Clinical Manifestations Of Hyperthyroidism Research Articles

A Review of Testing for Distinguishing Hashimoto's Thyroiditis in the Hyperthyroid Stage and Grave's Disease.

Hashimoto's thyroiditis (HT) and Graves' disease (GD) are two very common autoimmune thyroid diseases (AITD). In this review, we use "HT in the hyperthyroidism stage" to refer to early HT with clinical manifestations of hyperthyroidism. In clinical practice, it is not easy to distinguish between HT in the hyperthyroidism stage and GD as they exhibit very similar clinical symptoms. The current literature lacks so far studies that systematically compare and summarize hyperthyroidism due to HT and GD from varied aspects. It is necessary to focus on all the clinical indices of HT in the hyperthyroidism stage and GD, for accurate diagnosis. Multiple databases such as PubMed, CNKI, WF Data, and CQVIP Data were used to search the literature concerning HT in the hyperthyroidism stage and GD. The information extracted from the relevant literature was summarized and further analyzed. To differentially diagnose hyperthyroidism as HT or GD, it is recommended to first focus on serological tests, followed by imaging tests, as well as the thyroid I131 uptake index. In pathology, fine needle aspiration cytology (FNAC) is the gold standard for the differential diagnosis of HT and GD. Test results from cellular immunology and genetics could also be used to accurately diagnose between the two diseases, which may be further developed and studied in the future. In this paper, we reviewed and summarized the difference between HT in the hyperthyroidism stage and GD from the following six aspects: blood tests, imaging, thyroid I131 uptake, pathology, cellular immunology, and genetics.

Therapeutic Plasma Exchange for the Treatment of Hyperthyroidism: Approach to the Patient with Thyrotoxicosis or Antithyroid-Drugs Induced Agranulocytosis.

Primary hyperthyroidism is an endocrine disorder characterized by excessive thyroid hormone synthesis and secretion by the thyroid gland. Clinical manifestations of hyperthyroidism can vary from subclinical to overt forms. In rare cases, hyperthyroidism may represent a clinical emergency, requiring admission to an intensive care unit due to an acute and severe exacerbation of thyrotoxicosis, known as a thyroid storm. First-line treatment of hyperthyroidism is almost always based on medical therapy (with thioamides, beta-adrenergic blocking agents, glucocorticoids), radioactive iodine or total thyroidectomy, tailored to the patient's diagnosis. In cases of failure/intolerance/adverse events or contraindication to these therapies, as well as in life-threatening situations, including a thyroid storm, it is necessary to consider an alternative treatment with extracorporeal systems, such as therapeutic plasma exchange (TPE). This approach can promptly resolve severe conditions by removing circulating thyroid hormones. Here we described two different applications of TPE in clinical practice: the first case is an example of thyrotoxicosis due to amiodarone treatment, while the second one is an example of a severe adverse event to antithyroid drugs (agranulocytosis induced by methimazole).

A rare case of silent pituitary macroadenoma with positive TSH and prolactin immunostaining

Silent thyroid stimulating hormone (TSH)-immunostaining pituitary adenomas are rare tumors, they can be either pure or immunoreactive to other pituitary hormones. We report a case of a silent macroadenoma with both TSH and prolactin immunostaining but with no clinical manifestations of hyperthyroidism or hyperprolactinemia. Pituitary magnetic resonance imaging revealed a macroadenoma. Transsphenoidal surgery was incomplete. The immunohistochemical staining showed that tumor cells were reactive to TSH (60%) and to prolactin (40%). Control pituitary imaging revealed a residual macroadenoma, and dopaminergic agonist treatment was administered. Mixed TSH and prolactin pituitary adenomas are rare and usually diagnosed incidentally or in the face of compression signs. Hormonal examinations for all patients who have a pituitary adenoma should be performed even in the absence of symptoms of hypersecretion. Pathological examination with immunostaining is key to diagnosis of clinically silent pituitary adenomas. Complementary therapies can be used when surgery is incomplete or contraindicated such as dopamine agonists and somatostatin analogs.

Thyrotropin-Secreting Pituitary Adenoma Successfully Treated With Cabergoline

Background: Thyrotropin secreting pituitary adenomas (TSH-oma) account for less than 1% of pituitary adenomas and are a rare cause of hyperthyroidism. In this case, we describe the safe use of cabergoline with the subsequent achievement of euthyroid levels and the resolution of symptoms. Clinical Case: A 67-year-old female with a presumed history of hypothyroidism for the last 3 years managed with Armour thyroid was referred for fatigue associated with palpitations, intermittent diarrhea, insomnia, and anxiety. Her TSH was noted to be suppressed at that time, and her Amour thyroid was changed to Levothyroxine 25 mcg daily, which was eventually stopped as her symptoms persisted. Follow-up thyroid function tests (TFTs) showed elevated TSH (8.60 µU/mL, reference range 0.340 - 5.600 µU/mL), and elevated free T3 (10.8 pg/mL, reference range 2.7-4.7 pg/mL) and free T4 (2.0 ng/dL, reference range 0.8-1.5 ng/dL) levels. Further laboratory workup including basal prolactin, LH, FSH, hCG α-subunit, IGF-1, and ACTH levels were within the normal range. Physical examination showed diffuse thyroid enlargement. An I-123 thyroid uptake and scan showed uniform uptake throughout the gland with no focal hyperintense areas. A dedicated pituitary MRI was performed and revealed an 8 mm microadenoma in the posterior left adenohypophysis. The patient wanted to avoid any invasive treatment and refused trans-sphenoidal surgery and medical therapy was chosen. Unfortunately, using a somatostatin analog as part of the standard medical treatment was not an option due to the high cost and lack of insurance coverage. For these reasons, a trial of cabergoline was started to suppress TSH secretion. Atenolol 25 mg daily was added temporarily for the management of her sympathetic symptoms. On periodic follow-up, her symptoms gradually subsided, and TFTs remained within normal limits. Treatment was continued for one year. Conclusion: Clinical manifestations of hyperthyroidism with biochemical evidence of elevated thyroid hormone levels and TSH levels should raise a strong suspicion for central or secondary hyperthyroidism due to TSH secreting pituitary adenoma. Cabergoline might represent an effective alternative form of medical treatment for TSH-oma in certain situations where the first line therapeutic options are refractory, contraindicated, or declined.

Thyrotoxic dilated cardiomyopathy: personal experience and case collection from the literature.

SummaryThe authors examine several reports of the literature concerning thyrotoxic dilated cardiomyopathy. In particular, it is pointed out that this clinical manifestation of hyperthyroidism is rare in readily diagnosed and properly treated hyperthyroidism. Case reports are analyzed comparatively. A case deriving from the direct experience of the authors is also presented.Learning points:Dilated cardiomyopathy has been reported as the initial presentation of hyperthyroidism in only 6% of patients although <1% developed severe LV dysfunction.Clinical picture of thyrotoxic dilated cardiomyopathy can degenerate into an overt cardiogenic shock sometimes requiring the use of devices for mechanical assistance to the circulation, or extracorporeal membrane oxygenation.For thyrotoxic dilated cardiomyopathy, evidence-based pharmacologic measures valid for heart failure should always be supplemented by the administration of specific thyroid therapies such as thionamides (methimazole, carbimazole or propylthiouracil), whose relatively long latency of action should be supported by the i.v. administration of small doses of beta-blocker.In cases of cardiogenic shock, the administration of beta-blocker should be carried out only after the restoration of satisfactory blood pressure levels- with the prudent use of synthetic catecholamines, if necessary.

Aging Alters Phenotypic Traits of Thyroid Dysfunction in Male Mice With Divergent Effects on Complex Systems but Preserved Thyroid Hormone Action in Target Organs.

Clinical manifestation of hyperthyroidism and hypothyroidism vary with age, with an attenuated, oligosymptomatic presentation of thyroid dysfunction (TD) in older patients. We asked, whether in rodents TD phenotypes are influenced by age and whether this involves changes in systemic and/or organ thyroid hormone (TH) signaling. Chronic hyper- or hypothyroidism was induced in male mice at different life stages (5, 12, and 20 months). TH excess resulted in pronounced age-specific body weight changes (increase in youngest and decrease in old mice), neither explained by changes in food intake (similar increase at all ages), nor by thermogenic gene expression in brown adipose tissue (BAT) or TH serum concentrations. Relative increase in body temperature and activity were more pronounced in old compared to young hyperthyroid mice. An attenuated hypothyroid state was found in old mice for locomotor activity and in heart and BAT on functional (less bradycardia) and gene expression level (heart and BAT). In contrast, decrease in body weight was pronounced in old hypothyroid mice. Thus, age has divergent impact on features of TD in mice, whereby effects on highly complex systems, such as energy homeostasis are not proportional to serum TH state, in contrast to organ-specific responses in heart and BAT.

TSH-secreting pituitary adenoma: late diagnosis and effectiveness of therapy

The modern therapeutic and diagnostic algorithms allow timely detection of pituitary disorder to prescribe adequate treatment. Meanwhile, when interpreting the thyroid status, physicians need to take into account the extremely rare but the actually existing possibility of central thyrotoxicosis. The worldwide practice shows that diagnosis of this condition is rather challenging.&#x0D; We report a clinical case of a TSH-secreting pituitary adenoma in a 47-year-old female who received a long-term thyrostatic therapy for thyrotoxicosis. The patient was diagnosed with Graves’ disease; however, thyrotoxicosis was actually caused by TSH-oma. The key laboratory signs of central thyrotoxicosis included the combination of episodes of normal or elevated TSH level with the high or normal free T4 level. MRI showed a pituitary macroadenoma. The clinical manifestations of thyrotoxicosis made it possible to rule out the thyroid hormone resistance syndrome. The attempted therapy with octreotide eliminated the clinical and laboratory signs of thyrotoxicosis, so the conservative method was selected as first-line therapy. The features of clinical and laboratory signs, as well as the principles of differential diagnosis and modern methods for treating TSH-secreting pituitary adenomas are discussed.

Protocolo del manejo de la disfunción tiroidea en el paciente anciano

IntroductionThyroid dysfunction is a common condition in the elderly. PathogenesisIn the aging process there are changes in secretion, metabolism and action of thyroid hormones. Thyroid function tests could be difficult to interpret because of aging related changes in the thyroid. ManifestationsHypothyroidism symptoms such as fatigue, constipation or dry skin can mimic the typical changes during aging. The clinical manifestations of hyperthyroidism in the elderly are milder than in middle-aged people. The different types of thyroid cancer and nodules are usually associated with more aggressive forms of the disease. ManagementIn order to minimize the morbidity associated with thyroid dysfunction in the elderly it is essential to establish the appropriate treatment that should be tailored to an accurate diagnosis and appropriate monitoring.

Myocardial infarction as a first clinical manifestation of hyperthyroidism

Abstract Introduction Hyperthyroidism is a condition in which there is an increased secretion of thyroid hormones that exceeds the current needs of the body. Increased concentrations of hormones affect proper functioning of many organs and systems, including the cardiovascular system. Untreated hyperthyroidism may result in myocardial infarction (MI), which very rarely is its first clinical manifestation. Aim The aim of this work is to present the case of a male patient with no previous symptoms, in whom ST segment elevation myocardial infarction (STEMI) occurred as the first clinical manifestation of hyperthyroidism. Case study Presentation and analysis of the case of a 41-year-old male admitted with clinical and electrocardiographic features of anterior wall STEMI in the course of hyperthyroidism. Results and discussion The cause of ischemia and MI in patients with no previous coronary artery disease is not fully known. Probable predisposing factors may include increased serum thyroid hormone concentrations. It enhances the vasoconstrictor effect of catecholamines and hyperkinetic circulation, which may be the potential causes of ischemia. In addition, it predisposes to a hypercoagulable state, which is the cause of coronary thrombosis. Conclusions It is not only high cholesterol levels and anemia that are the possible causes of MI. Endocrine disorders, such as hyperthyroidism should always be taken into account.

Lithium-induced transient euthyroid hyperthyroxinemia: a case report.

To the Editor: Sixty years after its introduction, lithium remains a first-line medication in the treatment of bipolar disorder.1 While lithium treatment has been associated with a wide range of adverse effects,2,3 thyroid-related abnormalities, especially hypothyroidism, are the most commonly reported ones.4,5 Lithium-associated hyperthyroidism, however, is quite rare, and only a few sporadic case reports of thyrotoxicosis that developed after several years of lithium therapy or after stopping lithium3,6 are described in the literature. Lithium-induced euthyroid hyperthyroxinemia, described as an elevation in serum thyroid hormone levels without clinical manifestations of thyrotoxicosis,7 has not been reported to our knowledge. Stratakis and Chrousos8 described a case of transient euthyroid hyperthyroxinemia associated with discontinuation of chronic lithium treatment. We report a patient who developed transient euthyroid hyperthyroxinemia within a few weeks of initiation of lithium therapy. Case report. Ms A, a 24-year-old African American woman with a 4-year history of schizoaffective disorder, bipolar type (DSM-IV-TR), was admitted to our hospital in December 2011 with signs and symptoms consistent with mania with psychosis. At admission, she presented with a labile mood with aggressive and violent behavior, insomnia, poor concentration, pressured speech with racing thoughts, and increased psychomotor activity. She was also very paranoid, reported auditory hallucinations, and was often found responding to internal stimuli. She had no acute medical findings, except for past history of gastroesophageal reflux/dyspepsia symptoms and urinary urgency. She had never been pregnant, and her family history was negative for thyroid abnormalities. Her admission laboratory workup, including thyroid function, was unremarkable except for elevated serum total creatine kinase level of 574 U/L (normal range, 26–140 U/L), which subsequently normalized. She was started on lithium carbonate titrated to 900 mg daily, risperidone, and clonazepam. Under this regimen, her mood and psychotic symptoms started to improve. Serum lithium, free T4, and thyroid-stimulating hormone (TSH) levels were serially monitored over the course of her hospitalization (Figure 1). Figure 1. Serial Serum Levels of Lithium, TSH, and Free T4 in a Patient Treated With Lithium About 2.5 months after treatment initiation, we noticed an elevation in her free T4 levels with a slight decrease in TSH levels. During this period, she remained clinically euthyroid with no evidence of thyrotoxicosis. A full hyperthyroidism workup revealed the following: an elevated serum total thyroglobulin level over 180 ng/mL (normal range, 1.2–35 ng/mL), thyroid antibody levels within normal limits, no evidence of a thyroid nodule on ultrasonogram, a 0.9% I123 uptake at 4 hours (normal, 5%–15%) and a 0.3% uptake at 24 hours (normal, 5%–15%) on a thyroid uptake scan, and no evidence suggestive of an ectopic thyroid tissue. Lithium therapy was continued with careful monitoring for evidence of thyrotoxicosis. Elevation of free T4 and associated drop in TSH levels persisted for the next 2 months (Figure 1). During the fourth month of treatment, free T4 levels returned to within normal limits. The incidence of transient euthyroid hyperthyroxinemia in acute psychiatric inpatients at admission has been reported to be at 9%–18%.7 The subject in the present report had normal TSH and T4 levels at admission. To our knowledge, this is the first reported case of lithium-induced transient euthyroid hyperthyroxinemia. Although the role of lithium in thyroid hormone synthesis and release has been extensively investigated and reviewed,9 how it may induce euthyroid hyperthyroxinemia is unclear. From a clinical perspective, if a clinician finds elevated thyroxine levels in the absence of overt thyrotoxicosis in a patient started on lithium therapy, it would seem prudent to carefully monitor clinically for development of thyrotoxic symptoms without immediately resorting to an extensive and expensive diagnostic workup.

Liver Functional Behavior During Thyrotoxicosis: A Review

Thyroid and liver are among two vital and important organs which are interrelated in health and disease. The cooperation of thyroid and liver is extremely vital for a proper functional behavior for both thyroid and liver. Liver crucial role in the basic metabolic rate, growth and development is due to the liver ability to transfer the thyroid hormone and deliver it to the various organs intracellular due to thyroid hormone transporting system which is mediated by the liver. Thyrotoxicosis defined as the clinical manifestation of hyperthyroidism, a symptom with various adverse effects on the liver, heart, vascular, nervous and gastrointestinal systems. There are many reports demonstrating the negative side effect of hyperthyroidism on liver function tests which occur due to the accompanying clinical manifestation of thyrotoxicosis. In severe form of hyperthyroidism in addition to liver biochemical alteration and elevated liver enzymes, damages to hepatocytes will occur. Therefore it is strongly recommended that subjects with either of hyperthyroid or liver dysfunction should be carefully examined simultaneously for both organs to have a clear cut diagnosis and to assist the patient with proper therapeutically treatments. © 2013 Asian Network for Scientific Information.

Graves' Disease that Developed Shortly after Surgery for Thyroid Cancer

Graves' disease is an autoimmune disorder that may present with various clinical manifestations of hyperthyroidism. Patients with Graves' disease have a greater number of thyroid nodules and a higher incidence of thyroid cancer compared with patients with normal thyroid activity. However, cases in which patients are diagnosed with recurrence of Graves' disease shortly after partial thyroidectomy for thyroid cancer are very rare. Here we report a case of hyperthyroid Graves' disease that occurred after partial thyroidectomy for papillary thyroid cancer. In this case, the patient developed hyperthyroidism 9 months after right hemithyroidectomy, and antithyroglobulin autoantibody and thyroid stimulating hormone receptor stimulating autoantibody were positive. Therefore, we diagnosed Graves' disease on the basis of the laboratory test results and thyroid ultrasonography findings. The patient was treated with and maintained on antithyroid drugs. The mechanism of the recurrence of Graves' disease in this patient is still unclear. The mechanism may have been the improper response of the immune system after partial thyroidectomy. To precisely determine the mechanisms in Graves' disease after partial thyroidectomy, further studies based on a greater number of cases are needed.

Old men hyperthyroidism

Even the thyroid, like all the other organs and tissues, has undergone anatomic-functional modifications during the senescence. One of the characteristics of ageing is the significant increase of thyroid disease and their different clinical expression. Moreover, thyroid disease in older patients requires special attention because of the increased gravity caused by the frequent co-existence of other pathologies or the greater risk of pharmacological interferences and a lower metabolism of the drugs. In particular, hyperthyroidism in old men is a pathology that should not be undervalued because of the peculiarity of the clinical and prognostic aspects which characterize this age. The prevalence of hyperthyroidism increases 7 times in people over sixty-five years old and, including the subclinical hyperthyroidism; the percentage of people over sixty-five years old oscillates from 0,7% to 4% according to the casuistry. The most frequent causes of hyperthyroidism in old men are the toxic multinodular goiter and the autonomously functioning solitary nodules, which in the iodineless areas represent over the 70% of the causes; moreover hyperthyroidism exogenous (iodine and iodathe composts, like amiodarone, means of radiological contrast, ingestion of intentional or unintentional suppressive doses of thyroid hormone). The clinical manifestations of hyperthyroidism are peculiar and they are often different in old men with respect to young men. In old men the apatetica production is frequent with not many aspecific symptoms and cardiovascular complications (atrial fibrillation or other arrhythmias). Also the therapy is different in old men with respect to young men. In fact it must be individualized not only because of the causes, but also the age, by the risk factors of cardiovascular illnesses and by the presence of others illnesses, too.

Effects of the Thyromimetic Agent Diiodothyropropionic Acid on Body Weight, Body Mass Index, and Serum Lipoproteins: A Pilot Prospective, Randomized, Controlled Study

Widespread thyroid hormone actions offer the possibility of developing selective thyromimetic analogs with salutary metabolic properties. Consequently, effects of diiodothyropropionic acid (DITPA) on body weight, serum lipoproteins, and bone metabolism markers were studied in a prospective, controlled, double-blind 24-wk trial, which was primarily designed to assess treatment of stable chronic heart failure. Eighty-six patients (aged 66 +/- 11 yr, mean +/- sd) were randomized (1:2) to placebo or an escalating DITPA dose (90 to 180, 270, and 360 mg/d) over 8 wk until serum TSH was less than 0.02 mU/liter. Patients were studied at 2, 4, 6, 8, 16, and 24 wk and after 4 wk off study drug. Only 21 DITPA-treated and 27 placebo patients completed the full 24 wk of therapy. DITPA therapy lowered serum TSH levels and, to a lesser extent, serum T(3) and T(4), but there were no differences in clinical manifestations of thyrotoxicosis or hypothyroidism. Serum total and low-density lipoprotein cholesterol levels both decreased on DITPA; there was a transient decrease in triglycerides and no change in high-density lipoprotein cholesterol. DITPA therapy was associated with significant reduction in body weight, 12.5 lb at 24 wk. Increases in serum osteocalcin, N-telopeptide, and deoxypyridinoline levels were consistent with increased bone turnover on DITPA. This investigation of DITPA actions demonstrated its efficacy in reducing body weight and lowering total and low-density lipoprotein cholesterol levels. However, DITPA's adverse effects at doses used resulted in a high dropout rate and potentially dangerous skeletal actions were observed.

Serendipitous Identification of Graves' Disease in Identical Twins with Polydipsia

Graves' disease in adolescents and adults usually presents with classic symptoms including weight loss, frequent stools, irritability, and heat intolerance. However, the clinical manifestations of hyperthyroidism in young children are often subtle, unrecognized, and atypical. Here, we report a 6 year-old girl who presented for evaluation of increased. thirst. Review of systems was negative with respect to weight loss, irritability, palpitations, diarrhea, and school performance problems. Physical exam was unremarkable except for an enlarged thyroid gland. Her identical twin sister, who incidentally accompanied her to clinic, also had a previously unidentified goiter. Testing for diabetes was negative. Further laboratory investigation was consistent with Graves' disease in both girls. Polydipsia is a rare and unusual presenting feature of hyperthyroidism in children. The evolution of this case highlights the importance of maintaining a high index of suspicion for thyroid disease during childhood.

Hyperthyroid heart disease.

The heart is an organ sensitive to the action of thyroid hormone, and measurable changes in cardiac performance are detected with small variations in thyroid hormone serum concentrations. Most patients with hyperthyroidism experience cardiovascular manifestations, and the most serious complications of hyperthyroidism occur as a result of cardiac involvement. Recent studies provide important insights into the molecular pathways that mediate the action of thyroid hormone on the heart and allow a better understanding of the mechanisms that underlie the hemodynamic and clinical manifestations of hyperthyroidism. Several cardiovascular conditions and drugs can interfere with thyroid hormone levels and may pose a difficulty in interpretation of laboratory data in patients with suspected thyroid heart disease. The focus of this report is a review of the current knowledge of thyroid hormone action on the heart and the clinical and hemodynamic laboratory findings as well as therapeutic management of patients with hyperthyroid heart disease.

MECHANISMS OF THYROID HORMONE ACTION: Implications for the Clinical Manifestation of Thyrotoxicosis

Serum thyroid hormone concentrations alone do not explain the variability and severity of the range of symptoms observed in thyrotoxic patients. Despite gaps in our understanding of the links between the clinical manifestations of thyrotoxicosis and the underlying mechanisms, much has been learned. A limited number of markers directly reflect T3 action. The future elucidation of T3 targets that mediate these effects should ultimately lead to additional clinical markers of tissue-specific T3 action. The availability of such tests should allow for more specific treatment of individual patients.

Thyroid hormone and the cardiovascular system

Thyroid hormone has many effects on the heart and vascular system.1 Many of the clinical manifestations of hyperthyroidism are due to the ability of thyroid hormone to alter cardiovascular hemodynamics.2 The hemodynamic effects of hypothyroidism are opposite to those of hyperthyroidism, although the clinical manifestations are less obvious. This review will integrate what is known about the mechanisms of thyroid hormone action on the heart2–5 with recent observations from both experimental and clinical studies of hyperthyroidism and hypothyroidism. We will also address the potential role of thyroid hormone treatment in patients with acute or chronic cardiac disease. Effects of . . .

The Heart and Thyroid Disease

This article discusses the effects of thyroid hormone on the heart, cardiovascular symptoms and signs in elderly patients with hyperthyroidism and hypothyroidism, and the diagnosis and therapy of hyperthyroidism and hypothyroidism in elderly patients. Cardiovascular symptoms of hyperthyroidism include palpitations, angina, pectoris, and dyspnea on exertion, orthopnea, or paroxysmal nocturnal dyspnea. Atrial fibrillation or congestive heart failure may be the only clinical manifestation of hyperthyroidism in elderly patients with apathetic hyperthyroidism. Atrial fibrillation with a rapid ventricular rate due to hyperthyroidism should be treated with propranolol to control the rapid ventricular rate. Elderly patients with coronary artery disease and hypothyroidism should be treated cautiously with thyroid hormone replacement to avoid precipitating or exacerbating angina pectoris, precipitating acute myocardial infarction, and precipitating or aggravating ventricular arrhythmias or congestive heart failure.

Signification diagnostique d'une hormone thyréotrope abaissée en médecine interne

In an attempt to determine the significance of low plasma thyrotropin (TSH) concentrations in internal medicine and the usefulness of systematic TSH assays in hospitals, 732 consecutive TSH measurements were performed in first-admission patients. TSH concentrations below 0.15 mU/l were found in 33 patients (4.5%) divided into 4 groups: a) in 5 patients a second assay made within 10 days of the first one showed no fall in TSH levels; b) 5 patients had known endocrine disease; c) in 8 patients hyperthyroidism could be asserted; the diagnosis had not been suspected in 3 elderly women and 1 pregnant women; d) 15 patients remained with low TSH concentrations but had normal free T3 and free T4 levels; in this group a goitre was detected in 7 patients and 8 had a severe chronic disease. These results showed that a TSH concentration below 0.15 mU/l corresponded to hyperthyroidism in less than one out of three patients in this population and that the 0.07 to 0.15 mU/l range is particularly misleading. A second TSH assay, free T3 and free T4 measurements ant thorough investigations in search of a goitre must be made. Severe organic diseases and several drugs may induce a fall in TSH. All considered, the 1% prevalence of hyperthyroidism in this population does not justify systematic TSH assays, but in subjects over 60 years of age, the clinical manifestations of hyperthyroidism may be misleading or unrecognized, and TSH assays should be widely performed.