Goitrous Hypothyroidism Induced by Amino-glutethimide, Anticonvulsant Drug

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Abstract
Thyroidal enlargement and hypothyroidism were observed in 3 children who had been treated for seizures with amino-glutethimide (Elipten). Evidence for a block in organification of iodine in these patients was deduced from their low PBI and BEI values, high thyroidal uptake of l31I and discharge of greater than 50% of thyroidal radioactivity following administration of thiocyanate. Extraction and chromatography of plasma and urine revealed noabnormal iodinated compounds. Four additional children receiving amino-glutethimide were clinically euthyroid and exhibited no abnormalities of PBI or radioiodine studies. The role of amino-glutethimide in the production of goitrous hypothyroidism was verified by discontinuing the drug in the affected children and observing disappearance of the goiter and restoration of normal thyroid function. The nature of the antithyroidal effect of aminoglutethimide was investigated in rats fed a diet containing amino-glutethimide. Thyromegaly, diminished production of thyroxine and diiodotyrosine and an accumulation of thyroidal inorganic iodide were observed. This block in organification of iodide is similar to the action of propylthiouracil and amino-benzene derivatives to which amino-glutethimide bears a structural resemblance. The reasons for the variable responses observed in children receiving amino-glutethimide are not known but it is clear that amino-glutethimide can cause hypothyroidism and goiter in some patients.