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Elevation in Serum Thyroglobulin during Prolonged Antarctic Residence: Effect of Thyroxine Supplement in the Polar 3,5,3'-Triiodothyronine Syndrome

Internal Medicine Service, Madigan Army Medical Center (N.V.D., H.L.R.), Tacoma, Washington 98431; New Mexico Resonance (L.M.), Albuquerque, New Mexico 89111; Veterans Affairs Puget Sound Health Care System, Tacoma, Washington 98493, and Division of Metabolism, Endocrinology, and Nutrition, University of Washington (G.R.M.), Seattle, Washington 98195; Endocrine Service, William Beaumont Army Medical Center (H.L.), El Paso, Texas 79920; Department of Exercise Science and Physical Education, McDaniel College (H.S.C.), Westminster, Maryland 21157; Department of Family and Preventive Medicine, University of California (L.A.P.), San Diego, California 92093; U.S. Food and Drug Administration (K.R.), Rockville, Maryland 20857; and Multicare Medical Group (H.L.R.), Tacoma, Washington 98415

Address all correspondence and requests for reprints to: Dr. Nhan Van Do, Stanford Medical Informatics, Medical School Office Building, x-215, 251 Campus Drive, Stanford, California 94305-5479. E-mail: nhan.do{at}us.army.mil.

Extended Antarctic residence (AR) is associated with an increase in serum TSH, a decrease in free T₄, and an increase in T₃ production and clearance. It is not clear whether these adaptations reflect changes in clearance alone or whether intrinsic thyroidal synthetic activity also changes. Thyroglobulin (Tg) secretion is an independent marker of intrinsic thyroid activity whose kinetics are independent of those of T₃ and T₄. In this study we examined changes in Tg levels in healthy subjects before and during AR and their responses to thyroid supplementation to help determine whether alterations in thyroid activity, and not just kinetics of clearance, underlie the changes seen with the polar T₃ syndrome. In cohort 1, we compared measurements of TSH and Tg in 12 subjects before deployment and monthly for 11 months during AR. In cohort 2, we compared the same measurements in 12 subjects monthly for 11 months of AR. Subjects were randomized to receive either placebo or levothyroxine in cohort 1 for 7 months and in cohort 2 for 11 months. Tg increased over baseline during the first 4 months of AR by 17.0 ± 4.6% and after 7 more months by 31.7 ± 4.3% over baseline in the placebo group of both cohorts (P < 0.0002). When L-T₄ was taken, Tg returned to a value not different from baseline (4.5 ± 3.9%). The percent changes from baseline in serum TSH and Tg during AR were highly correlated (P < 0.00003) in the placebo group for both cohorts. The rise in Tg with TSH and the reduction in Tg with L-T₄ provide evidence of target tissue response to TSH and further confirm the TSH rise as physiologically significant. The results also suggest that the adaptive changes in thyroid hormone economy with AR reflect TSH-dependent changes in thyroid synthetic activity, which may help explain a portion of the increases in T₃ production found with AR.

This work was supported in part by National Science Foundation Grant OPP-9418466.

The opinions expressed herein are those of the authors and are not to be construed as reflecting the views of the Department of the Army, the Department of Defense, the National Science Foundation, or the U.S. Food and Drug Administration.

Results from this work were presented in part at the 83rd Annual Meeting of The Endocrine Society, Denver, CO, June 20–23, 2001.

Abbreviations: AR, Antarctic residence; FT₃, free T₃; FT₄, free T₄; PG, placebo group; T₄G, T₄-treated group; Tg, thyroglobulin.

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