Adrenocortical reserves in hyperthyroidism
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ORIGINAL ARTICLE
Adrenocortical reserves in hyperthyroidism Kemal Agbaht • Sevim Gullu
Received: 6 January 2013 / Accepted: 18 March 2013 Ó Springer Science+Business Media New York 2013
Abstract Explicit data regarding the changes in adrenocortical reserves during hyperthyroidism do not exist. We aimed to document the capability (response) of adrenal gland to secrete cortisol and DHEA-S during hyperthyroidism compared to euthyroidism, and to describe factors associated with these responses. A standard-dose (0.25 mg/i.v.) ACTH stimulation test was performed to the same patients before hyperthyroidism treatment, and after attainment of euthyroidism. Baseline cortisol (Cor0), DHEA-S (DHEA-S0), cortisol binding globulin (CBG), ACTH, calculated free cortisol (by Coolen’s equation = CFC), free cortisol index (FCI), 60-min cortisol (Cor60), and DHEA-S (DHEA-S60), delta cortisol (DCor), delta DHEA-S (DDHEA-S) responses were evaluated. Forty-one patients [22 females, 49.5 ± 15.2 years old, 32 Graves disease, nine toxic nodular goiter] had similar Cor0, DHEA-S0, CFC, FCI, and DHEA-S60 in hyperthyroid and euthyroid states. Cor60, DCor, and DDHEA-S were lower in hyperthyroidism. In four (10 %) patients the peak ACTH-stimulated cortisol values were lower than 18 lg/ dL. When the test repeated after attainment of euthyroidism, all of the patients had normal cortisol response. Regression analysis demonstrated an independent association of Cor60 with free T3 in hyperthyroidism. However, the predictors of CFC, FCI, and DHEA-S levels were serum creatinine levels in hyperthyroidism, and both creatinine and transaminase levels in euthyroidism. ACTHstimulated peak cortisol, delta cortisol, and delta DHEA-S levels are decreased during hyperthyroidism, probably due
K. Agbaht (&) S. Gullu Department of Endocrinology and Metabolic Diseases, Faculty of Medicine, Ibn-i Sina Hospital, Ankara University, Sihhiye, Ankara, Turkey e-mail: [email protected]; [email protected]
to increased turnover. Since about 10 % of the subjects with hyperthyroidism are at risk for adrenal insufficiency, clinicians dealing with Graves’ disease should be alert to the possibility of adrenal insufficiency during hyperthyroid stage. Keywords Hyperthyroidism Adrenocortical insufficiency ACTH stimulation test Delta cortisol response Delta DHEA-S response
Introduction Adrenal insufficiency may complicate thyrotoxicosis that can be life-threatening in individual cases [1]. These observations had been paid some attentions in the past. Indeed, though the clinical studies investigating adrenocortical reserves in hyperthyroidism go back to 1950s [2], the literature still lacks conclusive data regarding the changes in metabolism of adrenal cortex-derived steroids in hyperthyroidism. In the clinical literature, one of the earliest reports in the field was by Felber et al. [2] in 1959, in which the authors evaluated the response of urinary 17-hydroxycorticosteroids and 17-ketosteroids to the 48-h intravenous ACTH test, in 12 hyperthyroid patients. They p
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