Autoimmune thyroiditis, Hashimoto's goitre, and premyxoedema.
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Biomedical subjects
Publications and source records attributed to P A Bastenie.
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Cross sectional and prospective surveys of thyroid autoimmunity have been performed in two cohorts of men, 280 living in west Finland and 269 in east Finland. In both populations, aged 50 to 69 years at the first survey, risk factors for coronary heart-disease (C.H.D.) were common. The incidence of C.H.D. was shown to be related to the presence of thyroid antibodies. The results of the cross-sectional studies were not conclusive. The five-year follow-up study emphasised that in both areas asymptomatic thyroid autoimmunity, independently of other known risk factors, was a predictor of subsequent development of C.H.D. The importance of asymptomatic autoimmune thyroid-itis as a risk factor for C.H.D. increases with age.
The clinical picture of mild hypothyroidism consists of mild, often non-specific signs. In general, the diagnosis can only be made in the laboratory. Estimations of protein-bound iodine, thyroxine and tri-iodothyronine in the serum are often within normal limits. A rise in serum TSH and in doubtful cases, the excessive liberation of TSH during the TRH-TSH test confirm the diagnosis. As mild hypothyroidism is often due to auto-immune thyroiditis, the demonstration of anti-thyroid antibodies may guide the clinician.
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Within the first 36 hours following myocardial infarction, serum total thyroxine (T4) levels were supranormal in most cases in contrast to normal thyrotropin values. After one week, T4 levels dropped to normal while TSH values rose significantly. These findings suggest that, in the acute phase of myocardial infarction, the secretion of thyroid hormones is increased, thereby inhibiting the pituitary thyrotropes. The stimulation of thyroid secretion might be due to the high levels of blood catecholamines generally found in patients with myocardial infarction.
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