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Hypothyroidism is the most common thyroid abnormality in children. It can develop at any age among previously healthy children, although it is more common among girls. Growth retardation is an early sign. There are various causes of acquired hypothyroidism (Table 521-1). Iodine deficiency remains a major cause worldwide; however, the worldwide incidence is decreasing. Symptomatic iodine deficiency is uncommon in North America because of fortification of salt and the presence of iodine in dairy products. In the United States, acquired hypothyroidism is most often caused by autoimmune thyroiditis (Hashimoto thyroiditis) characterized by high levels of circulating antithyroid antibodies. Among other causes of acquired juvenile hypothyroidism are exposure to goitrogenic agents, thyroid dysgenesis, late onset of hypothyroidism caused by an inborn error of thyroidal biosynthesis, acquired hypothalamic or pituitary hypothyroidism, or endemic factors.
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AUTOIMMUNE (HASHIMOTO) THYROIDITIS
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The spectrum of autoimmune thyroid disease in children includes euthyroid goiter, hypothyroid goiter, Graves disease, hashitoxicosis, nodular goiter, thyroid antigen-antibody nephritis, and several endocrine deficiency diseases. The last includes diabetes mellitus, adrenal insufficiency, hypoparathyroidism, moniliasis, and, less commonly, pernicious anemia and thrombocytopenia. The most common clinical association is Hashimoto thyroiditis and diabetes mellitus with or without adrenal cortical insufficiency (Schmidt syndrome).
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Hashimoto thyroiditis is the most common thyroid disorder in children, with a marked predilection for females. Chronic thyroiditis is the most common cause of goiter and hypothyroidism among children older than 6 years in North America. It occurs in a genetically predisposed population: 30% to 40% of patients have a family history of thyroid disease.
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Circulating thymus-dependent (T) lymphocytes sensitized against the particulate portion of thyroid cells (microsomes and cell membranes) are found in almost all patients with Hashimoto thyroiditis and Graves disease. A genetically determined defect in the immune surveillance system has been postulated. Both T lymphocytes sensitized against thyroidal components and humoral antibodies directed at various thyroidal components produce the thyroid abnormality. The latter are produced by B rather than T lymphocytes. It is known that the interaction of T and B lymphocytes plays a crucial role in the elaboration of immunoglobulins by B lymphocytes.
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Age-specific incidence rates for Graves disease and Hashimoto thyroiditis show an increasing rate of onset through the fifth decade and a decline thereafter, possibly suggesting ...