EFFECT OF ORAL AND INTRAVENOUS COBALTOUS CHLORIDE ON THYROID FUNCTION

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Abstract
Following oral administration of cobaltous chloride (37.5 mg of cobalt per day) for more than ten days, there was marked depression of thyroidal I131 uptake at half an hour and at twenty-four hours, in 2 of 4 patients. In 1 of these subjects, half an hour after administration of I131, thyroidal radioactivity was discharged almost completely by 1.0 Gm. of NaSCN intravenously. In 1 of 2 subjects who received both oral and supplemental intravenous cobalt, early thyroidal uptake was depressed and the thyroidal radio-activity accumulated at sixteen minutes was discharged by NaSCN. In 3 of 6 subjects receiving intravenous cobalt immediately before, and in some cases immediately after intravenous I131, there was a depression of early thyroidal uptake and partial discharge of accumulated thyroidal I131 by NaSCN. These results demonstrate that the action of cobalt is to block organic binding of radioiodide by the thyroid. Results of distribution and excretion studies of Co60Cl2 with and without carrier, in human subjects suggest that under load conditions only about 10 per cent of the administered dose is absorbed. Variations in absorption and in blood and thyroidal cobalt levels may account for the conflicting reports concerning the effect of therapeutic dosages of cobalt on thyroid function in human subjects. Results of studies with Co60Cl2 in rats yielded no evidence for concentration of cobalt by the thyroid to an extent significantly greater than could be accounted for by the plasma content of the gland.