SERUM PROTEIN-BOUND IODINE LEVELS FOLLOWING ADMINISTRATION OF THYROXINE IN VARIOUS DISEASES*†

Abstract

IT IS known that serum protein-bound iodine (PBI) levels may be altered in circumstances other than hyper- or hypothyroidism (1). For example there are the increases associated with pregnancy (2–5) and muscular dystrophy (6, 7) and the decreases which may be noted in cirrhosis (8) or in subjects receiving cortisone or ACTH (9–14). It has also been reported that in patients with leukemia or lymphomata there may be an increase in the PBI level and the basal metabolic rate may be above the normal range (15–18). In none of the instances listed have the mechanisms involved in the particular PBI change been satisfactorily identified. It is nonetheless obvious that in these clinical and experimental situations new steady states have been established involving possible alterations in the production or release of thyroxine by the thyroid gland, the binding of thyroxine by serum proteins, the distribution of thyroxine in body fluids, or the subsequent removal of thyroxine from the proteins or from the circulation, alone or in combination. The sodium salt of l-thyroxine¹ has therefore been given by mouth in such conditions, in an attempt to establish the participation of these components, if any, in the serum protein-bound iodine changes.