Decreased serum TSH levels are not associated with mortality in the adult northeast German population
ABSTRACT Results of cohort studies on the association between decreased serum TSH levels and mortality are conflicting. Some studies demonstrated an increased mortality risk in subjects with decreased serum TSH levels, others did not. Even meta-analyses revealed contradictory results. We undertook the present study to investigate the association between decreased serum TSH levels and mortality in the large population-based Study of Health in Pomerania (SHIP).
Data from 3651 individuals from SHIP without known thyroid disorders or thyroid treatment were analyzed. Serum TSH, free triiodothyronine, and free thyroxine levels were determined by immunochemiluminescent procedures. Decreased TSH was defined as serum TSH levels below 0.25 mIU/l. Cox regression was used to associate decreased TSH levels with mortality.
The median duration of follow-up was 8.5 years (30 126 person years). During follow-up, 299 individuals (6.9%) died corresponding to a death rate of 9.92 deaths per 1000 person years. Survival time was shorter in subjects with decreased serum TSH levels compared to euthyroid individuals. After adjustment for age and sex, however, there was no association between decreased serum TSH levels and all-cause mortality (hazard ratio: 0.95; 95% confidence interval: 0.67; 1.36). Likewise, decreased serum TSH levels were neither associated with cardiovascular nor with cancer mortality.
There is no independent association of decreased serum TSH levels with all-cause, cardiovascular, and cancer mortality in the adult northeast German population. Although our study has some strengths, we cannot finally conclude on therapeutical implications in individuals with subclinical thyroid diseases.
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ABSTRACT: Thyroid hormones are of crucial importance for the functioning of nearly every organ. Remarkably, disturbances of thyroid hormone synthesis and function are among the most common endocrine disorders affecting approximately one third of the working German population. Over the last ten years our understanding of biosynthesis and functioning of these hormones has increased tremendously. This includes the identification of proteins involved in thyroid hormone biosynthesis like Thox2 and Dehal where mutations in these genes are responsible for certain degrees of hypothyroidism. One of the most important findings was the identification of a specific transporter for triiodothyronine (T3), the monocarboxylate transporter 8 (MCT8) responsible for directed transport of T3 into target cells and for export of thyroid hormones out of thyroid epithelial cells. Genetic disturbances of MCT8 in patients result in a biochemical constellation of high T3 levels in combination with low or normal TSH and thyroxine levels leading to a new syndrome of severe X-linked mental retardation. Importantly mice lacking MCT8 presented only with a mild phenotype, indicating that compensatory mechanisms exist in mice. Moreover, it has become clear that not only genomic actions of T3 exist. T3 is also capable to activate adhesion receptors and it signals via activation of PI3K and MAPK pathways. Most recently, thyroid hormone derivatives were identified, the thyronamines which are decarboxylated thyroid hormones initiating physiological actions like lowering body temperature and heart rate, thereby acting in opposite direction to the classical thyroid hormones. So far it is believed that thyronamines function via the activation of a G-protein coupled receptor, TAAR1. The objective of this review is to summarise the recent findings in thyroid hormone synthesis and action and to discuss their implications for diagnosis of thyroid disease and for treatment of patients.Thyroid Research 08/2011; 4 Suppl 1(Suppl 1):S9. DOI:10.1186/1756-6614-4-S1-S9
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ABSTRACT: Background Subclinical thyroid dysfunction may be a risk factor for mortality in patients with heart failure, and it may be associated with dilated cardiomyopathy (DCM). The present study is the cohort study to examine the possible association between subclinical thyroid dysfunction and all-cause mortality in DCM patients as the current evidence on this association remains elusive. Methods and Results A total of 963 DCM patients were evaluated for thyroid function. Of these patients, 7.1% (n=68) had subclinical hyperthyroidism (defined as serum TSH <0.35 μIU/mL), 84.7% (n=816) had euthyroidism (TSH 0.35-5.5 μIU/mL), and 8.2% (n=79) had subclinical hypothyroidism (TSH >5.5 μIU/mL). There was a significant difference in the all-cause mortality rate between patients with euthyroidism and patients with subclinical hyper- and hypothyroidism (21%, 38.2%, and 26.6%, respectively, log-rank χ2=13.104, P=0.001) with mean follow-up 3.5 years. After adjustment for other confounding factors at baseline, QRS duration, N-terminal fragment pro-brain natriuretic peptide, NYHA functional class, left atrium diameter and subclinical hyperthyroidism (HR 1.793, 95% CI 1.010-3.183, P=0.046) emerged as significant predictors of all-cause mortality. Conclusion Subclinical hyper- and hypothyroidism in DCM patients had higher all-cause mortality rate. However, only subclinical hyperthyroidism, not subclinical hypothyroidism, was an independent predictor for increased risk of all-cause mortality.Journal of Cardiac Failure 07/2014; 20(7). DOI:10.1016/j.cardfail.2014.05.002 · 3.07 Impact Factor
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ABSTRACT: This paper considers a model of an insurance company which is allowed to invest a risky asset and to purchase proportional reinsurance. The objective is to find the policy which maximizes the expected total discounted dividend pay-out until the time of bankruptcy and the terminal value of the company under liquidity constraint. We find the solution of this problem via solving the problem with zero terminal value. We also analyze the influence of terminal value on the optimal policy.Acta Mathematica Scientia 05/2011; 31(3):1077-1090. DOI:10.1016/S0252-9602(11)60299-3 · 0.62 Impact Factor