title: Tumour necrosis factor blockers do not increase overall tumour risk in patients with rheumatoid arthritis, but may be associated with an increased risk of lymphomas.
abstract: OBJECTIVE
  To determine whether TNF blockers increase tumour risk in patients with RA.
  
  
  METHODS
  The South Swedish Arthritis Treatment Group register (SSATG) comprises over 90% of anti-TNF treated patients with RA in the area. 757 patients treated with etanercept or infliximab included between 1 February 1999 and 31 December 2002 were identified. 800 patients with conventional antirheumatic treatment in a community based cohort served as a comparison cohort. Tumours and deaths were identified in the cancer registry and population census registers. Patients were followed up from initiation of anti-TNF treatment or 1 July 1997 for the comparison group, until death or 31 December 2002.
  
  
  RESULTS
  In the anti-TNF group, 16 tumours (5 lymphomas) were identified in 1603 person-years at risk, and in the comparison group 69 tumours (2 lymphomas) in 3948 person-years. Standardised incidence ratios (SIRs) for total tumour relative risk for the anti-TNF group and the comparison group were 1.1 (95% confidence interval (CI) 0.6 to 1.8) and 1.4 (95% CI 1.1 to 1.8), respectively. The lymphoma relative risk (RR) was 11.5 (95% CI 3.7 to 26.9) and 1.3 (95% CI 0.2 to 4.5), respectively The total tumour RR excluding lymphoma was 0.79 (95% CI 0.4 to 1.42) and 1.39 (95% CI 1.08 to 1.76), respectively. Proportional hazard analysis for lymphomas yielded RR 4.9 (95% CI 0.9 to 26.2) in anti-TNF treated versus untreated patients.
  
  
  CONCLUSIONS
  Community based patients with RA treated conventionally had an increased overall tumour risk compared with the background population. A possible additional increased risk for lymphoma associated with TNF blockers was based on few cases and needs confirmation.
authors.affiliation: Department of Rheumatology, Lund University Hospital, SE 221 85 Lund, Sweden. Pierre.geborek@reum.lu.se
authors.forename: P
authors.initials: P
authors.lastname: Geborek
authors.forename: A
authors.initials: A
authors.lastname: Bladström
authors.forename: C
authors.initials: C
authors.lastname: Turesson
authors.forename: A
authors.initials: A
authors.lastname: Gulfe
authors.forename: I F
authors.initials: IF
authors.lastname: Petersson
authors.forename: T
authors.initials: T
authors.lastname: Saxne
authors.forename: H
authors.initials: H
authors.lastname: Olsson
authors.forename: L T H
authors.initials: LT
authors.lastname: Jacobsson
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000009:adverse effects; D018501:Antirheumatic Agents / Q000009:adverse effects*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D004812:Epidemiologic Methods; D000068800:Etanercept; D005260:Female; D019337:Hematologic Neoplasms / Q000139:chemically induced; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects; D007155:Immunologic Factors / Q000009:adverse effects*; D000069285:Infliximab; D008223:Lymphoma / Q000139:chemically induced* / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D018124:Receptors, Tumor Necrosis Factor; D013548:Sweden / Q000453:epidemiology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D007155:Immunologic Factors; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068800:Etanercept