title: Dehydroepiandrosterone sulphate is increased and dehydroepiandrosterone-response to corticotrophin-releasing hormone is decreased in the hyperthyroid state compared with the euthyroid state.
abstract: OBJECTIVE
  Dehydroepiandrosterone (DHEA) and DHEA-sulphate (S) have been suggested to play protective roles in many pathological states, some of which are observed in hyperthyroidism. If DHEA and DHEA-S levels change in hyperthyroidism, they might participate as a possible causative link with such pathophysiological changes in hyperthyroidism. However, the CRH-ACTH-DHEA system in hyperthyroidism has not been clearly defined. We examined plasma levels of DHEA and DHEA-S together with ACTH and cortisol in both hyperthyroid (Hyper) and euthyroid states (Eu).
  
  
  METHODS
  Eighteen patients (5 men and 13 women, aged 46.9 +/- 2.8 years) with Graves' disease were studied before treatment and again in the euthyroid state following treatment with methimazole. A 100 microg hCRH stimulation test and a low-dose (0.5 microg) 1-24 ACTH stimulation test were performed on separate days. Basal levels and A area under the response curve (AUC) were compared between Hyper and Eu.
  
  
  RESULTS
  DHEA-S was higher in Hyper than in Eu. However, basal DHEA did not differ between Hyper and Eu. The ratio of DHEA to DHEA-S was lower in Hyper than in Eu. AAUC of DHEA during a CRH test was lower in Hyper than in Eu. However, AAUC of DHEA during an ACTH test was similar in both Hyper and Eu. Basal ACTH was higher in Hyper than in Eu. In both CRH and ACTH tests, AAUC of cortisol response was lower in Hyper than in Eu, although the basal cortisol level was not different.
  
  
  CONCLUSIONS
  The balance of the conversion between DHEA-S and DHEA in the hyperthyroid state favoured DHEA-S. Similar to cortisol, the DHEA response in the CRH test in hyperthyroidism seemed to be insufficiently compensated for by increased ACTH, although the DHEA response to low-dose ACTH was similar in the hyperthyroid and euthyroid states. Increased DHEA-S might play some role in the pathological states in many organs in hyperthyroidism.
authors.affiliation: Department of Internal Medicine, Matsunami General Hospital, Kasamatsu, Gifu-Prefecture, Japan. nyamakita@matsunami-hsp.or.jp
authors.forename: N
authors.initials: N
authors.lastname: Yamakita
authors.forename: T
authors.initials: T
authors.lastname: Murai
authors.forename: Y
authors.initials: Y
authors.lastname: Kokubo
authors.forename: M
authors.initials: M
authors.lastname: Hayashi
authors.forename: A
authors.initials: A
authors.lastname: Akai
authors.forename: K
authors.initials: K
authors.lastname: Yasuda
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D013956:Antithyroid Agents / Q000627:therapeutic use; D019540:Area Under Curve; D003346:Corticotropin-Releasing Hormone; D003687:Dehydroepiandrosterone / Q000097:blood*; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006980:Hyperthyroidism / Q000097:blood*; D008297:Male; D008713:Methimazole / Q000627:therapeutic use; D008875:Middle Aged; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D013956:Antithyroid Agents; D014284:Triiodothyronine; D003687:Dehydroepiandrosterone; D008713:Methimazole; D019314:Dehydroepiandrosterone Sulfate; D000324:Adrenocorticotropic Hormone; D013972:Thyrotropin; D003346:Corticotropin-Releasing Hormone; D013974:Thyroxine; D006854:Hydrocortisone