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). CONCLUSION: 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.
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 RApatients. 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). CONCLUSION: 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.