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Dissociation of the Early Decline in Serum T₃ Concentration and Serum IL-6 Rise and TNF in Nonthyroidal Illness Syndrome Induced by Abdominal Surgery

Departments of Medicine (M.Mi., A.G.V., M.Ma., V.K.) and Surgery (F.K.), Division of Endocrinology, University of Patras Medical School, University Hospital, Patras 26500, Greece

Address all correspondence and requests for reprints to: Dr. Apostolos G. Vagenakis, University Hospital, P. O. Box 1045, Patras 26500, Greece. E-mail: vag.inmd{at}med.upatras.gr

Abstract

The etiology of the prompt decline in serum T₃ in patients with nonthyroidal illness syndrome has not been adequately explained. It has been attributed to various parameters, including test artifacts, inhibitors of T₄ and T₃ binding to proteins, decreased 5'-deiodinase activity, and circulating cytokines. Currently, much attention is centered on the role of IL-6 and TNF in developing the nonthyroidal illness syndrome through an effect on the hypothalamus, pituitary, and possibly 5'-deiodinase activity.

We therefore studied the relation of the endogenous serum IL-6 and TNF rise early in the course of nonthyroidal illness syndrome to the early decline in serum T₃ in 19 apparently healthy individuals, aged 43 ± 16 yr, who underwent elective abdominal surgery for cholelithiasis or gastroplasty. Serum T₃, free T₃, T₄, free T₄, rT₃, TSH, IL-6, and TNF were measured before and at various time intervals up to 42 h after skin incision. We observed a prompt decline in serum T₃ 30 min before skin incision, which continued to decline throughout the observational period. The magnitude of the decline reached 20% from the baseline value at 2 h. The early decline of T₃ was attenuated and lasted from the 2–8 h, probably due to the sharp increase in serum TSH that started immediately after the entrance to the operating room and lasted for 2 h. In contrast, serum T₄ and free T₄ concentrations were increased soon after skin incision and remained elevated during the first postoperative day. Serum rT₃ increased approximately 6 h after the initiation of surgery and remained elevated thereafter. Serum IL-6 remained essentially undetectable for 2 h after skin incision, whereas serum T₃ was low. Two hours after skin incision, serum IL-6 increased sharply and remained elevated throughout the observational period. Serum TNF remained essentially undetectable throughout the postoperative period. Serum cortisol increased rapidly upon entrance to the operating room and remained elevated throughout the postoperative period.

We conclude that the decline in serum T₃ early in the course of nonthyroidal illness syndrome is not due to increased serum IL-6 or TNF levels. The brisk TSH secretion soon after the onset of the syndrome attenuates the decline in serum T₃ due to T₃ secretion from the thyroid. The early and brisk cortisol response to surgery may at least in part explain the early decrease in serum T₃ in nonthyroidal illness syndrome.

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