title: [Meta analysis of infection risks of anti-TNF-α treatment in rheumatoid arthritis].
abstract: OBJECTIVE
  To systematically evaluate the risks of anti-TNF-α treatment-associated infection, severe infection and tuberculosis in rheumatoid arthritis (RA) patients, and to reduce the infection incidences associated with anti-TNF-α therapy.
  
  
  METHODS
  We used Meta analysis to systematically review randomized controlled trials on anti- TNF-α treatment associated risks of infection, severe infection and tuberculosis in RA patients.
  
  
  RESULTS
  Although no statistically significant differences were detected in TB risk between anit- TNF-α treatment and the control group (0.5% vs 0.07%; P=0.27, OR=1.85, 95% CI: 0.62-5.52), there still existed a clinically obvious elevation of TB risk in monoclonal anti-TNF-α treatment, which was illustrated by the results that no TB case was reported in the etanercept group, but 11 TBs in 2050 infliximab-treated cases, and 3 TBs in 722 adalimumab-treated cases. The total infection and severe infection risks were also significantly higher in patients receiving anti-TNF-α treatment (P<0.05). Subanalysis revealed that etanercept showed no significantly higher infection or severe infection risk than control group (P>0.05), while both kinds of monoclonal antibodies of TNF-α blockers showed a significantly elevated infection or severe infection risks (P<0.05). High doses of anti-TNF-α treatment were associated with statistically increased risks of severe infection (6.0% vs 2.8%, P=0.04, OR=1.68, 95% CI: 1.02-2.78).
  
  
  CONCLUSIONS
  The TB risk of anti-TNF-α treatment deserves close attention, especially in places with high rate of BCG vaccination and MTb infection. Monoclonal anti-TNF-α treatment brings higher risks of infection and severe infection than soluble TNF-α receptor.
authors.affiliation: Department of Rheumatology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
authors.forename: Xi
authors.initials: X
authors.lastname: Xie
authors.forename: Jinwei
authors.initials: J
authors.lastname: Chen
authors.forename: Youming
authors.initials: Y
authors.lastname: Peng
authors.forename: Jiesheng
authors.initials: J
authors.lastname: Gao
authors.forename: Jing
authors.initials: J
authors.lastname: Tian
authors.forename: Guanghui
authors.initials: G
authors.lastname: Ling
authors.forename: Jinfeng
authors.initials: J
authors.lastname: Du
authors.forename: Ni
authors.initials: N
authors.lastname: Mao
authors.forename: Peijun
authors.initials: P
authors.lastname: Wu
authors.forename: Fen
authors.initials: F
authors.lastname: Li
mesh_terms: D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000009:adverse effects* / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000009:adverse effects* / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D002681:China / Q000453:epidemiology; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects / Q000627:therapeutic use; D007239:Infections / Q000453:epidemiology / Q000209:etiology* / Q000276:immunology; D000069285:Infliximab; D016032:Randomized Controlled Trials as Topic; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D014376:Tuberculosis / Q000453:epidemiology / Q000209:etiology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
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