Salicylates and Thyroid Function
نویسنده
چکیده
In the preceding paper (1) it was pointed out that the administration of sodium salicylate to man induces a number of changes suggestive of thyrotoxicosis. There is an elevated basal metabolic rate (BMR), negative nitrogen balance, a fall in the cholesterol level of the hypothyroid subject, and an accelerated fractional disappearance rate of labeled thyroxine from the circulation. Paradoxically, salicylate-induced hypermetabolism is not accompanied by certain of the clinical characteristics of hyperthyroidism and is associated with depressed thyroid function as measured by thyroidal radioiodine uptake and clearance, or the serum protein bound iodine (PBI) concentration. The salicylate level in the serum of such patients is not high enough to interfere with in vitro iodine metabolism in rat thyroid slices, and in acute experiments in rats no depression of the iodide concentrating mechanism can be demonstrated at blood salicylate levels comparable to those attained in the above patients (1). Similar findings had previously been recorded in rats and in man treated with 2,4-dinitrophenol (2-4). It was subsequently shown (5) that this thyroid depression produced by 2,4-dinitrophenol probably resulted from inhibition at a pituitary or higher level. The absence of a direct or immediate effect of salicylates on thyroid tissue, despite marked thyroid depression upon more prolonged exposure to the drug, suggested that this effect may also result from a decrease in thyroid stimulation by thyrotropin (TSH). It is the purpose of this report to suggest a locus of salicylate action and to present some observations on the nature of the inhibitory effect.
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تاریخ انتشار 2013