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Hyperthyroidism


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Introduction
Thyroid hormones affect virtually every organ system. In the child, thyroid hormone is critical for normal growth and development. In the adult, the major role of thyroid hormone is to maintain metabolic stability.

Reservoirs of thyroid hormone in the thyroid gland and blood provide constant thyroid availability. In addition, the hypothalamic-pituitary-thyroid axis is sensitive to small changes in circulating thyroid hormone concentrations. Alterations in thyroid hormone secretion maintain peripheral free thyroid hormone levels within a narrow range.(1)

The thyroid gland uses iodine to make thyroid hormones, the two most important being thyroxine (T4) which has four iodine molecules attached to its chemical structure, and triiodothyronine (T3), which has three. Iodine can be found in seafood, bread, salt, and seaweed. More than 99 percent of all thyroid hormones are bound to proteins in the blood and do not interact with body cells. Only a fraction are free; however, these are the important and active hormones that directly interact with body cells to help regulate metabolism.

Normally, the rate of production of thyroid hormone is controlled by the pituitary gland. When there is insufficient thyroid hormone in the body for normal functioning of cells, the pituitary releases TSH (Thyroid stimulating hormone). TSH "stimulates" the thyroid gland to produce more thyroid hormone.

Measurement of radioactive iodine uptake (RAIU) is critical in the evaluation of the clinically thyrotoxic patient. An elevated RAIU indicates true hyperthyroidism; that is, the patient's thyroid gland is actively overproducing T4, T3, or both. Conversely, a low RAIU indicates the excess thyroid hormone is not a consequence of thyroid gland hyperfunction. The importance of differentiating true hyperthyroidism from other causes of thyrotoxicosis lies in the widely different prognosis and treatment of diseases in the two categories.(1)

Thyrotoxicosis results when tissues are exposed to excessive levels of T4, T3, or both.(2) Like many endocrine disorders, thyrotoxicosis occurs more frequently in women, with an estimated annual incidence of 3 per 1000. Some causes of thyrotoxicosis in patients with increased RAIU include:

  • TSH-induced hyperthyroidism
  • TSH secreting tumors
  • Selective pituitary resistance to T4
  • Thyroid stimulators other than TSH
  • Graves' Disease (thyroid stimulating antibodies)
  • Trophoblastic diseases (HCG)
  • Thyroid autonomy
  • Toxic adenoma
  • Multinodular goiter

Some causes of thyrotoxicosis in patients with decreased RAIU include:

  • Inflammatory thyroid disease (subacute thyroiditis, painless thyroid)
  • Ectopic thyroid tissue (struma ovarii, metastatic follicular carcinoma)
  • Exogenous sources of thyroid hormone ( medication and food)
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Footnotes
1 DiPiro, et al. Pharmacotherapy, A Pathophysiologic Approach, fourth edition. Stamford, Conn: Appleton and Lange; 1999:1244-1248.
2 Kannan CR, Seshadri KG. Thyrotoxicosis. Dis Mon. 1997;43:601-677.
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