A survey of goitre was made in the goitrous regions on the coast of Hokkaido, the northern island of Japan. Prevalence of goitre was confirmed in Hidaka coast and Rishiri Island. All goitrous patients were clinically euthyroid. The usual diet of the inhabitants of these districts consisted of a large quantity of iodine-rich seaweeds. Urinary excretion of iodine in five patients exceeded 20 mg per day. Studies of 131I and 127I metabolism were performed both during ingestion and after restriction of seaweed. When the patients were taking their usual diet, the mean thyroidal 131I uptake in 57 patients was 9.6% at 3 hours and 11.7% at 24 hours. In five of seven patients plasma inorganic iodine and thyroidal iodine space were markedly increased. Significant discharge of thyroidal 131I followed administration of thiocyanate. After withdrawal of seaweed from their usual diet, the plasma inorganic iodine was below 2 μg/100 ml but the thyroidal stable iodine uptake was higher than normal, depending on increase in thyroidal 131I clearance rate. No discharge was shown by thiocyanate block. Plasma PBI and thyronine-iodine level and serum T3 resin uptake were within the normal range. Radiochromatography of the thyroid tissue of the goitrous patients showed an increase in MIT/DIT ratio and a decrease in T3 + T4 proportion. No evidence for peripheral defect in DIT-131I deiodination was obtained. In a few patients restriction of seaweed induced a marked decrease in the size of goitre. The major cause of the endemic coast goitre seems to be excessive and longstanding intake of iodine from seaweed, and the similarities of iodine metabolism between the endemic coast goitre and iodide goitre arc discussed.

The effects of repeated doses of oral cholecystographic agents on serum thyroxine (T4), 3,3′,5-triiodothyronine (T3), 3,3′,5′-triiodothyronine (rT3) and thyrotrophin (TSH) concentrations were studied in 37 euthyroid male subjects. Iobenzamic acid, tyropanoic acid, iopanoic acid, and ipodate sodium, in a dosage of 3 g for 3 days, respectively, induced a significant decrease in serum T3 and an increase in rT3 within 24 h after the initial dose, followed by an increase in TSH and a slight increase in T4. The extent of the changes in rT3 varied between the agents, ipodate causing the greatest change, but without any relation to the changes in T3 or T4. Responses of serum T4, T3, rT3 and TSH concentrations to exogenous thyrotrophin-releasing hormone (TRH) and bovine TSH were also studied before and after 3-day doses of iopanoic acid. In 11 subjects given iopanoic acid, the response of TSH to TRH (500 μg, iv) was increased but the T3 response was unchanged. A dose of TSH (10 U.S.P. units, im) caused a significant increase in serum T3 and a decrease in TSH concentrations in 5 subjects both before and after cholecystography. It is thus suggested that in euthyroid subjects given multiple doses of oral cholecystographic agents, (1) the primary and consistent events are the reciprocal changes of serum T3 and rT3. although the extent of the changes is not coordinately reciprocal; (2) the responsiveness of the pituitary thyrotrophs and thyroid to TRH is preserved; and (3) the high basal and TRH-induced TSH in the serum may be ascribed to the decrease in the serum T3 concentration.

We have previously shown that some oral cholecystographic agents induce marked increase in basal and TRH-stimulated TSH concentrations in normal subjects. To define the relationship between circulating iodothyronines and pituitary secretion after oral cholecystography, temporal changes in the responses of serum TSH and PRL to a fixed dose of TRH (500 micrograms iv) and in serum T4, T3, and rT3 concentrations were assessed before, immediately after, and then at weekly intervals after the three daily doses of iopanoic acid (Ip). Both basal and TRH-stimulated TSH concentrations were significantly increased at the end of the period of Ip administration when the serum T3 concentration was decreased, were still above the pretreatment level 1 week after the course of Ip when the serum T3 had returned to pre-Ip levels, and returned toward normal 2 weeks after the course of Ip. The changes in serum T3 concentration were accompanied by reciprocal changes in rT3 concentration. PRL secretion was not significantly changed. To evaluate further the relationship between the enhanced TSH secretion and the changes in serum iodothyronine concentrations, subjects were given oral doses of T3 (5 micrograms every 4 h) or T4 (50 micrograms every 8 h) during the administration of Ip. In the subjects given Ip plus T3, serum T3 concentrations were maintained at pre-Ip levels, and both basal and TRH-stimulated TSH concentrations were not different from the control. Administration of T4 did not completely prevent the Ip-induced increment of TSH secretion. It is suggested that in subjects given Ip, 1) the serum T3 level is, at least partly, a determining factor for TSH secretion; and 2) the set-point of TSH secretion is appropriately tuned to either reduction or elevation of serum T3 concentration by a mechanism that is different from that in fasting subjects.

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