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This is a short review about thyroid dysfunction in the elderly. Screening investigations from the United States have shown that nearly every 4th woman above the age of 65 is affected. Therefore a state-of-the-art article about this phenomenon seems justified. Epidemiologic studies show that the pattern of thyroid dysfunction depends on the iodine-nutrient status, thyrotoxicosis being more common in countries with iodine deficiency, overt and subclinical hypothyroidism occurring very frequently in areas with sufficient iodine supplementation. After discussing the state of the art of what is known about physiologic changes induced by age in the hypothalamic-pituitary-thyroid axis, it is pointed out that abnormal values of thyroid function parameters in serum should be further investigated. Symptoms of thyroid dysfunction are very rare and often unspecific. Therefore, laboratory screening in women above the age of 65 seems to be justified. Finally, the differences of treating elderly patients with thyroid dysfunction in comparison to treating young patients is discussed. In this discussion the impact of subclinical disturbances of thyroid dysfunction is included.

This review discusses the clinically relevant effects of thyroid hormone excess on the heart. Tachycardia and atrial fibrillation are usually reversible after euthyroidism is restored. Atrial fibrillation may, however, take several months to return to sinus rhythm. The increase in contractility leads to an increase of cardiac output. The development of a relative myocardial hypertrophy following long-term high-dose therapy with thyroid hormones is controversial. Cardiac failure at stress in spite of an increased cardiac output at rest is a phenomenon typical for thyrotoxicosis. Reports of dilated cardiomyopathy associated with Graves' disease and evidence for TSH-receptors in the human myocardium suggest a relationship between these two diseases. Endomyocardial biopsy studies have, however, failed to prove this hypothesis. Mitral valve prolapse is more frequent in hyperthyroid patients than in normals. Thyroid hormone excess as well as the autoimmune origin of the disease are suggested as etiology for this phenomenon. The frequently observed angina pectoris seems to be a consequence of the increase in consumption of oxygen in the presence of an unchanged oxygen supply rather than of obstruction of coronary circulation. Well documented cases of myocardial infarction patients with thyroid hormone excess and normal coronary arteries in angiography substantiate this theory. Finally diagnostic and therapeutic options of the two forms of thyrotoxicosis induced by the antiarrhythmic drug amiodarone are presented.

Myocardial ischemia is a rare but severe and possibly life threatening manifestation of hyperthyroidism, but does not usually result in persistent ischemia. We report on a 71-year-old woman who had undergone total thyroidectomy with subsequent irradiation because of follicular carcinoma 3 years ago. Since then, she had been maintained on oral levothyroxine replacement therapy at a dose of 0.15 mg alternating with 0.2 mg daily. When latent hypothyroidism became evident despite replacement therapy, the dose of levothyroxine was increased to 0.3 mg a day. Three weeks later, the patient suffered from an acute posterior myocardial infarction, although she had no previous history of coronary artery disease. Subsequent coronary arteriograms revealed no evidence of disease of the major vessels. Myocardial scintigraphy 3 weeks after infarction still revealed a persistent perfusion defect. Since it is known that thyroid hormones increase oxygen demand, the rapid elevation of oxygen utilization caused by thyrotoxicosis factitia is likely to be responsible for this patient's myocardial infarction. The case illustrates that a sudden increase in levothyroxine replacement dose should be avoided.

This paper tries to evaluate the importance of IFN-alpha induced thyroid dysfunction. Based on our own experience and reported data we present the results obtained in a total of 588 patients, in whom thyroid function and thyroid antibody occurrence was monitored during therapy with IFN-alpha: About 10% of these patients developed thyroid dysfunction during IFN-alpha treatment. Half of them reacted with hypothyroidism, 3% with hyperthyroidism and in 2% a biphasic (hyperthyroidism followed by hypothyroidism) pattern of reaction was observed. The frequency of these thyroid dysfunctions was increased in female patients and in patients with preexisting thyroid antibodies. The risk to develop thyroid dysfunction is reduced to 7% in patients with no pretherapeutic thyroid antibodies. The evolution of the thyroid ailment is variable and therefore unpredictable. In many patients there is no need to stop treatment with IFN-alpha nor to treat the thyroid dysfunction specifically. IFN-alpha induced autoimmune- phenomena seem to be etiologically important for the development of thyroid disease during IFN-alpha. The reported data allow in our view some basic recommendations for the clinician: thyroid function and thyroid antibodies should be evaluated before the start of treatment with IFN-alpha. During therapy with IFN-alpha these parameters should be regularly (eg every 4 months) monitored. In patients with thyroid autoantibodies or dysfunction already before IFN-alpha the control intervals should not be longer than every two months.

Iodine-induced thyroid dysfunction will become more important in Austria in the near future, because of the augmentation of the iodine content in salt in 1990. This review therefore tries to summarize the diagnostic and therapeutic problems that may arise in iodine-induced thyroid disease. After discussion of the physiologic reaction of the normal thyroid to iodine the most frequently used iodine-containing drugs used in Austria are presented. Special emphasis is laid on iodine containing antiseptics and on the antiarrhythmic drug amiodarone. The influence of iodine supplementation on the reaction of diseased thyroid glands to iodine overload is stressed. The diagnosis of iodine induced thyroid dysfunction is relatively simple, once it is thought of. Amiodarone-iodine induced thyroid disease may be an exception, because of the intrinsic effect of this drug on thyroid hormone metabolism. Since high intra-thyroidal iodine content inhibits the action of thyrostatics, therapy of iodine-induced hyperthyroidism may be complicated. Alternative possibilities such as cortisone, perchlorate or surgery in thyroid storm are presented. Substitution with 1-thyroxine in iodine-induced hypothyroidism may be harmful in elderly patients with cardiac problems. In conclusion, this review tries to present the state of the art of the solution of diagnostic and therapeutic problems in thyroid dysfunction due to iodine administration.

The present concept for the etiology of thyroid disease permits the definition of three separate entities occuring with hyperthyroidism: Graves' Disease, Toxic Nodular Goitre, Autonomous Adenoma. Physiopathological properties of these entities lead to a rational therapeutic strategy for each one of them.

Serum angiotensin converting enzyme activities were significantly increased in 26 untreated hyperthyroid patients (20.3 +/- 5.4 U/ml; P less than 0.001) compared with healthy control subjects (13.1 +/- 2.3 U/ml). In 12 patients a significant fall in enzyme activities was observed after treatment compared with pretreatment serum ACE levels (P less than 0.001). Eight patients with hypothyroidism (15.7 +/- 5.1 U/ml) and 11 athyreotic patients, totally thyroidectomized for well-differentiated thyroid cancer, showed no significant differences in serum ACE activities (14.3 +/- 2.2 U/ml) compared with control subjects. After thyroid hormone supplementation a significant increase in serum ACE activity (P less than 0.05) was found in the athyreotic patients. Addition of increasing amounts of L-thyroxine to a serum sample of an athyreotic patient showed no significant effect on ACE activity in vitro. We suggest that the elevated serum ACE activity in hyperthyroidism is not from the thyroid gland, but represents a direct effect of thyroid hormone on ACE synthesis and/or release from endothelial cells.

The binding of 125I-insulin to insulin receptors on circulating mononuclear leukocytes was studied in ten patients with hyperthyroidism and 20 euthyroid normal volunteers. The hyperthyroid patients demonstrated significantly elevated glucose levels following an oral glucose load, despite normal insulin secretion. The infusion of insulin resulted in a delayed hypoglycaemic effect in the hyperthyroid patients; however, the inhibition of the endogenous insulin secretion as indicated by suppression of C-peptide levels was not different from euthyroid control subjects. Insulin binding to monocytes was significantly decreased in the hyperthyroid patients. Scatchard analysis of binding data indicates that a decrease of receptor number rather than receptor affinity seems to be the cause of the lowered insulin binding in hyperthyroid patients with diffuse toxic goitre. The findings of decreased insulin receptor number, mild degree of glucose intolerance despite normal insulin secretion and the delayed hypoglycaemic effect following insulin infusion suggest that peripheral insulin resistance could be involved in the highly complex pathophysiology of glucose intolerance in hyperthyroidism.