title: Comparison of the clinical characteristics of vasculitis occurring during anti-tumor necrosis factor treatment or not in rheumatoid arthritis patients. A systematic review of 2707 patients, 18 vasculitis.
abstract: OBJECTIVE
  Comparison of vasculitis occurring in rheumatoid arthritis (RA) patients undergoing anti-tumor necrosis factor (TNF) treatment and those not.
  
  
  METHODS
  Systematic, retrospective, observational study of all RA patients in one center (1997-2004). Vasculitis cumulative incidence in RA patients was calculated in patients receiving anti-TNF or those not. Clinical characteristics of RA and vasculitis were collected. Begaud's imputability tables were used to evaluate the role of anti-TNF in inducing vasculitis.
  
  
  RESULTS
  Out of 2707 RA patients, 440 received an anti-TNF. A vasculitis occurred in 6 patients treated with anti-TNF (cumulative incidence: 1.3%), and in 12 patients treated without anti-TNF (cumulative incidence: 0.5%). Characteristics of patients not treated with anti-TNF or treated were respectively (mean): age (years) at vasculitis occurrence: 66.5 vs. 55.3, disease duration (years): 12.2 vs. 13.8, extra-articular features before vasculitis: 16% vs. 60%, number of previous DMARDs: 3.2 vs. 4.5, corticosteroid cumulated dosage (grams): 40.8 vs. 64.3. Vasculitis was cutaneous (58% vs. 67%), neurologic (58% vs. 67%), visceral (8% vs. 17%), and required a treatment in 66% vs. 83%. Using Begaud's tables, anti-TNF could be responsible for inducing vasculitis in 2 out of 6 patients.
  
  
  CONCLUSIONS
  In RA, vasculitis is more frequent during anti-TNF treatment than without anti-TNF. Anti-TNF could be responsible for inducing vasculitis in 2 patients. Patients treated with anti-TNF had more severe RA. It remains to be determined whether vasculitis is a consequence of anti-TNF inefficacy or whether it is treatment-related. In vasculitis occurring with anti-TNF, classical treatment seems more suitable than a switch to another anti-TNF.
authors.affiliation: Université René Descartes, Faculté de Médecine, AP-HP, Hôpital Cochin, Service de Rhumatologie B, Paris, France. sandre.guignard@free.fr
authors.forename: S
authors.initials: S
authors.lastname: Guignard
authors.forename: L
authors.initials: L
authors.lastname: Gossec
authors.forename: F
authors.initials: F
authors.lastname: Bandinelli
authors.forename: M
authors.initials: M
authors.lastname: Dougados
mesh_terms: D000068879:Adalimumab; D000368:Aged; D000911:Antibodies, Monoclonal / Q000009:adverse effects; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000150:complications* / Q000188:drug therapy*; D004359:Drug Therapy, Combination; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D018124:Receptors, Tumor Necrosis Factor; D012189:Retrospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014657:Vasculitis / Q000150:complications* / Q000209:etiology*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept