The previous report from this clinic showed goiter areas on the seashore of Hokkaido, the northern island of Japan, where most inhabitants are taking a large quantity of iodine-rich seaweeds. In these goitrous patients, urinary excretion of iodine was high, and withdrawal of seaweed from their usual diet induced decrease in size of goiter (Higuchi 1964). It seems contradictory because the principle cause of endemic goiter is considered to be a lack of iodine. The present paper deals with various parameters of thyroid function in this peculiar endemic seashore goiter.
1. Basal metabolic rate, plasma protein-bound iodine and serum total cholesterol were within normal ranges.
2. Thyroidal I
131 uptake was determined in the goitrous patients under different dietary conditions. In thirty-five patients taking their usual diet, mean I
131 uptake rates were 9.6% at 3 hours and 11.7% at 24 hours. While, after restriction of seaweeds from their usual diet, the uptake was high, with a mean of 21.2% at 3 hours and 41.5% at 24 hours in fiftyseven patients. There was a significant difference between the two dietary groups (P>0.001).
3. Metabolism of radioactive and stable iodine was studied both during ingestion and after withdrawal of seaweed. After intravenous administration of tracer I
131, serial registrations of radioactivity were made in the plasma and urine as well as over the thyroid gland. When the patients were taking their usual diet containing about 10 to 20 grams of dried seaweed, radioactivity over the thyroid initially increased with time to a peak within a few hours, and subsquently decreased exponentially at same rate as plasma radioiodine. Plasma inorganic iodine (PII) was high, ranging 13.7 to 44.5 ug/ 100 ml, and marked increment of thyroidal iodine space (Ts), and thyroidal iodine content (TI = (PII× Ts) was shown in five of seven patients. After withdrawal of seaweed, thyroidal radioiodine increased gradually, until a peak was reached 24 hours or later after injection of I
131. PII was below 2 μg/100ml. However, stable iodine uptake by the thyroid (SIU=PII×k) was high in four out of six patients, depending on the increase in thyroidal I
131 clearance rate.
4. After a single injection of TSH (125 Ms units), “low thyroid reserve” of I
131 uptake or of plasma PBI was noted in two out of five patients. In three patients response was normal or Subnormal.
5. The Inhibitory effect of carrier iodide on thyroidal I
131 uptake was studied by the method, as described by Feinberg et al. (1959). In nine patients with seashore goiter, the magnitude of inhibition by 2 mg of carrier iodide (as I
127) was variable, and did not differ from those in euthyroid and thyrotoxic patients.
In regard of iodine metabolism, it is confirmed that, in the endemic seashore goiter, the thyroid can accumulate an extraordinarily large amount of stable iodine in spite of markedly increased PII. It is stressed that the seashore goiter in Hokkaido is similar to the goiter induced by iodide ingestion in several points. These facts appear to support the view that the most important pathogenetic factor of the seashore goiter is excessive and longstanding intake of iodide from seaweeds in their diet.
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