon Treatment ◽

Normal Thyroid ◽

Normal Thyroid Function ◽

Hbsag Loss

Objective To investigate the influence of thyroid dysfunction on the antiviral efficacy of α-interferon in adult patients with chronic hepatitis B (CHB). Methods We performed a retrospective study of 342 patients with CHB who underwent interferon treatment for >12 weeks. Patients with thyroid dysfunction before or during treatment were defined as the thyroid dysfunction group (n = 141) and those with normal thyroid function were defined as the normal thyroid function group (n = 201). The prevalences of hepatitis B virus (HBV) DNA undetectability, low hepatitis B surface antigen (HBsAg) titre (<250 IU/mL), HBsAg loss, and hepatitis B envelope antigen loss were compared. Results During interferon treatment, 69 of 270 (25.6%) participants with normal thyroid function at baseline developed thyroid dysfunction, whereas 11 of 72 (15.3%) with thyroid dysfunction at baseline regained normal thyroid function. The thyroid dysfunction group had significantly higher prevalences of low HBsAg titre (29.8% vs. 18.9%) and HBV DNA undetectability (66.0% vs. 40.3%). Multivariate logistic regression analysis showed that thyroid dysfunction was associated with HBsAg loss (odds ratio 4.945, 95% confidence interval 1.325–18.462). Conclusions These results suggest that thyroid dysfunction is not an absolute contraindication, but is associated with HBsAg loss, in patients with CHB undergoing α-interferon treatment.

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Thyroid-stimulating hormone decreases the risk of osteoporosis by regulating osteoblast proliferation and differentiation

BMC Endocrine Disorders ◽

10.1186/s12902-021-00715-8 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Tuo Deng ◽

Wenwen Zhang ◽

Yanling Zhang ◽

Mengqi Zhang ◽

Zhikun Huan ◽

...

Keyword(s):

Thyroid Function ◽

Thyroid Stimulating Hormone ◽

Mrna Levels ◽

Dependent Manner ◽

Osteoblast Proliferation ◽

Normal Thyroid ◽

Normal Thyroid Function ◽

Gene And Protein Expression ◽

Proliferation And Differentiation ◽

Stimulating Hormone

Abstract Background As the incidence of secretory osteoporosis has increased, bone loss, osteoporosis and their relationships with thyroid-stimulating hormone (TSH) have received increased attention. In this study, the role of TSH in bone metabolism and its possible underlying mechanisms were investigated. Methods We analyzed the serum levels of free triiodothyronine (FT3), free thyroxine (FT4), and TSH and the bone mineral density (BMD) levels of 114 men with normal thyroid function. In addition, osteoblasts from rat calvarial samples were treated with different doses of TSH for different lengths of time. The related gene and protein expression levels were investigated. Results A comparison of the BMD between the high-level and low-level serum TSH groups showed that the TSH serum concentration was positively correlated with BMD. TSH at concentrations of 10 mU/mL and 100 mU/mL significantly increased the mRNA levels of ALP, COI1 and Runx2 compared with those of the control (P < 0.05, P < 0.01). Bone morphogenetic protein (BMP)2 activity was enhanced with both increased TSH concentration and increased time. The protein levels of Runx2 and osterix were increased in a dose-dependent manner. Conclusions The circulating concentrations of TSH and BMD were positively correlated with normal thyroid function in males. TSH promoted osteoblast proliferation and differentiation in rat primary osteoblasts.

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