Classification of thyroid diseases: suggestions for a revision.

Abstract

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 hyperto 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. In the 1980s, the importance of environmental contributions and the reversibility of some thyroid diseases were recognized (21). In the 1990s the importance of the transient and bipolar clinical evolution of several thyroid diseases was stressed, and the need to update the nomenclature of thyroid diseases was acknowledged (22). Some recent books on internal medicine have begun to report some of the newly identified thyroid diseases as special topics, taking into account molecular mechanisms of thyroid diseases and the evolution of autoimmune thyroid diseases (23, 24). The new classification of thyroid diseases presented herein is a proposal to stimulate discussion of previous classification to codify these diseases in a clinically useful manner. New terms are often forged to eliminate the criticism of those already existing; in turn, they become similarly criticized. The writer is perfectly aware that his proposal is based on his own experience, and he hopes that it will be subject to the positive criticism needed to generate an updated classification.