Manifestations Of Hyperthyroidism Research Articles

Smoking and Other Lifestyle Factors and the Risk of Graves’ Hyperthyroidism

Hyperthyroidism caused by Graves' disease is common in women, yet little is known about risk factors for the disease. We sought to determine whether lifestyle factors, including smoking, alcohol consumption, physical activity level, and body mass index, are risk factors for Graves' hyperthyroidism. This analysis was conducted using data from the Nurses' Health Study II, among 115109 women aged 25 to 42 at entry. Incident reports of women with Graves' hyperthyroidism, confirmed to have the disorder, were included. During 1 328 270 person-years of follow-up, incident diagnoses of Graves' hyperthyroidism were confirmed in 543 women; the 12-year incidence was 4.6 per 1000 women. Cigarette smoking was a predictor of Graves' hyperthyroidism. The hazard ratio among current smokers was 1.93 (95% confidence interval [CI], 1.54-2.43), and among past smokers it was 1.27 (95% CI, 1.03-1.56), after adjusting for recent pregnancy, parity, and other variables. Among current smokers, the hazard ratio increased with the intensity of smoking and was 2.63 (95% CI, 1.71-4.04) among women who smoked 25 or more cigarettes daily. Obesity was associated with a decreased risk of Graves' hyperthyroidism. The hazard ratio for the disorder among women with a body mass index of 30 kg/m(2) or higher was 0.68 (95% CI, 0.49-0.92). Alcohol intake and physical activity level were not associated with risk of Graves' hyperthyroidism. Smoking is a risk factor for Graves' hyperthyroidism in women. Obesity may be associated with a reduced risk, although weight loss as the first manifestation of hyperthyroidism cannot be excluded.

Thyroid storm as precipitating factor in onset of coma in an elderly woman: case report and literature review

Thyroid storm is an uncommon but life-threatening manifestation of hyperthyroidism which, unless appropriately treated by combined therapy, causes 30-60% of deaths in hospitalized patients. Mental deterioration leading to apathy and eventually coma is a rare clinical presentation of this pathology, frequently observed in the elderly. We present the case of a 77-year-old hypertensive woman who was hospitalized for fast onset of coma, probably due to the unusual combination of a hypernatremic hyperosmolar state and an unexpected thyroid storm (TS). Although not definitely ascertained, the possible etiology was the hyperthyroid phase of chronic autoimmune thyreopathy (Hashitoxicosis). Notably, the significant adjunctive role of thyroid hyperfunction in the pathogenesis of coma was confirmed by the fact that, although metabolic abnormalities were overcome, complete and satisfactory recovery of the patient's mental and physical condition occurred only with normalization of thyroid hormones by antithyroid treatment. Our case highlights the importance of properly evaluating thyroid function in elderly patients who show a sudden progressive impairment in their mental condition, for early detection of potentially fatal conditions such as thyroid storm or myxedematous coma.

Thyroid receptor ligands. 1. Agonist ligands selective for the thyroid receptor beta1.

Endogenous thyroid receptor hormones 3,5,3',5'-tetraiodo-l-thyronine (T(4), 1) and 3,5,3'-triiodo-l-thyronine (T(3), 2) exert a significant effects on growth, development, and homeostasis in mammals. They regulate important genes in intestinal, skeletal, and cardiac muscles, the liver, and the central nervous system, influence overall metabolic rate, cholesterol and triglyceride levels, and heart rate, and affect mood and overall sense of well being. The literature suggests many or most effects of thyroid hormones on the heart, in particular on the heart rate and rhythm, are mediated through the TRalpha(1) isoform, while most actions of the hormones on the liver and other tissues are mediated more through the TRbeta(1) isoform of the receptor. Some effects of thyroid hormones may be therapeutically useful in nonthyroid disorders if adverse effects can be minimized or eliminated. These potentially useful features include weight reduction for the treatment of obesity, cholesterol lowering for treating hyperlipidemia, amelioration of depression, and stimulation of bone formation in osteoporosis. Prior attempts to utilize thyroid hormones pharmacologically to treat these disorders have been limited by manifestations of hyperthyroidism and, in particular, cardiovascular toxicity. Consequently, development of thyroid hormone receptor agonists that are selective for the beta-isoform could lead to safe therapies for these common disorders while avoiding cardiotoxicity. We describe here the synthesis and evaluation of a series of novel TR ligands, which are selective for TRbeta(1) over TRalpha(1). These ligands could potentially be useful for treatment of various disorders as outlined above. From a series of homologous R(1)-substituted carboxylic acid derivatives, increasing chain length was found to have a profound effect on affinity and selectivity in a radioreceptor binding assay for the human thyroid hormone receptors alpha(1) and beta(1) (TRalpha(1) and TRbeta(2)) as well as a reporter cell assay employing CHOK1-cells (Chinese hamster ovary cells) stably transfected with hTRalpha(1) or hTRbeta(1) and an alkaline phosphatase reporter-gene downstream thyroid response element (TRAFalpha(1) and TRAFbeta(1)). Affinity increases in the order formic, acetic, and propionic acid, while beta-selectivity is highest when the R(1) position is substituted with acetic acid. Within this series 3,5-dibromo-4-[(4-hydroxy-3-isopropylphenoxy)phenyl]acetic acid (11a) and 3,5-dichloro-4-[(4-hydroxy-3-isopropylphenoxy)phenyl]acetic acid (15) were found to reveal the most promising in vitro data based on isoform selectivity and were selected for further in vivo studies. The effect of 2, 11a, and 15 in a cholesterol-fed rat model was monitored including potencies for heart rate (ED(15)), cholesterol (ED(50)), and TSH (ED(50)). Potency for tachycardia was significantly reduced for the TRbeta selective compounds 11a and 15 compared with 2, while both 11a and 15 retained the cholesterol-lowering potency of 2. This left an approximately 10-fold therapeutic window between heart rate and cholesterol, which is consistent with the action of ligands that are approximately 10-fold more selective for TRbeta(1). We also report the X-ray crystallographic structures of the ligand binding domains of TRalpha and TRbeta in complex with 15. These structures reveal that the single amino acid difference in the ligand binding pocket (Ser277 in TRalpha or Asn331 in TRbeta) results in a slightly different hydrogen bonding pattern that may explain the increased beta-selectivity of 15.

Amiodarone-induced Thyrotoxicosis Presenting as Hypokalemic Periodic Paralysis

Thyroid disorder is a well-recognized side effect of amiodarone therapy. Thyrotoxicosis is less common than hypothyroidism. Hypokalemic periodic paralysis is one manifestation of thyrotoxicosis, and is more often seen in Oriental and Latin American men than in other demographic groups. This phenomenon, however, has not been previously described in thyrotoxicosis due to amiodarone usage. We describe a case of amiodarone-induced thyrotoxicosis in a 34-year-old man who presented with sudden lower extremity weakness, heat intolerance, and weight loss. Physical examination demonstrated fine tremors. Serum potassium level was 2.2 mEq/L on admission. Gastrointestinal and renal causes of potassium loss were excluded by history and physical examination. Further biochemical testing demonstrated abnormal thyroid function. The urinary potassium and serum bicarbonate, magnesium, and calcium levels were within normal limits. Lower extremity weakness resolved immediately after potassium replacement therapy. Methimazole therapy was initiated, and the patient was clinically euthyroid on discharge.

Subacute Thyroiditis Manifesting as Fever of Unknown Origin

Subacute thyroiditis (SAT) usually occurs in women in middle age with a viral prodrome, thyroid or neck tenderness, classic symptoms of thyrotoxicosis, and elevated erythrocyte sedimentation rate (ESR). We report a case in an 81-year-old man who initially had 2 days of fever to 101.2 degrees F, confusion, and bilateral lower extremity weakness. Extensive evaluation was remarkable only for the following laboratory values: thyrotropin (TSH) 0.02 microIU/mL, free thyroxine (FT4) 3.1 ng/dL, free triiodothyronine (FT3) 6.0 pg/mL, and ESR 98 mm/hr. One week later, the patient had persistent fevers to 102 degrees F; no source was found. The fever resolved, and 3 months later the patient had profound hypothyroidism (TSH >44.0 microIU/mL, FT4 0.4 ng/dL, ESR 13 mm/hr). A painless thyroid gland and atypical manifestations of hyperthyroidism are unusual in SAT. When fever is of unknown origin, SAT should be considered even if classic features are absent.

Is it hyperthyroidism?

PREVIEWAlthough hyperthyroidism is a common endocrine disorder, recognizing it is not always simple. Frequency and severity of symptoms vary significantly from one patient to another. For example, weight loss despite good appetite is a classic manifestation of thyrotoxicosis, but some patients, particularly those who are young, gain weight. In addition, manifestations are sometimes atypical. For instance, older patients may present with only atrial fibrillation, heart failure, or weight loss and cachexia. In this article, Dr Haddad describes how to distinguish euthyroid hyperthyroxinemia from true thyroid disease and summarizes how to choose among treatment approaches.

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 . . .

Subacute Thyroiditis Presenting as Cushing’s Syndrome

Subacute thyroiditis is a benign, self-limited disorder characterized by hyperthyroidism that resolves spontaneously. Although cortisol metabolism is accelerated in hyperthyroidism, cortisol levels are usually normal. We describe a child with subacute thyroiditis whose presenting complaints and preliminary evaluation suggested a diagnosis of Cushing's syndrome. There was spontaneous improvement in the signs and symptoms with concomitant normalization of laboratory values. We conclude that hypercortisolism may be a manifestation of hyperthyroidism, and the evaluation of Cushing's syndrome should include thyroid function tests.

Thyrotoxic Encephalopathy and Recurrent Seizures

Epilepsy is a rare but possible manifestation of thyrotoxicosis. The patient reported here developed recurrent, generalized and focal seizures, as presenting symptoms of a thyrotoxic encephalopathy. Intercritic EEG records showed triphasic waves. Seizures and signs of encephalopathy disappeared and the EEG reverted to normal only after treatment of the thyroid hyperfunction. It is concluded that thyroid function should be evaluated in cases of otherwise unexplained encephalopathy with untreatable seizures and triphasic waves.

Persistent chorea as a manifestation of thyrotoxicosis

We report a case of persistent chorea as a manifestation of thyrotoxicosis. The chorea was severe and persisted after the patient was rendered euthyroid. Dopamine antagonists only partially suppressed the involuntary movements during the first few months. It was eventually controlled with haloperidol, but whenever she discontinues the treatment the chorea has returned during the 16 months since she first presented.

Thyrotoxicosis and Abdominal Pain

<h3>To the Editor.—</h3> Although it has been reported in the literature,¹abdominal pain is now rarely seen as a primary manifestation of hyperthyroidism. Also, the inability to swallow saliva has not been regarded as a manifestation of thyrotoxicosis. We describe a patient whose unusual symptoms of abdominal pain and spitting masked the diagnosis of thyrotoxicosis. <h3>Report of a Case.—</h3> A 44-year-old man was admitted to the Kaiser/Permanente Medical Center in Hayward, Calif, in February 1979 with a one-month history of an 18-kg weight loss and vague diffuse abdominal pain. Physical examination findings were normal except for a pulse rate of 100 beats per minute and a generalized abdominal tenderness. His weight was 97 kg and his face expressionless. No goiter was at first appreciated because of a "bull neck." There was no evidence of congestive heart failure or hepatomegaly. Attention was focused on his abdomen, and numerous x-ray films,

Thyroxine-binding Globulin in Hepatoma

<h3>To the Editor.—</h3> Systemic manifestations of hepatoma include hypoglycemia, erythrocytosis, and hypercalcemia, among others.¹Mildly elevated levels of thyroxine-binding globulin (TBG) have been recognized in a minority of patients with hepatoma.²The case described herein demonstrates that increased TBG activity in hepatoma may lead to extreme elevation of circulating thyroid hormone in a clinically euthyroid patient. Because fever, weight loss, hypercalcemia, and other manifestations of hyperthyroidism can be seen due to hepatoma, the finding of a markedly elevated serum thyroxine (T₄) or triiodothyronine (T₃) level must be interpreted carefully in patients with hepatoma. <h3>Report of a Case.—</h3> A 52-year-old woman consulted her physician because of anorexia, weight loss, and an enlarging epigastric mass. She had not noted changes in hair, skin, or bowel habit. She had no past history of thyroid disease and serum T₄level was normal five years previously. She denied the use

Pulling the Therapeutic Rug

Primum nil nocere is a principle to be kept in mind not only when therapy is initiated, but also when it is terminated. There may be iatrogenic hazard in abrupt withdrawal of a drug. A recent example of such a hazard is the severe angina, myocardial infarction, and death that can occur in patients with coronary artery disease when therapy with propranolol is suddenly discontinued ( JAMA 237:53, 1977). Sudden discontinuance of therapy with propranolol may also precipitate acute thyrotoxicosis in persons whose hyperthyroid condition had been disguised by use of the drug. Shenkman et al 1 reported on three patients in whom florid clinical manifestations of hyperthyroidism on abrupt withdrawal of propranolol led to the unsuspected diagnosis. The threat of a superimposed acute thyrotoxic state to a heart already damaged by ischemic or hypertensive disease cannot be overemphasized. Equally florid, albeit more transient than the acute thyrotoxicosis of propranolol withdrawal,

Effect of adrenergic blockade and specific antithyroid therapy on electrocardiographic changes in hyperthyroidism.

Abstract:Considerable controversy still exists whether the cardiovascular manifestations of hyperthyroidism are due to the direct action of an increased amount of thyroid hormones on the heart or due to increased adrenergic activity of catecholamines. In this study, electrocardiograms (ECG) were rec

Beta-adrenergic receptor blocking drugs in hyperthyroidism.

β-Adrenergic receptor blockade reduces many of the clinical manifestations of hyperthyroidism particularly tachycardia and dysrhythmias. β-Adrenergic receptor blocking drugs without intrinsic sympathomimetic activity are superior to those possessing it, probably because of the increased sensitivity to adrenergic receptor stimulation which is found in this condition. However, such treatment should not be considered as a long-term substitute for specific antithyroid therapy.

Paroxysmal Atrial Tachycardia: A Presenting Manifestation of Hyperthyroidism: Case Report

Paroxysmal Atrial Tachycardia: A Presenting Manifestation of Hyperthyroidism: Case Report

Effect of reserpine on the increase in myocardial adenyl cyclase activity produced by thyroid hormone.

SummaryThyroid hormone activates adenyl cyclase present in a particulate preparation of cat myocardium, an action that might contribute to the hyperdynamic circulatory state present in hyperthyroidism. Although the marked improvement in the cardiac manifestations of hyperthyroidism produced by reserpine is thought to be due to depletion of the norepinephrine stores of adrenergic nerve terminals, such improvement might be partly caused by an inhibitory effect of reserpine on the thyroid hormone-mediated activation of adenyl cyclase. We therefore examined the effects of reserpine on the capacity of thyroid hormone to activate adenyl cyclase in particulate preparations of cat myocardium. The results demonstrated that reserpine did not impair activation of adenyl cyclase by thyroxine and triiodothy-roxine when: (i) reserpine was present in the incubation mixture; and (ii) when cats had been pretreated with reserpine 24 hr prior to sacrifice. Half maximal activity in both the reserpine pretreated and normal ca...

Choreoathetosis as a manifestation of thyrotoxicosis.

Choreoathetosis as a manifestation of thyrotoxicosis.

Involvement of bulbar muscles in thyrotoxic myopathy.

SummaryTwelve cases of thyrotoxic myopathy, with involvement of bulbar muscles, are reported. It appears likely that this manifestation of thyrotoxicosis is not as uncommon as has previously been suggested.

Hypercalcaemia in thyrotoxicosis with and without hyperparathyroidism.

Summary Two cases of thyrotoxicosis with hypercalcaemia are reported. The hypercalcaemia in one of the patients was a manifestation of hyperthyroidism and in the other was due to co-existent hyperparathyroidism. The literature is reviewed and the effect of thyroid hormone on calcium metabolism is discussed. Routine plasma calcium estimations should be performed in all cases of thyrotoxicosis.