Physiopathology of iodine deficiency

The process of goitrogenesis is likely to be the consequence of an increased TSH stimulation linked to an initial reduction of circulating thyroid hormone caused by iodine deficiency (ID). Other growth factors associated to TSH may have a role in the pathogenesis of goiter. Natural history of goiter is the evolution towards nodularity and functional autonomy. This phenomenon is due to the heterogeneity of thyroid follicular cells, some of which, with an intrinsic elevated growth rate, under the stimulation of ID progress to nodule formation and hyperfunction. In multinodular goiter TSH receptor mutations activating adenylate cyclase-cAMP pathway were found. In a recent epidemiological survey it was shown that nodular goiter increased with the age, being about 1% in schoolchildren and 23% in the adults (56-75 years). Also nodular autonomy and hyperthyroidism were more frequent in the 36-75 year age group. Severe ID is also cause of endemic cretinism. In Europe minor neuropsychological impairments and cognitive deficits were described in areas of moderate ID. The exposure to a mild ID during fetal life causes minor neuropsychological damage. In conclusion, ID is responsible of goiter and its evolution towards nodularity and functional autonomy. Severe ID is also cause of endemic cretinism, while cognitive deficits and minor neuropsychological impairments were found in mild to moderate ID.