title: Low levels of dehydroepiandrosterone sulphate in plasma, and reduced sympathoadrenal response to hypoglycaemia in premenopausal women with rheumatoid arthritis.
abstract: OBJECTIVE
  To evaluate the function of the hypothalamic-pituitary-adrenal axis and sympathoadrenal system in premenopausal women with rheumatoid arthritis (RA).
  
  
  METHODS
  Insulin-induced hypoglycaemia (0.1 IU/kg) was produced in 15 glucocorticoid-naive patients with long term RA with low disease activity and in 14 healthy women matched for age and body mass index. Concentrations of glucose, adrenocorticotropic hormone (ACTH), cortisol, Delta4-androstenedione (ASD), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS), 17alpha-hydroxyprogesterone (17OHP), epinephrine (EPI), norepinephrine (NE), interleukin 6 (IL6), and tumour necrosis factor alpha (TNFalpha) were analysed in plasma.
  
  
  RESULTS
  Patients had comparable responses of glucose, cortisol, ACTH, ASD, and 17OHP to hypoglycaemia, without any signs of hypothalamic insufficiency. Patients had lower basal DHEAS than controls (3.03 (0.37) micromol/l v 5.1 (0.9) micromol/l, respectively; p<0.05); borderline lower basal DHEA levels (p = 0.067); while the response of DHEA to hypoglycaemia was comparable to that of controls. Patients with RA had lower EPI (p = 0.005) and NE (p<0.001) responses to hypoglycaemia. TNFalpha and IL6 were higher (p<0.05) in patients with RA (TNFalpha 8 (2.8) pg/ml in RA v 1.1 (0.5) pg/ml in controls and IL6 15.1 (6.7) pg/ml v 1.4 (0.7) pg/ml).
  
  
  CONCLUSIONS
  Lower basal DHEAS levels, without concomitant differences or changes in DHEA, ASD, 17OHP, and cortisol responses to hypoglycaemia in patients with RA, indicate an isolated decrease in adrenal androgen production. Significantly lower responses of EPI and NE to hypoglycaemia may suggest sympathoadrenal hyporeactivity in patients with RA.
authors.affiliation: Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 833 06 Bratislava, Slovakia. richard.imrich@savba.sk
authors.forename: R
authors.initials: R
authors.lastname: Imrich
authors.forename: J
authors.initials: J
authors.lastname: Rovensky
authors.forename: F
authors.initials: F
authors.lastname: Malis
authors.forename: M
authors.initials: M
authors.lastname: Zlnay
authors.forename: Z
authors.initials: Z
authors.lastname: Killinger
authors.forename: R
authors.initials: R
authors.lastname: Kvetnansky
authors.forename: M
authors.initials: M
authors.lastname: Huckova
authors.forename: M
authors.initials: M
authors.lastname: Vigas
authors.forename: L
authors.initials: L
authors.lastname: Macho
authors.forename: J
authors.initials: J
authors.lastname: Koska
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000503:physiopathology; D001786:Blood Glucose / Q000378:metabolism; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D017697:Premenopause / Q000097:blood*; D013564:Sympathetic Nervous System / Q000503:physiopathology
chemical_list: D001786:Blood Glucose; D019314:Dehydroepiandrosterone Sulfate; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone