Hyperthyroidism and Thyrotoxicosis

F. Bandeira et al. (eds.), Endocrinology and Diabetes: A Problem-Oriented Approach, DOI 10.1007/978-1-4614-8684-8_2, © Springer Science+Business Media New York 2014 The term thyrotoxicosis applies to a clinical condition resulting from increased thyroid hormone action. It can result from excess thyroid hormone synthesis followed by release for which the term hyperthyroidism is applicable. Thyrotoxicosis can also result from a destructive process in the thyroid resulting in unregulated excess release of stored thyroid hormones without increased production [ 1 , 2 ]. The thyrotoxicosis syndrome may also be due to exogenous source either iatrogenic or factitious. Hyperthyroidism is considered subclinical when mild increase in peripheral thyroid hormone levels, although within normal laboratory reference range, is in excess for that individual. Hypothalamus–pituitary axis senses the excess and the negative feedback mechanism results in suppressed or abnormally low thyrotrophic hormone (TSH). Thus it can be argued that this is a biochemical rather than a clinical term. Subclinical hyperthyroidism may be symptomatic or asymptomatic but in either case has adverse effects [ 3 ]. In the United States subclinical hyperthyroidism is more common (0.7 %) than clinical hyperthyroidism (0.5 %), however much less common than subclinical hypothyroidism (3–10 %). If biologic activity of thyroid hormones is reduced such as in thyroid hormone resistance [ 4 ], increased peripheral thyroid levels do not result in thyrotoxicosis syndrome. Thyrotoxicosis is a syndrome with many diverse etiologies [ 1 ]. When clinical symptomatology or biochemical fi ndings establish excess thyroid hormone effect, diagnostic measures should be directed at fi nding the specifi c etiology, since management and therapy will depend on the etiology. Graves’ hyperthyroidism is the most common cause of hyperthyroidism in the United States. Toxic multinodular goiter and toxic adenomas are the next common causes. Nodular toxic goiter is more common in older individuals and in geographic areas with historical iodine defi ciency [ 5 ]. Inappropriate excess thyroxine (T4) therapy or T4 suppressive therapies for follicular cell-derived thyroid cancer are also common causes of subclinical hyperthyroidism. The fi rst step after establishing the diagnosis of thyrotoxicosis syndrome, if not contraindicated because of pregnancy or lactation, is to obtain a radioactive iodine uptake of thyroid. High radioactive iodine uptake (RAIU) in iodinesuffi cient areas is consistent with Graves’ hyperthyroidism and very rarely TSH-producing pituitary adenoma. Occasionally toxic nodular goiter may have mildly elevated uptake but usually uptake is normal and sometimes low [ 6 ]. In Graves’ disease degree of elevated uptake is usually proportional to the severity of Graves’ disease; subclinical cases may have normal uptake. Very low and near-zero RAIU is consistent with silent thyroiditis, subacute thyroiditis, postpartum thyroiditis, iodine-induced hyperthyroidism, V. Fatourechi , M.D. (*) Endocrinology, Metabolism and Nutrition , Mayo Clinic College of Medicine , 200 First Street, SW , Rochester , MN 55905 , USA e-mail: [email protected] 2 Hyperthyroidism and Thyrotoxicosis