Find information on thousands of medical conditions and prescription drugs.


Hyperthyroidism (or "overactive thyroid gland") is the clinical syndrome caused by an excess of circulating free thyroxine (T4) or free triiodothyronine (T3), or both. more...

Hairy cell leukemia
Hallermann Streiff syndrome
Hallux valgus
Hantavirus pulmonary...
HARD syndrome
Harlequin type ichthyosis
Hartnup disease
Hashimoto's thyroiditis
Hearing impairment
Hearing loss
Heart block
Heavy metal poisoning
HELLP syndrome
Hemifacial microsomia
Hemolytic-uremic syndrome
Hemophilia A
Hemorrhagic fever
Hepatic encephalopathy
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatocellular carcinoma
Hepatorenal syndrome
Hereditary amyloidosis
Hereditary angioedema
Hereditary ataxia
Hereditary ceroid...
Hereditary coproporphyria
Hereditary elliptocytosis
Hereditary fructose...
Hereditary hemochromatosis
Hereditary hemorrhagic...
Hereditary spastic...
Hereditary spherocytosis
Hermansky-Pudlak syndrome
Herpes zoster
Herpes zoster oticus
Hidradenitis suppurativa
Hip dysplasia
Hirschsprung's disease
Hodgkin lymphoma
Hodgkin's disease
Horner's syndrome
Horseshoe kidney
Howell-Evans syndrome
Human parvovirus B19...
Hunter syndrome
Huntington's disease
Hurler syndrome
Hutchinson Gilford...
Hutchinson-Gilford syndrome
Hydatidiform mole
Hydrops fetalis
Hypereosinophilic syndrome
Hyperimmunoglobinemia D...
Hyperkalemic periodic...
Hyperlipoproteinemia type I
Hyperlipoproteinemia type II
Hyperlipoproteinemia type...
Hyperlipoproteinemia type IV
Hyperlipoproteinemia type V
Hypertensive retinopathy
Hypertrophic cardiomyopathy
Hypokalemic periodic...
Hypoplastic left heart...
Hypothalamic dysfunction


Major causes in humans are:

  • Graves' disease (the most common etiology with 70-80%)
  • Toxic thyroid adenoma
  • Toxic multinodular goitre

Other causes of hyperthyroxinemia (high blood levels of thyroid hormones) are not to be confused with true hyperthyroidism and include subacute and other forms of thyroiditis (inflammation). Thyrotoxicosis (symptoms caused by hyperthyroxinemia) can occur in both hyperthyroidism and thyroiditis. When it causes acutely increased metabolism, it is sometimes called "thyroid storm".

Signs and symptoms

Major clinical features in humans are weight loss (often accompanied by a ravenous appetite), fatigue, weakness, hyperactivity, irritability, apathy, depression, polyuria, and sweating. Additionally, patients may present with a variety of symptoms such as palpitations and arrhythmias (notably atrial fibrillation), dyspnea, infertility, loss of libido, nausea, vomiting, and diarrhea. In the elderly, these classical symptoms may not be present and they may present only with fatigue and weight loss leading to apathetic hyperthyroidism

Neurological manifestations are tremor, chorea, myopathy, and periodic paralysis. Stroke of cardioembolic origin due to coexisting atrial fibrillation may be mentioned as one of the most serious complications of hyperthyroidism.

As to other autoimmune disorders related with thyrotoxicosis, an association between thyroid disease and myasthenia gravis has been well recognised. The thyroid disease, in this condition, is often an autoimmune one and approximately 5% of patients with myasthenia gravis also have hyperthyroidism. Myasthenia gravis rarely improves after thyroid treatment and relation between two entities is yet unknown. Some very rare neurological manifestations that are reported to be dubiously associated with thyrotoxicosis are pseudotumor cerebri, amyotrophic lateral sclerosis and a Guillain-Barré-like syndrome.


A diagnosis is suspected through blood tests, by measuring the level of TSH (thyroid stimulating hormone) in the blood. If TSH is low, there is likely to be increased production of T4 and/or T3. Measuring specific antibodies, such as anti-TSH-receptor antibodies in Graves' disease, may contribute to the diagnosis. In all patients with hyperthyroxinemia, scintigraphy is required in order to distinguish true hyperthyroidism from thyroiditis.


The major and generally accepted modalities for treatment of hyperthyroidism in humans are:


Surgery (to remove the whole thyroid or a part of it) is not extensively used because most common forms of hyperthyroidism are quite effectively treated by the radioactive iodine method. However, some Graves' disease patients who cannot tolerate medicines for one reason or another or patients who refuse radioiodine opt for surgical intervention. The procedure is relatively safe - some surgeons are even treating partial thyroidectomy on an out-patient basis.


[List your site here Free!]

Subclinical Hyperthyroidism: Controversies in Management
From American Family Physician, 2/1/02 by Diane K. Shrier

Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable. The thyroid-stimulating hormone value is typically measured in a third-generation assay capable of detecting approximately 0.01 [micro]U per mL (0.01 mU per L). Subclinical hyperthyroidism may be a distinct clinical entity, related only in part to Graves' disease or multinodular goiter. Persons with subclinical hyperthyroidism usually do not present with the specific signs or symptoms associated with overt hyperthyroidism. A detailed clinical history should be obtained, a physical examination performed and thyroid function tests conducted as part of an assessment of patients for subclinical hyperthyroidism and to evaluate the possible deleterious effects of excess thyroid hormone on end organs (e.g., heart, bone). A reasonable treatment option for many patients is a therapeutic trial of low-dose antithyroid agents for approximately six to 12 months in an effort to induce a remission. Further research regarding the etiology, natural history, pathophysiology, and treatment of subclinical hyperthyroidism is warranted. (Am Fam Physician 2002;65:431-8. Copyright[C] 2002 American Academy of Family Physicians.)

Subclinical hyperthyroidism is an entity that is being increasingly recognized, probably because of the aging of the U.S. population and the development of assays with enhanced thyroid-stimulating hormone (TSH) sensitivity. Subclinical hyperthyroidism is defined as clinical euthyroidism in the context of normal serum free thyroxine (T4) and triiodothyronine (T3) levels, with a TSH level suppressed below the normal range, usually undetectable.(1-9)

Measurement of only total T4 and T3 levels is insufficient because some patients have a total T4 or T3 level within the normal range; however, their free, or unbound, fractions are increased. The TSH value is measured in a third-generation assay capable of detecting 0.01 [micro]U per mL (0.01 mU per L). Patients usually are euthyroid without the specific signs or symptoms associated with overt hyperthyroidism (although nonspecific signs or symptoms such as malaise, tachycardia, nervousness, and anxiety may be present).10-22 Atrial fibrillation may be the primary manifestation of subclinical hyperthyroidism in elderly patients.(3) Physical examination will not reveal an enlarged thyroid gland in most patients.(5)

The pathophysiology of subclinical hyperthyroidism relates to the sensitivity of the pituitary gland to respond to minor elevations in serum or tissue T4 and T3 levels. Although these levels remain within the normal range, minimal increases in these thyronines are sufficient not only to decrease the serum TSH level by several logarithms (from about 1.0 [micro]U per mL [1.0 mU per L] to less than 0.01 [micro]U per mL [0.01 mU per L]), but also to induce abnormalities in several organs, including the heart and bones. The normal range must be considered as a reference, but it is possible to have important pathophysiologic manifestations of altered T4 or T3 at the tissue level even though the peripheral serum thyronine levels are considered normal.

Etiology and Differential Diagnosis

While the diagnostic criteria and treatment modalities for overt hyperthyroidism are well known, the literature on assessment and treatment of patients with subclinical hyperthyroidism is markedly less extensive.(1-10,13-17,23,24) The precise pathophysiology, natural history, prevalence, risks and long-term outcome of subclinical hyperthyroidism are unknown. It is assumed that most elderly patients with subclinical hyperthyroidism have a multinodular goiter, but several other conditions should be considered in the differential diagnosis.

Transient suppression of a TSH level that returns to the normal range within several months is thought to be caused by silent thyroiditis.(1,6,25) A suppressed serum TSH level may be related to nonthyroidal illness, steroid or dopamine administration, or pituitary dysfunction; therefore, it is important to exclude these conditions.(1,6,7) Abnormalities in the TSH level may presage the development of overt hyperthyroidism (Graves' disease, multinodular goiter, or Hashimoto's disease/ Hashitoxicosis), in which case the free T3 and T4 levels will gradually rise outside of the normal range, resulting in the development of the classic symptoms and signs of hyperthyroidism. The etiology of subclinical hyperthyroidism further includes partially or insufficiently treated overt hyperthyroidism, multinodular goiter, Graves' disease (early in its course), iodine-associated hyperthyroidism, solitary autonomous adenoma and thyroiditis (subacute, silent, postpartum).(1,6,13) In this discussion, we are specifically excluding consideration of patients who are taking exogenous thyroid hormone that is suppressing TSH.

It is important to exclude the recent administration of radio contrast material or exogenous iodine exposure, and to consider other causes of hyperthyroidism (e.g., trophoblastic tumors, exogenous thyroid hormone ingestion).(25,26) In subclinical hyperthyroidism, a 24-hour radioactive iodine uptake (RAIU) will generally be elevated in patients with Graves' disease, multinodular goiter, and solitary autonomous nodule; whereas, the RAIU will be less than 5 percent at 24 hours (normal range, 5 to 30 percent at 24 hours) in patients in the hyperthyroid phase of subacute, silent, or postpartum thyroiditis and in patients taking excess exogenous thyroid hormone.(26)

One difficulty in interpreting the literature relating to subclinical hyperthyroidism is the inclusion of patients with differing etiologies. It is assumed that the frequency of complications of subclinical hyperthyroidism relates to the perturbed T3 and T4 levels and not to the underlying cause.(1,3,6,27) Most patients with subclinical hyperthyroidism are ambulatory outpatients who are otherwise relatively healthy or have stable, chronic medical conditions. Results of long-term studies suggest that subclinical hyperthyroidism may develop into overt disease at a rate of at least 1 to 3 percent per year.(2,3,9-12) Abnormalities in the TSH level may remain for months or years in the absence of overt clinical symptoms, with a potentially increased risk to the patient of developing cardiac and bone density abnormalities.

Cardiac Abnormalities and Bone Loss

Patients with subclinical hyperthyroidism are at increased risk for cardiac abnormalities and bone loss, and strong consideration should be given to initiating treatment and restoring the TSH level to within the normal range.(3,17,24,26,28) The risk of atrial fibrillation is increased three to fivefold in persons older than age 60 studied for about a decade, compared with those with normal TSH values.(3) One study evaluated cardiac function and exercise tolerance in 10 dyspneic subjects with symptoms of adrenergic overactivity on l-thyroxine therapy (for five to nine years' duration) sufficient to suppress serum TSH level.(29) Resting baseline left ventricular diastolic filling was impaired and, during submaximal physical exercise, a decrease in left ventricular ejection fraction was observed in the l-thyroxine treated group, compared with a normal increase observed in the control group. Exercise capacity in duration and peak workload was reduced in the l-thyroxine-treated group, and cardiac parameters improved with administration of a beta blocker for four months.

In another study, an increase in left ventricular mass, prolonged isovolumetric relaxation time, and reduced early diastolic filling velocity were observed in l-thyroxine-treated subjects who had a suppressed serum TSH concentration.(30) In 19 study subjects receiving long-term l-thyroxine suppressive therapy, increases in intraventricular septal thickness and left ventricular posterior wall thickness were noted, compared with the control group. Exercise tolerance, maximal oxygen consumption (VO2) at peak exercise, and anaerobic threshold were also reduced in the l-thyroxine-treated group. Each of these cardiac changes returned to the normal range with modulation of the l-thyroxine dose that maintained the serum TSH concentration at a less suppressed level.(31) Atrial fibrillation and other arrhythmias may occur when tissues are exposed to excess thyroid hormones. The long-term clinical implications of these cardiac changes are unknown, but they are concerning, and further studies are warranted.(32)

The issue of increased bone loss in patients with subclinical hyperthyroidism has also been studied, although the published reports are generally small studies that were not controlled, prospective, long-term, or double blinded.(5,6,20,33-40) Premenopausal women with subclinical hyperthyroidism do not appear to be at increased risk of bone loss; whereas, two meta-analyses conclude that postmenopausal women with hyperthyroidism may be at increased risk of bone loss.(20,40) An analysis of 1,250 subjects enrolled in 41 studies revealed that in postmenopausal women, suppressive thyroid hormone therapy was associated with significant bone loss in the lumbar spine and femoral areas.(40) Results of another trial similarly led to the conclusion that postmenopausal women had enhanced bone loss when taking suppressive doses of thyroid hormone.(20)

The effects on bone mineral density appear to be comparable in women with a suppressed TSH level secondary to excess exogenous l-thyroxine compared with women with endogenous subclinical hyperthyroidism. In a prospective, nonrandomized two-year study, 16 postmenopausal women with nodular goiter and subclinical hyperthyroidism were treated with radioiodine therapy; 12 were followed without treatment and served as the control subjects.(5) The TSH level in women treated with radioiodine returned to the normal range, while the TSH level in women in the control group remained suppressed. Bone mineral density measurements of the hip and spine revealed an increase of approximately 1 to 2 percent in the radioiodine-treated women, while a 2 to 5 percent decrease was measured in the women in the control group. Differences in both the spine and the hip were statistically different in the control and treated groups.

The frequency of neuropsychiatric abnormalities in patients with subclinical hyperthyroidism has also been studied. Results suggest that patients with subclinical hyperthyroidism experienced reduced feelings of well-being, as well as feelings of fear, hostility, and an inability to concentrate.(41)

Diagnostic Assessment and Follow-Up

A clinical algorithm (Figure 1) outlines diagnostic assessment and therapeutic recommendations. After an initial clinical history and physical examination, patients who appear to have subclinical hyperthyroidism without a clear etiology should be re-evaluated with repeat serum free T4, T3, and TSH tests. We recommend monitoring thyroid function tests monthly for three months before making a more definitive therapeutic decision, but other reasonable periods of monitoring may be also be considered.

If the low serum TSH concentration persists, it is recommended that a 24-hour RAIU and a thyroid scan (after excluding pregnancy) be performed. In addition, thyroid sonography may be indicated in some instances to assess patients for nodules and heterogeneity. The sonogram may be helpful in allowing detection of nonpalpable nodules requiring biopsy and may provide information about the presence of cervical lymphadenopathy associated with silent or subacute thyroiditis. In select patients at increased risk for cardiac or osseous abnormalities, a bone mineral density study of the hip and spine and electrocardiography may be indicated as part of the treatment regimen.(3,18,23,33,34) Occasionally, use of a 24-hour Holter monitor may be indicated in documenting arrhythmias.

Treatment Options

Treatment modalities in patients with subclinical hyperthyroidism have not been studied long-term, and alternative treatment options have not been compared in controlled clinical studies. As has been noted, "Few data are available to guide clinical decisions regarding the treatment of endogenous subclinical thyrotoxicosis."(1) We conducted a computer-derived search for evidence-based studies relating to subclinical hyperthyroidism and found few prospective, randomized, controlled studies. Therefore, individual studies, case reports, and personal clinical experience must serve as the parameters for assessing patients with subclinical hyperthyroidism. These patients could be treated with either antithyroid agents, surgery, or radioactive iodine or, alternatively, these patients could simply be monitored periodically.(26) In general, in patients with a clearly detectable TSH level that is only slightly below the normal range, long-term monitoring seems most appropriate to determine if the TSH level will remain constant.

Currently, most endocrinologists in the United States recommend definitive treatment of patients with overt hyperthyroidism by ablating thyroid function with radioactive iodine (perhaps after the short-term use of antithyroid agents) and then maintaining the patient on life-long thyroid hormone replacement therapy.(26) In Japan, the preferred initial mode of treatment of patients with overt hyperthyroidism is the use of long-term antithyroid medications.(42) It is unknown if the same paradigm should apply to patients with subclinical hyperthyroidism.

Patients with subclinical hyperthyroidism may respond to treatment differently than patients with overt Graves' disease and multinodular goiters, although subclinical hyperthyroidism likely represents a form of one or more of these basic disease processes. Unlike patients with overtly symptomatic multinodular goiter, some patients with subclinical hyperthyroidism appear to undergo a sustained remission following a trial of antithyroid agents.

A decision regarding treatment of patients with subclinical hyperthyroidism that is based on evidence-based research is problematic because prospective controlled studies comparing different therapies do not exist. Patients with persistent thyroid function abnormalities without another discernible etiology or overt clinical symptoms might benefit from a course of low-dose antithyroid therapy. Definitive therapy (e.g., radioiodine, surgery) in patients without specific signs or symptoms seems to be unnecessarily aggressive--at least at the outset of disease.

Typically, the RAIU is normal or only slightly increased in patients with subclinical hyperthyroidism, and thyroid tissue heterogeneity may make it more difficult to determine the appropriate dose of radioactive iodine necessary to ablate the thyroid. Financial considerations and issues of potential noncompliance and drug interactions need to be considered with an aging population. The potential risks and benefits of each treatment option should be discussed with the patient, whose preference will weigh in the decision.

Some patients respond very well to a six- to 12-month trial of low-dose antithyroid agents. The risk of bone marrow suppression and hepatic toxicity is low with the dosages required.(35) After obtaining baseline thyroid function tests, complete blood count and liver function tests, periodic reassessment should be performed while antithyroid agents are administered. Patients should be informed of specific symptoms of a potential adverse reaction and told to contact their physician as soon as possible should they occur. The trial dose of antithyroid agent is modulated to maintain the TSH level within the normal range and discontinued after about six to 12 months of therapy. Initially, periodic monitoring of thyroid function tests and thyroid status should be performed every several months and less frequently thereafter. Methimazole (Tapazole), in dosages of about 5 mg daily, should be used since this medication can be administered once daily. It is a pregnancy category D drug and contraindicated in women of child-bearing age and nursing mothers. Propylthiouracil (50 to 100 mg daily) is preferred in patients who are of child-bearing potential, since in the United States, propylthiouracil has been used preferentially during pregnancy to treat hyperthyroidism.(18,35) If hyperthyroidism recurs after a trial of antithyroid agents, either another trial of antithyroid agents could be initiated or definitive therapy (e.g., iodine(131) therapy) or surgery could be considered.


The analysis of a low TSH level and subclinical hyperthyroidism raises the controversial issue of screening. The American Thyroid Association(43) recommends that serum TSH concentration screening be instituted at age 35 years in both men and women and be repeated every five years. Of course, if symptoms develop or if risk factors are present (e.g., thyroid antibodies), more frequent testing may be in order. It is recommended, based on a literature review,(7) that TSH screening in women older than 50 years may be indicated; the U.S. Preventive Services Task Force,(44) however, does not recommend screening for thyroid disease in asymptomatic children or adults. The guidelines of the American College of Physicians that were reviewed in the Helfand article(7) are also critically reviewed in an editorial(4) and three other articles.(45-47)

Dr. Burman has served as consultant and lecturer for Knoll Pharmaceutical Co. and Novartis.

DIANE K. SHRIER, M.D., is clinical professor of psychiatry and pediatrics at George Washington University Medical Center, and senior consultant psychiatrist at Walter Reed Army Medical Center, both in Washington, D.C., where she also has a private practice in child, adolescent and adult psychiatry. Dr. Shrier received her medical degree from Yale University School of Medicine, New Haven, Conn. She completed a residency in psychiatry and a fellowship in child psychiatry at Albert Einstein College of Medicine, Bronx Municipal Hospital Center, Bronx, N.Y.

KENNETH D. BURMAN, M.D., is chief of the Endocrine Section at Washington Hospital Center, Washington D.C., professor in the Department of Internal Medicine at the Uniformed Services University of the Health Sciences, Bethesda, Md., and clinical professor in the Department of Medicine at Georgetown University and George Washington University Medical Center, both in Washington, D.C. Dr. Burman received his medical degree from the University of Missouri Medical School, Columbia, Mo. He completed a residency in internal medicine at Barnes Hospital, St. Louis, and a fellowship in endocrinology at Walter Reed Army Medical Center, Washington, D.C. Dr. Burman was formerly chief of the Endocrine Department at Walter Reed Army Medical Center and endocrine consultant to the Surgeon General.

Address correspondence to Kenneth D. Burman, M.D., Chief of Endocrine Section, Washington Hospital Center, 110 Irving St., N.W., Washington DC 20010. Reprints are not available from the authors.


(1.) Werner SC, Ingbar SH, Braverman LE, Utiger RD. Subclinical thyrotoxicosis. In: Braverman LE, Utiger RD, et al., eds. Werner and Ingbar's The thyroid: a fundamental and clinical text. 7th ed. Lippincott Williams & Wilkins, 1996.

(2.) Vanderpump MP, Tunbridge WM, French JM, Appleton D, Bates D, Clark F, et al. The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey. Clin Endocrinol 1995;43:55-68.

(3.) Sawin CT, Geller A, Wolf PA, Belanger AJ, Baker E, Bacharach P, et al. Low serum thyrotropin concentrations as a risk factor for atrial fibrillations in older persons. N Engl J Med 1994;331:1249-52.

(4.) Cooper DS. Subclinical thyroid disease: a clinician's perspective [Editorial]. Ann Intern Med 1998;129: 135-8.

(5.) Faber J, Jensen IW, Petersen L, Nygaard B, Hegedus L, Siersbaek-Nielsen K. Normalization of serum thyrotrophin by means of radioiodine treatment in subclinical hyperthyroidism: effect on bone loss in postmenopausal women. Clin Endocrinol 1998;48: 285-90.

(6.) Haden ST, Marqusee E, Utiger RD. Subclinical hyperthyroidism. Endocrinologist 1996;6:322-7.

(7.) Helfand M, Redfern CC. Screening for thyroid disease: an update. Ann Intern Med 1998;129:144-58.

(8.) Marqusee E, Haden ST, Utiger RD. Subclinical thyrotoxicosis. Endocrinol Metab Clin North Am 1998;27:37-49.

(9.) Stott DJ, McLellan AR, Finlayson J, Chu P, Alexander WD. Elderly patients with suppressed serum TSH but normal free thyroid hormone levels usually have mild thyroid overactivity and are at increased risk of developing overt hyperthyroidism. Q J Med 1991;78:77-84.

(10.) Samuels MH. Subclinical thyroid disease in the elderly. Thyroid 1998;8:803-13.

(11.) Eggertsen R, Petersen K, Lundberg PA, Nystrom E, Lindstedt G. Screening for thyroid disease in a primary care unit with a thyroid stimulating hormone assay with a low detection limit. BMJ 1988;297: 1586-92.

(12.) Parle JV, Franklyn JA, Cross KW, Jones SC, Sheppard MC. Prevalence and follow-up of abnormal thyrotropin (TSH) concentrations in the elderly in the United Kingdom. Clin Endocrinol 1991;34:77-83.

(13.) Surks MI, Ocampo E. Subclinical thyroid disease. Am J Med 1996;100:217-23.

(14.) Utiger RD. Subclinical hyperthyroidism--just a low serum thyrotropin concentration, or something more? N Engl J Med 1994;331:1302-3.

(15.) Wallace K, Hofmann MT. Thyroid dysfunction: How to manage overt and subclinical disease in older patients. Geriatrics 1998;53:32-41.

(16.) Woeber KA. Subclinical thyroid dysfunction. Arch Intern Med 1997;157:1065-8.

(17.) Braverman LE. Subclinical hypothyroidism and hyperthyroidism in elderly subjects: should they be treated? J Endocrinol Invest 1999;22(10 suppl):1-3.

(18.) Madeddu G, Spanu A, Falchi A, Nuvoli S. Clinical and laboratory assessment of subclinical thyroid disease. Rays 1999;24:229-42.

(19.) Kasagi K, Kousaka T, Misaki T, Iwata M, Alam MS, Konishi J. Comparison of serum thyrotrophin concentrations determined by a third generation assay in patients with various types of overt and subclinical thyrotoxicosis. Clin Endocrinol 1999;50:185-9.

(20.) Faber J, Galloe AM. Changes in bone mass during prolonged subclinical hyperthyroidism due to l-thyroxine treatment: a meta-analysis. Eur J Endocrinol 1994;130:350-6.

(21.) Bagchi N, Brown TR, Parish RF. Thyroid dysfunction in adults over age 55 years. A study in an urban US community. Arch Intern Med 1990;150:785-7.

(22.) Sundbeck G, Jagenburg R, Johansson PM, Eden S, Lindstedt G. Clinical significance of low serum thyrotropin concentration by chemiluminometric assay in 85-year-old women and men. Arch Intern Med 1991;151:549-56.

(23.) Biondi B, Fazio S, Carella C, Amato G, Cittadini A, Lupoli G, et al. Cardiac effects of long term thyrotropin-suppressive therapy with levothyroxine. J Clin Endocrinol Metab 1993;77:334-8.

(24.) Franklyn JA. Thyroid disease and its treatment: short- and long-term consequences. J R Coll Physicians Lond 1999;33:564-7.

(25.) Dorfman SG, Cooperman MT, Nelson RL, Depuy H, Peake RL, Young RL. Painless thyroiditis and transient hyperthyroidism without goiter. Ann Intern Med 1977;86:24-8.

(26.) Burman KD. Hyperthyroidism. In: Becker KL, Bilezikian, et al., eds. Principles and practice of endocrinology and metabolism. 2d ed. Philadelphia: J.B. Lippincott, 1995.

(27.) Burman KD, Pandian R. Clinical utility of assays for TSH receptor antibodies. Endocrinologist 1998;8: 284-90.

(28.) Stanbury JB, Ermans AE, Bourdoux P, Todd C, Oken E, Tonglet R, et al. Iodine-induced hyperthyroidism: occurrence and epidemiology. Thyroid 1998;8:83-100.

(29.) Biondi B, Fazio S, Cuocolo A, Sabatini D, Nicolai E, Lombardi G, et al. Impaired cardiac reserve and exercise capacity in patients receiving long-term thyrotropin suppressive therapy with levothyroxine. J Clin Endocrinol Metab 1996;81:4224-8.

(30.) Fazio S, Biondi B, Carella C, Sabatini D, Cittadini A, Panza N, et al. Diastolic dysfunction in patients on thyroid-stimulating hormone suppressive therapy with levothyroxine: beneficial effect of beta-blockade. J Clin Endocrinol Metab 1995;80: 2222-6.

(31.) Mercuro G, Panzuto MG, Bina A, Leo M, Cabula R, Petrini L, et al. Cardiac function, physical exercise capacity, and quality of life during long-term thyrotropin-suppressive therapy with levothyroxine: effect of individual dose tailoring. J Clin Endocrinol Metab 2000;85:159-64.

(32.) Fadel BM, Ellahham S, Ringel MD, Lindsay J, Wartofsky L, Burman KD. Hyperthyroid heart disease. Clin Cardiol 2000;23:402-8.

(33.) Engler H, Oettli RE, Riesen WF. Biochemical markers of bone turnover in patients with thyroid dysfunctions and in euthyroid controls: a cross-sectional study. Clin Chim Acta 1999;289(1-2):159-72.

(34.) Gurlek A, Gedik O. Effect of endogenous subclnical hyperthyroidism on bone metabolism and bone mineral density in premenopausal women. Thyroid 1999;9:539-43.

(35.) Burman KD. How serious are the risks of thyroid hormone over-replacement? Thyroid Today 1995; 18:1-9.

(36.) Solomon BL, Wartofsky L, Burman KD. Prevalence of fractures in postmenopausal women with thyroid disease. Thyroid 1993;3:17-23.

(37.) Rosen HN, Moses AC, Garber J, Ross DS, Lee SL, Ferguson L, Chen V, et al. Randomized trial of pamidronate in patients with thyroid cancer: bone density is not reduced by suppressive doses of thyroxine, but is increased by cyclic intravenous pamidronate. J Clin Endocrinol Metab 1998;83: 2324-30.

(38.) Greenspan SL, Greenspan FS. The effect of thyroid hormone on skeletal integrity. Ann Intern Med 1999;130:750-8.

(39.) Hanna FW, Pettit RJ, Ammari F, Evans WD, Sandeman D, Lazarus JH. Effect of replacement doses of thyroxine on bone mineral density. Clin Endocrinol 1998;48:229-34.

(40.) Uzzan B, Campos J, Cucherat M, Nony P, Boissel JP, Perret GY. Effects on bone mass of long term treatment with thyroid hormones: a meta-analysis. J Clin Endocrinol Metab 1996;81:4278-89.

(41.) Bommer M, Eversmann T, Pickardt R, Leonhardt A, Naber D. Psychopathological and neuropsychological symptoms in patients with subclinical and remitted hyperthyroidism. Klin Wochenschr 1990; 68:552-8.

(42.) Wartofsky L, Glinoer D, Solomon B, Nagataki S, Lagasse R, Nagayama Y, Izumi M. Differences and similarities in the diagnosis and treatment of Graves' disease in Europe, Japan, and the United States. Thyroid 1991;1:129-35.

(43.) Ladenson PW, Singer PA, Ain KB, Bagchi N, Bigos ST, Levy EG, et al. American Thyroid Association guidelines for detection of thyroid dysfunction. Arch Intern Med 2000;160:1573-5.

(44.) U.S. Preventive Services Task Force. Guide to clinical preventive services. 2d ed. Baltimore: Williams & Wilkins, 1996.

(45.) Kaplan MM. Clinical perspectives in the diagnosis of thyroid disease. Clin Chem 1999;45(8 pt 1): 1377-83.

(46.) Arbelle JE, Porath A. Practice guidelines for the detection and management of thyroid dysfunction. A comparative review of the recommendations. Clin Endocrinol 1999;51:11-8.

(47.) Griffin G. Screening for subclinical thyroid disease. J Fam Pract 1998;47:248-9.

COPYRIGHT 2002 American Academy of Family Physicians
COPYRIGHT 2002 Gale Group

Return to Hyperthyroidism
Home Contact Resources Exchange Links ebay