Pathophysiology of Endemic Goiter

Endemic goiter is the end result of the physiologic and morphologic changes in the thyroid gland as an adaptation to an insufficient supply of dietary iodine. When iodine intake is low, thyroid hormone synthesis is impaired. This impairment leads to an increased thyroidal clearance of iodide from the plasma and decreased urinary excretion of iodide, an adaptation toward iodine conservation.

T3, being three to four times more potent than T4 but containing only three fourths as much iodine as T4, is preferentially synthesized over T4. There is also increased peripheral conversion of T4 to T3 21

Clinical euthyroidism is thus maintained, but biochemically the pattern of low serum T4, elevated TSH, and normal or supranormal T3 is often found.22"24 In severe thyroid failure, such as that in endemic cretinism, serum T3 and T4 concentrations are low and serum TSH concentration is markedly elevated. In less severe thyroid endemism, serum T3 and T4 concentrations may remain normal. The serum TSH level may also be normal or moderately elevated, and there may be an exaggerated TSH response to thyrotropin-releasing hormone (TRH) simulation, implying an increase in the pituitary reserve of TSH and subclinical hypothyroidism.

Such changes are thought to be mediated through an elevation in the serum TSH level. However, a wide variation in the level of TSH has been observed in normal and goitrous individuals in endemic areas.25 Such dissociation between goiter size and biochemical findings suggests the possible role of circulating thyroid growth factors, such as epidermal growth factors, or an autoimmune process in the pathogenesis of goiter.26 Activity of thyroid growth-promoting immunoglobulin (TGI) has been demonstrated in patients with sporadic and endemic goiter.27 However, conflicting results were obtained, and the methods of detection of such activity have been criticized, with this uncertainty leaving an unsettled role of TGI in goitrogenesis.28 30

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