Classification of Thyroid Diseases: Suggestions for a Revision

Extract

The last comprehensive classification of thyroid diseases has been reported by the American Thyroid Association in 1969. It was based largely on thyroid function; classification by etiology was considered premature, by pathology nonuseful to the clinician (1), and the clinical evolution and follow-up have not yet been evaluated. Goiter, without specifying the dimension of the enlargement, was a focal point of the classification, divided into nontoxic and toxic forms (2). With the adoption of American Thyroid Association classification, the American Thyroid Association voted that the classification “…. be reviewed periodically and revised as further knowledge might require” (1).

During the last 30 yr books on thyroid (3, 4) and endocrine diseases have not revised the classification or nomenclature of thyroid diseases (5–7). No revision has been made despite our greater understanding of the molecular mechanisms underlying hormonogenesis. We now distinguish thyroid dysfunction at the target tissue level and can identify receptor and postreceptor pathophysiology as syndromes of resistance to thyroid hormones (8, 9). We now recognize genetic defects of thyroid hormonogenesis (3, 4), postpartum thyroiditis (10), the evolution of diffuse to nodular goiter (11–14), and the complex effects of iodine on the function of endemic goiter (15). However, recent technology has allowed many countries to screen for congenital hypothyroidism, so that the clinical consequences of this syndrome should disappear as a clinical entity throughout the world in the next 10–20 yr (15, 16). We now better recognize the clinical evolution of thyroid diseases that frequently change their functional behavior with time from that observed at the onset of disease, i.e. from hyper- to hypofunction (17–20). The clinical evolution of thyroid function is of fundamental clinical importance, because it implies continuous follow-up with consequent updating of therapy. Today the presence of goiter cannot be considered a basis for classification, but only a parameter. We often see diseases before goiter onset, and environmental factors can affect thyroid function without a modification of thyroid morphology. In fact, many thyroid diseases occur without the presence of goiter, i.e. thyrotoxicosis factitia, postpartum thyroiditis, and even Graves’ disease.