The use of radioactive iodine in studying the pathologic physiology of thyroid disease.

It was in May, 1938 that Hertz et al. (1) published the first report on biological studies with a radioactive isotope of iodine. By today's standards these first studies were done under the least favorable conditions with an isotope whose half life of 25 minutes limited the studies that could be done. Notwithstanding the limitations put on these investigators they not only reaffirmed certain principles of thyroid physiology, but with other investigators, Hamilton (2), Hamilton and Soley (3), and LeBlond and Sue (4), who began working with radioactive isotopes of iodine in other laboratories at about the same time, they pioneered in a new field of investigating the thyroid. Today we have a small army of investigators bringing together a variety of disciplines, i.e., physics, chemistry, embryology, physiology, histochemistry, pathology and clinical medicine in studying with radioactive iodine and other tools normal and morbid physiology of the thyroid. Many of these investigators are students whose primary interests are related to studies of normal and abnormal function of the thyroid. These students are delighted to have made available so many new technics with which to increase our knowledge of thyroid physiology. Many of the investigators in this field are interested primarily in isotopic methods and their application to studies in biology. They probably have been attracted to this field because of the unique avidity of the thyroid for iodine which makes this an ideal tissue for applying isotopic methods, and for studying the biologic effects of irradiation with such isotopes. At the present time, it seems quite proper to ask questions such as those posed by Dr. William T. Salter preceding the 1948 Symposium on Radio Iodine at the Brookhaven National Laboratory. "1. How has radio iodine improved our knowledge of iodine metabolism and of the physiology and the therapy of the thyroid? 2. How do the results harmonize with past experience?" The purpose of this paper is to review the contributions made to our knowledge of human thyroid disease by studies with radioactive iodine. The earliest studies done at the clinical level by Hamilton and Soley (3) reaffirmed our previous concepts that the human thyroid has an avidity for iodine. These investigators compared the collection by the thyroid of iodine labelled with radio iodine and its excretion in the urine and feces in normal subjects and in patients having various thyroid disorders. They found that an orally administered dose of labelled iodine was absorbed rapidly and could be detected in the thyroid within 20 minutes. In normal subjects 74 to 89 per cent of the dose was excreted during a five-day period with the major portion appearing during the first 24 hours. Two myxedematous patients excreted 91 and 94 per cent in the urine during five days but at a much slower rate than did the normals. Thyrotoxic patients previously treated with iodine excreted about the same amount of iodine as did normal individuals. Fecal excretion of these labelled doses of iodine averaged only about 1 per cent of the dose. In another series of studies Hamilton and Soley (5) recorded the characteristic collection curves obtained by in sivo measurements for various thyroid states. The curve that they observed to be typical for normal thyroids was a smooth curve which leveled off to a flat plateau in two days. The initial collection by thyroids of hyperthyroid patients was greater and much more rapid than in normal thyroids but decreased almost as rapidly to a plateau lower than that of the normal thyroids. This phenomenon was also observed in two goiterous hypothyroid children (Hamilton, et al. [6]). This rapid decrease to a lower than normal plateau following an increased pickup observed in the goiterous children and hyperthyroid individuals might be attributed to the fact that these investigators were using 14 mgm. of inert iodide as carrier. This concept is supported by their failure to observe the rapid loss of radio iodine from the thyroid when a carrier dose of 0.1 pg. of sodium iodide was given.