The Clinical Efficacy of Type 2 Inflammation-Specific Agents Targeting Interleukins in Reducing Exacerbations in Severe Asthma: A Meta-Analysis
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Purpose: Monoclonal antibodies against type 2 inflammatory pathways are currently promising therapeutics for severe asthma. The aim of this study was to determine how well type 2 (T2) inflammation-specific agents targeting interleukins reduce the rate ofasthma exacerbations (AE) in patients with severe asthma. Materials and Methods: We performed a systematic review and meta-analysis in accordance with PRISMA guidelines. A systematicliterature search was conducted in PubMed, Embase, and the Cochrane Central Register. The primary outcome was the reductionrate of annualized AEs. Results: We analyzed 17 studies comprising 11800 subjects. A total of 6197 patients received T2-specific agents (benralizumab,dupilumab, lebrikizumab, mepolizumab, reslizumab, and tralokinumab). Overall, T2-specific agents were significantly associatedwith a lower risk of AE, compared with placebo [rate ratio (RR) 0.58, 95% confidence interval (CI) 0.51 to 0.66]. Among all studiedagents, only tralokinumab did not demonstrate a reduction in AE. The efficacy of T2-specific agents in reducing AE was maintainedregardless of the pathway used. A subgroup analysis indicated that T2-specific agents further reduced the risk of AE in patients witheosinophil counts of ≥300 cells/μL (RR 0.41, 95% CI 0.32 to 0.53). Conclusion: Our findings suggest that T2-specific agents are significantly associated with a reduced rate of AE, compared withplacebo. Their efficacy appears to be enhanced in patients with eosinophil counts of ≥300 cells/μL.
Abstract
Purpose: Monoclonal antibodies against type 2 inflammatory pathways are currently promising therapeutics for severe asthma. The aim of this study was to determine how well type 2 (T2) inflammation-specific agents targeting interleukins reduce the rate ofasthma exacerbations (AE) in patients with severe asthma. Materials and Methods: We performed a systematic review and meta-analysis in accordance with PRISMA guidelines. A systematicliterature search was conducted in PubMed, Embase, and the Cochrane Central Register. The primary outcome was the reductionrate of annualized AEs. Results: We analyzed 17 studies comprising 11800 subjects. A total of 6197 patients received T2-specific agents (benralizumab,dupilumab, lebrikizumab, mepolizumab, reslizumab, and tralokinumab). Overall, T2-specific agents were significantly associatedwith a lower risk of AE, compared with placebo [rate ratio (RR) 0.58, 95% confidence interval (CI) 0.51 to 0.66]. Among all studiedagents, only tralokinumab did not demonstrate a reduction in AE. The efficacy of T2-specific agents in reducing AE was maintainedregardless of the pathway used. A subgroup analysis indicated that T2-specific agents further reduced the risk of AE in patients witheosinophil counts of ≥300 cells/μL (RR 0.41, 95% CI 0.32 to 0.53). Conclusion: Our findings suggest that T2-specific agents are significantly associated with a reduced rate of AE, compared withplacebo. Their efficacy appears to be enhanced in patients with eosinophil counts of ≥300 cells/μL.
참고문헌 (44)
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