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Relationship between Thyrotropin and Thyroxine Changes during Recovery from Severe Hypothyroxinemia of Critical Illness^*

Ewen Downie Metabolic Unit, Monash University Department of Medicine, and Intensive Care Unit Alfred Hospital, Melbourne, Australia 3181

Address all correspondence and request for reprints to: Dr. D. J. Topliss, Ewen Downie Metabolic Unit, Alfred Hospital, Commercial Road, Melbourne, Australia 3181

In a prospective study of critically ill hypothyroxinemic patients, we assessed the relationship between serum TSH and T₄ during the return of serum T₄ normal during recovery. In this longitudinal study of 60 patients with a variety of critical illnesses, including burns, septicemia, and acute renal failure, serum T₄ fell to less than 2.7 µg/dl (35 nmol/liter) in 24 patients, of whom 14 survived with return of T₄ to normal. A rise in total T₄ of more than 1.9 µg/dl (25 nmol/liter) within 96 h occurred 13 times in 10 patients, while 4 patients had slower increases in T₄. All 13 episodes of rapid T₄ rise [1.7 ± 0.8 (± SD) to 5.6 ± 2.1 µg/dl] were associated with a marked increase in serum TSH (1.1 ± 0.8 to 7.0 ± 5.2 mU/liter), and TSH was transiently above normal during 8 episodes of T₄ recovery. In the 6 episodes with sampling less than 6 h apart, the TSH rise consistently preceded the T₄ rise. In the 4 patients who received dopamine, TSH and T₄ remained low until cessation of therapy. During the TSH rise, only minor changes, which could not account for the increase in total T₄, occurred in T₄-binding globulin (12.9 ± 3.3 to 14. 8 ± 3.3 mg/liter), prealbumin (208 ± 73 to 234 ± 82 mg/liter), and albumin (28.3 ± 2.9 to 31.9 ± 2.9 g/liter). Mean free T₄ increased (0.60 ± 0.34 to 1.45 ± 0.56 ng/dl), as did total T₃ (16 ± 14 to 76 ± 44 ng/dl), during the phase of TSH rise, suggesting that the increase in TSH was not simply a consequence of diminished negative feedback due to increased plasma binding. The very close and consistent temporal relationship between TSH and T₄ during the recovery phase suggests that TSH may have an essential role in the return of T₄ to normal during recovery from critical nonthyroidal illness

^* Presented in part at the 67th Annual Meeting of the Endocrine Society, Baltimore, MD, June 19–21, 1985. This work supported in part by grants from the National Health and Medical Research Council of Australia and the Alfred Hospital Medical Research Committee.

Received July 11, 1985.

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