title: Anti-tumour necrosis factor antibody treatment does not change serum levels of cortisol binding globulin in patients with rheumatoid arthritis but it increases androstenedione relative to cortisol.
abstract: BACKGROUND
  Cortisol binding globulin (CBG) is produced by liver cells and is inhibited by proinflammatory cytokines such as interleukin (IL) 6. CBG serum levels are typically low during prolonged inflammatory processes. Thus, observed changes of cortisol during anti-tumour necrosis factor (TNF) treatment may be related to changes of CBG in rheumatoid arthritis (RA).
  
  
  OBJECTIVE
  To investigate the course of CBG during anti-TNF treatment in RA.
  
  
  METHODS
  13 patients with longstanding RA, without prior prednisolone treatment, were included in this longitudinal study with subcutaneous adalimumab.
  
  
  RESULTS
  Treatment with anti-TNF markedly decreased clinical markers of inflammation and serum IL6. Serum levels of cortisol, CBG, and the ratio of cortisol/CBG did not change markedly, whereas the ratio of serum CBG/IL6 increased (p = 0.004). In parallel, levels of adrenocorticotropic hormone decreased during the observation period. The ratio serum androstenedione/serum cortisol increased during the study (p = 0.036).
  
  
  CONCLUSIONS
  During anti-TNF treatment relatively normal levels of CBG and a normal ratio of CBG/cortisol are found. Changes of cortisol in relation to IL6 during anti-TNF treatment, seen previously, may not be related to changes of CBG.
authors.affiliation: Laboratory of Neuroendocrinoimmunology, Department of Internal Medicine I, University Hospital Regensburg 93042, Germany. rainer.straub@klinik.uni-regensburg.de
authors.forename: R H
authors.initials: RH
authors.lastname: Straub
authors.forename: P
authors.initials: P
authors.lastname: Sarzi-Puttini
authors.forename: F
authors.initials: F
authors.lastname: Atzeni
authors.forename: F
authors.initials: F
authors.lastname: Buttgereit
authors.forename: M
authors.initials: M
authors.lastname: Carrabba
authors.forename: M
authors.initials: M
authors.lastname: Cutolo
mesh_terms: D000068879:Adalimumab; D000368:Aged; D000369:Aged, 80 and over; D000735:Androstenedione / Q000097:blood*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy*; D015415:Biomarkers / Q000097:blood; D002352:Carrier Proteins / Q000097:blood*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008137:Longitudinal Studies; D008875:Middle Aged; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D015415:Biomarkers; D002352:Carrier Proteins; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; C027091:cortisol binding globulin; D000735:Androstenedione; D000068879:Adalimumab; D006854:Hydrocortisone