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Effects of Growth Hormone Therapy on Thyroid Function of Growth Hormone-Deficient Adults with and without Concomitant Thyroxine-Substituted Central Hypothyroidism

Effects of Growth Hormone Therapy on Thyroid Function of Growth Hormone-Deficient Adults with and... Administration of human GH to GH-deficient patients has yielded conflicting results concerning its impact on thyroid function, ranging from increased resting metabolic rate to induction of hypothyroidism. However, most studies have been casuistic or uncontrolled and have used pituitary-derived GH of varying purity, often contaminated with TSH. Therefore, we conducted a double blind, placebo-controlled cross-over study of the effect of 4 months of biosynthetic human GH therapy (Norditropin; 2 IU/m2 · day) on thyroid function in GH-deficient adults (8 females and 14 males; mean + SE age, 23.8 + 1.2 yr). One group (I) was euthyroid without T4 substitution (n = 13), whereas the other (group II) received T4 (n = 9). Serum T4 (nanomoles per L) decreased in both groups after GH treatment [group I, 100 + 8 (mean [ SE) vs. 89 + 8 (P < 0.01); group II, 145 + 18 vs. 115 + 10 (P < 0.05)]. Conversely, GH treatment caused an increase in serum T3 (nanomoles per L) in both groups[group I, 1.9 + 0.1 vs. 2.0 + 0.1 (P < 0.1); group II, 1.7 + 0.1 vs. 1.9 + 0.1 (P < 0.05)]. Similar changes were seen in serum free T4 and T3. The serum T3 level during the placebo period of group I was significantly lower than that in an age-matched reference group (P < 0.02). Serum rT3 (nanomoles per L) was low in group I and decreased significantly, as in group II, after GH treatment[group I, 0.26 + 0.02 (placebo) vs. 0.20 + 0.02 (GH; P < 0.01); group II, 0.38 + 0.05 (placebo) vs. 0.29 + 0.02 (GH; P < 0.01)]. Serum TSH decreased in both groups during GH therapy, though not significantly. Serum thyroglobulin was unaltered and did not differ from that in the reference group. In conclusion, our data are consistent with a GH-induced enhancement of peripheral deiodination of T4 to T3. GH thus seems to play an important role, either directly or indirectly, in the regulation of peripheral T4 metabolism. (J Clin Endocrinol Metab69: 1127, 1989) This content is only available as a PDF. Author notes * This work was supported in part by Aarhus University Research Foundation, the National Danish Health Foundation (H 11/84-87 and H 11/26-88), and the Danish Medical Research Council (12-7452). Copyright © 1989 by The Endocrine Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Clinical Endocrinology and Metabolism Oxford University Press

Effects of Growth Hormone Therapy on Thyroid Function of Growth Hormone-Deficient Adults with and without Concomitant Thyroxine-Substituted Central Hypothyroidism

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References (38)

Publisher
Oxford University Press
Copyright
Copyright © 1989 by The Endocrine Society
ISSN
0021-972X
eISSN
1945-7197
DOI
10.1210/jcem-69-6-1127
Publisher site
See Article on Publisher Site

Abstract

Administration of human GH to GH-deficient patients has yielded conflicting results concerning its impact on thyroid function, ranging from increased resting metabolic rate to induction of hypothyroidism. However, most studies have been casuistic or uncontrolled and have used pituitary-derived GH of varying purity, often contaminated with TSH. Therefore, we conducted a double blind, placebo-controlled cross-over study of the effect of 4 months of biosynthetic human GH therapy (Norditropin; 2 IU/m2 · day) on thyroid function in GH-deficient adults (8 females and 14 males; mean + SE age, 23.8 + 1.2 yr). One group (I) was euthyroid without T4 substitution (n = 13), whereas the other (group II) received T4 (n = 9). Serum T4 (nanomoles per L) decreased in both groups after GH treatment [group I, 100 + 8 (mean [ SE) vs. 89 + 8 (P < 0.01); group II, 145 + 18 vs. 115 + 10 (P < 0.05)]. Conversely, GH treatment caused an increase in serum T3 (nanomoles per L) in both groups[group I, 1.9 + 0.1 vs. 2.0 + 0.1 (P < 0.1); group II, 1.7 + 0.1 vs. 1.9 + 0.1 (P < 0.05)]. Similar changes were seen in serum free T4 and T3. The serum T3 level during the placebo period of group I was significantly lower than that in an age-matched reference group (P < 0.02). Serum rT3 (nanomoles per L) was low in group I and decreased significantly, as in group II, after GH treatment[group I, 0.26 + 0.02 (placebo) vs. 0.20 + 0.02 (GH; P < 0.01); group II, 0.38 + 0.05 (placebo) vs. 0.29 + 0.02 (GH; P < 0.01)]. Serum TSH decreased in both groups during GH therapy, though not significantly. Serum thyroglobulin was unaltered and did not differ from that in the reference group. In conclusion, our data are consistent with a GH-induced enhancement of peripheral deiodination of T4 to T3. GH thus seems to play an important role, either directly or indirectly, in the regulation of peripheral T4 metabolism. (J Clin Endocrinol Metab69: 1127, 1989) This content is only available as a PDF. Author notes * This work was supported in part by Aarhus University Research Foundation, the National Danish Health Foundation (H 11/84-87 and H 11/26-88), and the Danish Medical Research Council (12-7452). Copyright © 1989 by The Endocrine Society

Journal

Journal of Clinical Endocrinology and Metabolism – Oxford University Press

Published: Dec 1, 1989

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