PEDIATRICS Vol. 29 No. 5 May 1962, pp. 692-702
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CLINICAL AND LABORATORY ASPECTS OF THYROID FUNCTION

E. Mead Johnson Award Address, October, 1961

Donald E. Pickering M.D.1

1 Department of Pediatrics, University of Oregon Medical School

It is an honor to have been selected as a recipient of the E. Mead Johnson Award for Research in Pediatrics; more specifically, for research in thyroid gland function. At mid-century it seemed reasonable to explore quantitatively the role of thyroid in the developing primate and thus, hopefully, to provide a more secure base whereby therapeutic criteria could be ascertained.

The gross effects of thyroid ablation and their general elimination following administration of crude thyroid gland were known before the turn of the century, and thyroxine was identified as the primary thyroid gland hormone and was chemically characterized and synthesized during the first two decades of this century.

At the turn of the century the late Sir William Osler,1 in a classic presentation reviewing sporadic cretinism on this continent, in all optimism made the following statement.

Not the magic wand of Prospero or the brave kiss of the daughter of Hippocrates ever effected such a change as that which we are now enabled to make in these unfortunate victims, doomed heretofore to live in hopeless imbecility, an unspeakable affliction to their parents and to their relatives.

Unfortunately, the optimism expressed in this statement has not come to fruition. Mental retardation remains the most significant sequella of thyroid deficiency in the pediatric age group and is of high incidence in sporadic cretinism, without regard to clinical classification; i.e., whether the dysfunction represents athyrosis or an inborn error of hormonogenesis or is of some other origin.2,3

It has been the opinion of our group, both clinically and experimentally, that most cases of thyroid deficiency are treated too late and with far too little hormone.