We have critically reviewed the available information on iodine-induced hyperthyroidism (IIH) from published sources and other reports as well as the experience of the authors in Tasmania, Zaire, Zimbabwe, and Brazil. Administration of iodine in almost any chemical form may induce an episode of thyrotoxicosis (IIH). This has been observed in epidemic incidence in several countries when iodine has been given as prophylaxis in a variety of vehicles, but the attack rate as recorded has been low. IIH is most commonly encountered in older persons with long standing nodular goiter and in regions of chronic iodine deficiency, but instances in the young have been recorded. It customarily occurs after an incremental rise in mean iodine intake in the course of programs for the prevention of iodine deficiency, or when iodine-containing drugs such as radiocontrast media or amiodarone are administered. The biological basis for IIH appears most often to be mutational events in thyroid cells that lead to autonomy of function. When the mass of cells with such an event becomes sufficient and iodine supply is increased, the subject may become thyrotoxic. These changes may occur in localized foci within the gland or in the process of nodule formation. IIH may also occur with an increase in iodine intake in those whose hyperthyroidism (Graves' disease) is not expressed because of iodine deficiency. The risks of IIH are principally to the elderly who may have heart disease, and to those who live in regions where there is limited access to medical care. More information is needed on the long-term health impact of IIH or "subclinical" IIH, especially in the course of prophylaxis programs with iodized salt or iodinated oil in regions where access to health care is limited.

Abnormal thyroid function profoundly alters calcium metabolism. In 1929, Aub, Bauer, Heath, and Ropes (1) demonstrated in patients on constant low calcium diets that urinary and fecal excretion of calcium and phosphorus is frequently increased in hyperthyroidism and lower than normal in myxedema. These changes could not be ascribed to elevation of metabolism per se (1) acidosis (2) or vitarmin D deficiency (3); they were observed even in the absence of the parathyroid glands (4, 5). In addition, roentgenographic evidence of skeletal demineralization has been described in patients with thyrotoxicosis (6).The conventional balance techniques which have been used in the study of calcium metabolism in thyroid disease measure only net effects: they do not measure the processes of deposition and resorption of calcium. An indication of the skeletal turnover of calcium, however, can be obtained from serial observations of the specific activity of radioactive calcium (Ca45) in blood and urine after intravenous injection (7,8).The present study was designed to define the alterations in calcium metabolism in thyroid disease in man by using Ca45 and the technique of isotope dilution. Observations have been made in euthyroid, hyperthyroid, and myxedematous subjects, and, for purposes of comparison, in additional euthyroid patients with Paget's disease and with hypoparathyroidism. MATERIALS AND METHODSAll patients (Table I) were on the metabolic ward and were ambulatory throughout the study. Diets, which were constant and of neutral ash, contained from 0.08 to 0.23 grams of calcium per day (Table II). In order to avoid tetany, the two hypoparathyroid subjects were given 0.31 and 0.57 grams, respecfively, of calcium in their diets per day. Fluid intake was maintained at 2,000 to 2,500 ml. per day. Complete collections of urine and stool were begun after six days on the fixed diet. A three-day control collection of urine and feces was obtained prior to the administration of Ca.The stock solution of Ca"Cl, 2 was acidified with concentrated HCI, added to 0.9 per cent NaCI solution to give a final concentration of approximately 0.5 j&c per ml.saline at a pH of 6, and autoclaved. Five to seven microcuries were injected from a calibrated syringe into an antecubital vein one hour before breakfast. Blood samples were obtained by venipuncture from the opposite arm at frequent intervals. Fractional urine collections were made for the first three days following injection, and daily thereafter. Stool collections were made TABLE I

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SUMMARY Neurological examinations were made of 67 children and adults with congenital iodine‐deficiency disorder (endemic cretinism) in four rural villages in highland Ecuador. There was a distinct and readily identifiable pattern of neurological deficits. These included, to varying degrees: deaf‐mutism or lesser degrees of bilateral hearing‐loss or dysarthria; spasticity, particularly involving the proximal lower extremities; mental deficiency of a characteristic type; and rigidity and bradykinesia. Not all of these elements were found in all cases. Less common features were strabismus, kyphoscoliosis and frontal‐lobe signs. There were exceptional cases with hypotonia. In contrast, cerebellar function was largely spared, as were functions of emotion and attention, vegetative and autonomic functions, social interaction, and probably memory, except in the most severely involved. RÉSUMÉ Neurologie des affections congénitales de déficit en iode (crélinisme endémique) Des examens neurologiques ont été faits chez 67 enfants et adultes présentant une affection congénitale de déficit en iode (crétinisme endémique) dans quatre villages ruraux des hautes terres d'Equateur. II a été observé un regroupement particulier et rapidement identifiable des déficits neurologiques. Ceci incluait à des degrés divers: une surdimutité ou de moindre degré de perte auditive bilatérale ou dysarthrie; une spasticité atteignant tout spécialement la région proximale des membres inférieurs, un déficit mental d'un type caractéristique et une rigidité et bradykinésie. Tous ces éléments n'étaient pas présents dans tous les cas. Des signes moins habituels ont été le strabisme, la cyphoscoliose et les signes frontaux. Des cas exceptionnels d'hypotonie ont été observés. En revanche, la fonction cérébelleuse était largement épargnée comme l'étaient les fonctions d'émotion et d'attention, les fonctions du système végétatif et autonome, l'interaction sociale et probablement la mémoire, excepté dans les cas les plus graves. ZUSAMMENFASSUNG Die Neurologie der congenitalen Jodmangelkrankheit (endemischer Krelinismus) 67 Kinder und Erwachsene mit der congenitalen Jodmangelkrankheit (endemischer Kretinismus) aus vier ländlichen Gemeinden im Hochland von Ecuador wurden neurologisch untersucht. Es wurde ein bestimmtes und leicht erkennbares Muster neurologischer Ausfälle gefunden. Diese bestanden in unterschiedlicher Ausprägung in: Taubstummheit oder in abgeschwächter Form in bilateralem Hörverlust oder Dysarthrie; Spastik, wobei insbesondere der proximale Bereich der unteren Extremitäten betroffen war; eine charakteristische Art des Schwachsinns; Rigidität und Bradykinäsie. Nicht in jedem Fall wurden all diese Elemente gefunden. Die weniger häufigen Merkmale waren Strabismus, Kyphoskoliose und Frontalhirnzeichen. Es gab Ausnahmefälle mit Hypotonic Dagegen waren die cerebellären Funktionen, Gefühl und Aufmerksamkeit, vegetative und autonome Funktionen, soziale Interaktion und wahrscheinlich Gedächtnis normal mit Ausnahme der sehr schwer betroffenen Fälle. RE...

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Skeletal and systemic disease may be reflected in profound alterations of the metabolism of the bone salts. In human skeletal disease attention has focused, for the most part, on the altered metabolism of calcium. Several studies indicate that strontium may have a metabolic pathway similar to that of calcium and that radiostrontium, because of its ease of measurement, might be a convenient indicator for observing the transfer of calcium through the calcium-containing compartments of the body.The investigations to be reported here are concerned with the comparative distribution and fate of calcium and strontium in subjects with altered bone metabolism. Patients with thyroid and parathyroid disease, osteoporosis, and Paget's disease were studied after simultaneous intravenous administration of strontium85 and calcium45. The results indicate that Sr85 closely parallels Ca45 as an index of skeletal function. MATERIALS AND METHODSAll patients (Table I) were on the Metabolic Research Ward, were ambulatory throughout the study, and spent a few hours out of doors each day with a nurse in attendance. Each received a constant neutral ash diet containing 88 to 206 mg of calcium per day (Table II). The calculated daily magnesium intake did not exceed 200 mg. Fluid intake was kept between 2,000 and 2,500 ml per day. After a minimum of 7 days on the fixed diet, a 3-day control collection of urine and feces was obtained before administration of the labeled isotopes.The dose of labeled calcium and strontium was prepared from hydrochloric acid stock solutions of Ca"C121 of high specific activity, and from carrier-free Sr5'Cl,.

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