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Salsalate Administration—A Potential Pharmacological Model of the Sick Euthyroid Syndrome

Departments of Biochemistry (R.W.) and Medicine (J.C.N.), School of Medicine, Loma Linda University, Loma Linda, California 92354; and Quest Diagnostics Nichols Institute (R.B.W.), San Juan Capistrano, California 92690

Address all correspondence and requests for reprints to: R. Bruce Wilcox, Ph.D., Department of Biochemistry, Mortensen Hall, Room 209, Loma Linda University, Loma Linda, California 92354.

This study examined salsalate ingestion as a model of the sequelae of acute inhibition of thyroid hormone binding to serum protein. One dose of salsalate (60–65 mg/kg) was administered to healthy volunteers. Serum salsalate concentrations peaked at 2 h (82 µg/mL), then declined at 8 h to 1.2 µg/mL. Serum total T₄ (TT₄) and total T₃ (TT₃) concentrations declined for 4 h, then recovered by 96 h, while T₄ binding protein concentrations remained unchanged. TT₃ was reduced to a greater extent than TT₄ between 2 h and 72 h, and serum total reverse(r)T₃ (TrT₃) was transiently increased at 8 h. TSH concentrations fell while TT₄ and TT₃ fell, then recovered while TT₄, TT₃, and free T₃, but not free T₄, were still reduced. Subsequently, TSH overshot basal levels and continued to rise after 96 h while TT₄, TT₃, free T₄, free T₃, and TrT₃ were all at basal levels. We postulate that an acute release of T₄ and T₃ from circulating transport proteins, induced by an inhibitor of binding, can result in large and rapid redistribution of T₄ and T₃ into tissue compartments associated with transiently reduced peripheral tissue 5'-monodeiodination and deranged TSH regulation.

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