title: TNF inhibitors increase fat mass in inflammatory rheumatic disease: a systematic review with meta-analysis.
abstract: OBJECTIVE
  To assess body composition of patients with inflammatory rheumatic disease and the effect of TNF inhibitors on it.
  
  
  METHODS
  This was systematic review with meta-analysis of studies consulted on PubMed, Cochrane Library and EMBASE and assessing body composition in patients with rheumatoid arthritis or spondyloarthritis. We compared i) patients with healthy controls and ii) body components before and after TNF inhibitors.
  
  
  RESULTS
  Among the 703 articles reviewed, 19 met the inclusion criteria. In patients with rheumatoid arthritis, a significant increase in fat mass (+1.85 kg, p=0.02), adiposity (+3.53%, p<0.00001) and android mass (+1.7 kg, p<0.00001) and a significant decrease in lean mass (-3.03 kg, p=0.01), were observed. In patients with spondyloarthritis, a significant but modest increase in fat mass (+0.69 kg, p=0.03) and a significant decrease in lean mass (-3.74 kg, p=0.03) were observed. Nine studies assessed impact of TNF inhibitors on body composition, with an increase of fat mass in the short and long term in all studies. Data on lean mass were controversial. Two studies found an increase in visceral or android mass under TNF inhibitors.
  
  
  CONCLUSIONS
  Patients with inflammatory rheumatic disease have a significant decrease in lean mass and increase in fat mass. The use of TNF inhibitors is associated with a further increase in fat mass including android fat, which could potentially have cardiovascular consequences.
authors.affiliation: Rheumatology Department, Lapeyronie Hospital and Montpellier University, France.
authors.forename: Sarah
authors.initials: S
authors.lastname: Marouen
authors.affiliation: Rheumatology Department, Pellegrin Hospital and Bordeaux 2 University, France.
authors.forename: Thomas
authors.initials: T
authors.lastname: Barnetche
authors.affiliation: Rheumatology Department, Lapeyronie Hospital and Montpellier University; and Institute of Molecular Genetic, UMR5535, CNRS, Montpellier, France.
authors.forename: Bernard
authors.initials: B
authors.lastname: Combe
authors.affiliation: Rheumatology Department, Lapeyronie Hospital and Montpellier University; and Institute of Molecular Genetic, UMR5535, CNRS, Montpellier, France.
authors.forename: Jacques
authors.initials: J
authors.lastname: Morel
authors.affiliation: Rheumatology Department, Lapeyronie Hospital and Montpellier University; and Institute of Molecular Genetic, UMR5535, CNRS, Montpellier, France. c-daien@chu-montpellier.fr.
authors.forename: Claire I
authors.initials: CI
authors.lastname: Daïen
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects* / Q000503:physiopathology; D050154:Adiposity / Q000187:drug effects*; D000328:Adult; D000368:Aged; D018501:Antirheumatic Agents / Q000009:adverse effects*; D001688:Biological Products / Q000009:adverse effects*; D016009:Chi-Square Distribution; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012216:Rheumatic Diseases / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D018570:Risk Assessment; D012307:Risk Factors; D025241:Spondylarthritis / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D013997:Time Factors; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000276:immunology; D055815:Young Adult
chemical_list: D018501:Antirheumatic Agents; D001688:Biological Products; D014409:Tumor Necrosis Factor-alpha