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Hyperthyroidism

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...

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Causes

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.

Diagnosis

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.

Treatment

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

Surgery

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.

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A REVIEW OF HYPERTHYROIDISM: A TWENTY-FIVE YEAR EXPERIENCE
From Medicine and Health Rhode Island, 12/1/04 by Durkan, Maeve C

Hyperthyroidism is a common endocrine disorder. We retrospectively evaluated our 25-year database of 374 patients with hyperthyroidism, reviewing underlying etiologies, treatment strategies and success or failure of various treatments. We also evaluated the role of antibody titers in Graves' disease in predicting ultimate hypothyroidism. Graves' disease was diagnosed in 82% of patients and the remainder had a multinodular toxic goiter or toxic adenoma. 84% of patients were female with a female to male ratio of 5:1. The average age of onset of disease was 48 years (range 11 to 88 years). More than half the patients presented between 30 and 60 years of age (55%). 19% were 30 years of age or younger and 22% were between 60 and 79 years of age. 25% of patients had a clearly defined precipitating stress-event and 38% of patients had a positive family history of thyroid disease. 65% of patients had symptoms for several months to a year. 83% percent of patients had a goiter with an estimated gland weight of 30 to 100 grams. 28% of patients had clinical ophthalmopathy and 11 patients (

More than half of patients had positive anti-microsomal antibody titers. Of the 35 patients with recently measured TSI titers, 25 (71%) had positive titers, and all had Graves' disease. All patients exhibited TSH suppression. Approximately 90% had increased serum T4 levels. 3% (11 patients) had increased T3, and normal T4, consistent with T3 toxicosis. 3% (12 patients) had normal T3 and T4. 78% of patients had homogenous uptake on thyroid scan and the remainder had inhomogenous uptake, or uptake consistent with a toxic adenoma. Mean I^sup 123^ uptake was 47% at 6 hours and 57% at 24 hours. 116 patients received PTU or tapazole for 1 year or longer of whom only 16 patients have had a sustained remission. 20 patients were treated surgically and 8 of these patients were subsequently treated with I^sup 131^. Of those with antibody positivity, 29% became ultimately hypothyroid compared with 14% who had antibody negativity. 304 patients received I^sup 131^ of whom 251 received one therapeutic dose, 47 received 2 doses and 6 received 3 doses. Of those receiving one dose of I^sup 131^, 28% ultimately became hypothyroid and of these 58% were antimicrosomal antibody positive. Of those treated twice, 26% became hypothyroid (66% were antibody positive) and of those treated 3 times, 2 of 6 (33%) became hypothyroid. 73 patients with positive antibody titers developed hypothyroidism after I^sup 131^ while only 33 patients with negative antibody titers developed hypothyroidism.

Our findings support the general experience that Graves' disease is the most common cause of hyperthyroidism, with a female predominance, presenting most often between 30 and 60 years of age. Finally, more than half of the patients had positive antibody titers consistent with a concomitant underlying Hashimotos thyroiditis, in keeping with the general impression of a frequent association between Hashimotos thyroiditis and Graves' disease. The data suggest a greater incidence of I^sup 131^ induced hypothyroidism in patients with positive antibody titers.

MAEVE C. DURKAN, MD, JASMINE JOHN, MD, JOSEPH TUCCI, MD

ROGER WILLIAMS MEDICAL CENTER, BOSTON UNIVERSITY SCHOOL OF MEDICINE, BROWN UNIVERSITY SCHOOL OF MEDICINE

Copyright Rhode Island Medical Society Dec 2004
Provided by ProQuest Information and Learning Company. All rights Reserved

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