Administration of thyroxine in treated Graves' disease: effects on the level of antibodies to thyroid-stimulating hormone receptors and on the risk of recurrence of hyperthyroidism
Article Abstract:
Graves' disease is a condition in which excess thyroid hormone, or thyroxine, is manufactured by the thyroid gland. Thyroxine is normally produced in response to thyroid-stimulating hormone (TSH; also called thyrotropin), made in the pituitary gland and carried in the circulation to the thyroid gland, where it binds to receptors located on thyroid cells. The hyperthyroidism (elevated thyroxine levels) of Graves' disease is due mainly to the stimulation of these receptors by autoantibodies (antibodies made by the body to components of its own tissues) against the receptors, instead of by TSH; as a result of the stimulation, the cells produce more thyroxine. It is possible that the concentration of TSH-receptor antibodies rises during treatment in response to increased concentrations of TSH receptor proteins released when thyroid cells are stimulated by TSH. Reduction of TSH levels, then, might lead to lower levels of TSH-receptor antibodies; this can be accomplished by the administration of thyroxine. To test the effectiveness of thyroxine in treating Graves' disease, 109 patients with that disorder whose thyroxine levels had become normal after treatment were given either thyroxine and methimazole (an antithyroid drug), or a placebo (inactive drug) and methimazole. The patients' blood levels of thyroxine, TSH, TSH-receptor antibodies, and other relevant factors were measured regularly for several years. Results showed that concentrations of TSH-receptor antibodies decreased significantly during the initial treatment in all patients. The level fell still further for patients who received the thyroxine-methimazole combination, but held steady for those who received placebo-methimazole. Even after methimazole was discontinued, TSH-receptor antibody levels continued to decline for patients taking thyroxine. A smaller proportion of patients in this group suffered recurrences of hyperthyroidism during the three years after methimazole was discontinued. Thus, thyroxine appears beneficial for preventing hyperthyroidism in Graves' disease. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1991
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Treatment for Graves' disease: letting the thyroid rest
Article Abstract:
Graves' disease, a condition of hyperthyroidism (characterized by excess production of thyroid hormone), can be effectively treated, but patients and physicians may become concerned about the possible side effects of the three commonly used therapies. These are: antithyroid drugs, which may cause allergic reactions and (rarely) life-threatening side effects; removal of the thyroid gland (thyroidectomy), associated with discomfort and the need for lifelong consumption of thyroid hormones; and ingestion of radioactive iodine, considered undesirable by some people who fear exposure to radiation, and also necessitating hormone replacement therapy. A recent survey of clinicians from several countries revealed that the majority (69 percent) of those in the US would select radioactive-iodine therapy for a 43-year-old woman with Graves' disease, while most (88 percent) Japanese physicians would recommend an antithyroid drug. Though effective, none of these remedies actually treats the underlying abnormality in this disease, which is the production of antibodies against the thyrotropin (also called thyroid-stimulating hormone, TSH) receptor. TSH, manufactured in the pituitary, travels in the circulation to the thyroid where it stimulates the production of thyroid hormone (thyroxine). A novel approach to treating Graves' disease, presented in the April 4, 1991 issue of The New England Journal of Medicine, relies on administering thyroxine to patients to reduce the levels of TSH, which, in turn, leads to lower levels of the antigenic TSH-receptor protein. This led to a lower rate of recurrence of hyperthyroidism than is usual after antithyroid drug therapy, a result of clinical significance. The finding should be confirmed in other studies, and more information is needed about how such an effect might be produced. The recent characterization of the molecular structure of the TSH receptor offers additional hope for a better understanding of Graves' disease. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1991
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Thyroxine in goiter, Helicobacter pylori infection and chronic gastritis
Article Abstract:
A study was conducted to determine whether there is an increased need for thyroxine in patients with euthyroid multinodular goiter, Helicobacter pylori infection and impaired secretion of gastric acid. It was concluded that patients with impaired acid secretion require an increased dose of thyroxine, suggesting that normal gastric acid secretion is necessary for effective absorption of oral thyroxine.
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 2006
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