title: Impaired hypothalamo-pituitary-adrenal axis in patients with ankylosing spondylitis.
abstract: BACKGROUND
  To investigate the hypothalamic-pituitary- adrenal (HPA) axis in patients with ankylosing spondylitis (AS) and healthy controls.
  
  
  METHODS
  Forty-nine AS patients and 20 healthy controls were included. Lowdose ACTH test (LDST) was used to assess the HPA axis. Basal cortisol, stimulated peak cortisol levels, and acutephase reactants [C-reactive protein (CRP), erythrocyte sedimentation rate, and fibrinogen] were studied. Bath Ankylosing Spondylitis Functional Index, Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and Bath Ankylosing Spondylitis Metrology Index were also evaluated.
  
  
  RESULTS
  Patient and control groups were not different regarding age, sex, body mass index and waist circumference (WC). Basal cortisol levels did not show a significant difference between groups. However, cortisol increment after low-dose ACTH was significantly impaired in AS subjects with respect to controls (20.0+/-4.4 vs 24+/-2.2 microg/dl, p<0.001). Eleven AS patients had impaired cortisol peak after LDST when a cortisol cut-off is accepted as 500 nmol/l (18 microg/dl) and none of the controls exhibited a peak cortisol responses to LDST<500 nmol/l. Comparison of AS subjects who were receiving anti-tumor necrosis factor (TNF) (no.=23), and conventional therapy (no.=26) yielded similar basal and peak cortisol concentrations. Peak cortisol concentrations were associated with basal cortisol, impaired cortisol response, CRP, and fibrinogen. Impaired cortisol response (subjects with peak cortisol levels <18 microg/dl) was significantly correlated with basal and peak cortisol concentrations and BASDAI.
  
  
  CONCLUSIONS
  Our results indicate an increased prevalence of subclinical glucocorticoid deficiency in AS patients. Anti-TNF treatment seems not to have effect on HPA axis.
authors.affiliation: Department of Internal Medicine, Izmir Bozyaka Training and Research Hospital, Izmir, Turkey.
authors.forename: L
authors.initials: L
authors.lastname: Kebapcilar
authors.forename: O
authors.initials: O
authors.lastname: Bilgir
authors.forename: A
authors.initials: A
authors.lastname: Alacacioglu
authors.forename: Y
authors.initials: Y
authors.lastname: Yildiz
authors.forename: A
authors.initials: A
authors.lastname: Taylan
authors.forename: R
authors.initials: R
authors.lastname: Gunaydin
authors.forename: A
authors.initials: A
authors.lastname: Yuksel
authors.forename: B
authors.initials: B
authors.lastname: Karaca
authors.forename: I
authors.initials: I
authors.lastname: Sari
mesh_terms: D000293:Adolescent; D000324:Adrenocorticotropic Hormone; D000328:Adult; D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D013167:Spondylitis, Ankylosing / Q000503:physiopathology*
chemical_list: D000324:Adrenocorticotropic Hormone; D002097:C-Reactive Protein; D006854:Hydrocortisone