Thyroid Hormones and the Metabolic Syndrome

European Thyroid Journal 06/2013; 2(2):83-92. DOI: 10.1159/000351249
Source: PubMed


Clustering of various metabolic parameters including abdominal obesity, hyperglycaemia, low high-density lipoprotein cholesterol, elevated triglycerides and hypertension have been used worldwide as metabolic syndrome to predict cardiometabolic risk. Thyroid dysfunction impacts on various levels of these components.
The purpose of the present review is to summarize available data on thyroid hormone-dependent action on components of the metabolic syndrome.
A PubMed search for any combination of hyperthyroidism, thyrotoxicosis or hypothyroidism and metabolic syndrome, blood pressure, hypertension, hyperlipidaemia, cholesterol, high-density lipoprotein cholesterol, glucose, diabetes mellitus, body weight or visceral fat was performed. We included papers and reviews published between 2000 and today but accepted also frequently cited papers before 2000.
There is convincing evidence for a major impact of thyroid function on all components of the metabolic syndrome, reflecting profound alterations of energy homeostasis at many levels.
Even though the interactions shown in animal models and man are complex, it is evident that insulin sensitivity is highest and adverse thyroid effects on the metabolic system are lowest in euthyroid conditions.

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    ABSTRACT: Subclinical hypothyroidism (SCH) should be considered in two categories according to the elevation in serum thyroid-stimulating hormone (TSH) level: mildly increased TSH levels (4.0-10.0 mU/l) and more severely increased TSH value (>10 mU/l). An initially raised serum TSH, with FT4 within reference range, should be investigated with a repeat measurement of both serum TSH and FT4, along with thyroid peroxidase antibodies, preferably after a 2- to 3-month interval. Even in the absence of symptoms, replacement therapy with L-thyroxine is recommended for younger patients (<65-70 years) with serum TSH >10 mU/l. In younger SCH patients (serum TSH <10 mU/l) with symptoms suggestive of hypothyroidism, a trial of L-thyroxine replacement therapy should be considered. For such patients who have been started on L-thyroxine for symptoms attributed to SCH, response to treatment should be reviewed 3 or 4 months after a serum TSH within reference range is reached. If there is no improvement in symptoms, L-thyroxine therapy should generally be stopped. Age-specific local reference ranges for serum TSH should be considered in order to establish a diagnosis of SCH in older people. The oldest old subjects (>80-85 years) with elevated serum TSH ≤10 mU/l should be carefully followed with a wait-and-see strategy, generally avoiding hormonal treatment. If the decision is to treat SCH, then oral L-thyroxine, administered daily, is the treatment of choice. The serum TSH should be re-checked 2 months after starting L-thyroxine therapy, and dosage adjustments made accordingly. The aim for most adults should be to reach a stable serum TSH in the lower half of the reference range (0.4-2.5 mU/l). Once patients with SCH are commenced on L-thyroxine treatment, then serum TSH should be monitored at least annually thereafter.
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