title: Hypothalamic-pituitary-adrenocortical axis function in patients with polymyalgia rheumatica and giant cell arteritis.
abstract: BACKGROUND
  Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are 2 closely related syndromes affecting elderly people. One of the most striking features of these conditions is the development of the disease in an almost exclusive manner in people older than 50 years. Despite this close association with age, the pathogenic mechanisms that could explain this age-related predisposition are unknown. Aging is accompanied by a number of quantitative and qualitative changes in the endocrine system that may predispose to several pathologic conditions that occur in the elderly.
  
  
  OBJECTIVE
  To explore the hypothalamic-pituitary-adrenal axis in PMR and GCA.
  
  
  METHODS
  Basal levels of adrenal hormones as well as the response to low-dose adrenocorticotropin hormone (ACTH) were investigated in 20 patients with active untreated disease and compared with levels in 16 healthy age-matched controls.
  
  
  RESULTS
  Male patients with active disease had low basal levels of androstenedione compared to the controls. After low-dose ACTH challenge, cortisol and dehydroepiandrosterone reached higher levels in patients than in healthy subjects, indicating that the adrenal gland function was not suppressed. Furthermore, the authors did not find a clear relationship between the levels of acute phase reactants and adrenal hormones in the patient population.
  
  
  CONCLUSIONS
  The authors' findings are probably more compatible with the hypothesis that the abnormalities found in the patient group are the consequences of chronic illness rather than a crucial factor contributing to the pathogenesis of the disease.
authors.affiliation: Division of Immunology, Hospital Universitario Marqués de Valdecilla, Facultad de Medicina, Universidad de Cantabria, Santander, Spain.
authors.forename: Maria J Bartolome
authors.initials: MJ
authors.lastname: Pacheco
authors.forename: Jose A
authors.initials: JA
authors.lastname: Amado
authors.forename: Marcos
authors.initials: M
authors.lastname: Lopez-Hoyos
authors.forename: Ricardo
authors.initials: R
authors.lastname: Blanco
authors.forename: Maria T
authors.initials: MT
authors.lastname: Garcia-Unzueta
authors.forename: Vicente
authors.initials: V
authors.lastname: Rodriguez-Valverde
authors.forename: Victor M
authors.initials: VM
authors.lastname: Martinez-Taboada
mesh_terms: D019326:17-alpha-Hydroxyprogesterone / Q000097:blood; D000210:Acute-Phase Reaction / Q000276:immunology; D000324:Adrenocorticotropic Hormone / Q000627:therapeutic use; D000368:Aged; D000369:Aged, 80 and over; D003350:Cortodoxone / Q000097:blood; D003687:Dehydroepiandrosterone / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D005260:Female; D013700:Giant Cell Arteritis / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D011111:Polymyalgia Rheumatica / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*
chemical_list: D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D019326:17-alpha-Hydroxyprogesterone; D000324:Adrenocorticotropic Hormone; D003350:Cortodoxone; D006854:Hydrocortisone