title: Serum dehydroepiandrosterone, dehydroepiandrosterone sulfate, and pregnenolone sulfate concentrations in patients with hyperthyroidism and hypothyroidism.
abstract: BACKGROUND
  Dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) have been suggested to have protective effects against cardiovascular disease, cancer, immune-modulated diseases, and aging. We examined serum concentrations of DHEA, DHEA-S, and pregnenolone sulfate (PREG-S) in patients with thyroid dysfunction.
  
  
  METHODS
  Steroids extracted with methanol from serum sample were separated into an unconjugated fraction (DHEA) and a monosulfate fraction (DHEA-S and PREG-S), using a solid-phase extraction and an ion-exchange column. After separation of unconjugated steroids by HPLC, the DHEA concentration was measured by enzyme immunoassay. The monosulfate fraction was treated with arylsulfatase, and the freed steroids were separated by HPLC. The DHEA and PREG fractions were determined by gas chromatography-mass spectrometry, and the concentrations were converted into those of DHEA-S and PREG-S.
  
  
  RESULTS
  Serum concentrations of DHEA, DHEA-S, and PREG-S were all significantly lower in patients with hypothyroidism (n = 24) than in age- and sex-matched healthy controls (n = 43). By contrast, in patients with hyperthyroidism (n = 22), serum DHEA-S and PREG-S concentrations were significantly higher, but the serum DHEA concentration was within the reference interval. Serum concentrations of these three steroids correlated with serum concentrations of thyroid hormones in these patients. Serum albumin and sex hormone-binding globulin concentrations were not related to these changes in the concentration of steroids.
  
  
  CONCLUSIONS
  Serum concentrations of DHEA, DHEA-S, and PREG-S were decreased in hypothyroidism, whereas serum DHEA-S and PREG-S concentrations were increased but DHEA was normal in hyperthyroidism. Thyroid hormone may stimulate the synthesis of these steroids, and DHEA sulfotransferase might be increased in hyperthyroidism.
authors.affiliation: Clinical Chemistry Laboratory, Kobe Pharmaceutical University, 4-19-1, Motoyamakita-machi, Higashinada-ku, Kobe 658-8558, Japan.t-noriko@kobe pharma-u.ac.jp
authors.forename: N
authors.initials: N
authors.lastname: Tagawa
authors.forename: J
authors.initials: J
authors.lastname: Tamanaka
authors.forename: A
authors.initials: A
authors.lastname: Fujinami
authors.forename: Y
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: T
authors.initials: T
authors.lastname: Takano
authors.forename: S
authors.initials: S
authors.lastname: Fukata
authors.forename: K
authors.initials: K
authors.lastname: Kuma
authors.forename: H
authors.initials: H
authors.lastname: Tada
authors.forename: N
authors.initials: N
authors.lastname: Amino
mesh_terms: D000328:Adult; D003687:Dehydroepiandrosterone / Q000097:blood*; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood*; D005260:Female; D006801:Humans; D006980:Hyperthyroidism / Q000097:blood*; D007037:Hypothyroidism / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011284:Pregnenolone / Q000097:blood*; D013963:Thyroid Hormones / Q000097:blood
chemical_list: D013963:Thyroid Hormones; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D011284:Pregnenolone