Key result
Azilsartan added to etanercept improves pain, disease activity, CRP, and ESR in active rheumatoid arthritis.
Why the study?
The involvement of the renin-angiotensin system in inflammatory processes suggests that blocking RAS may enhance treatment efficacy in active rheumatoid arthritis patients poorly responding to methotrexate.
Does azilsartan improve clinical outcomes in patients with active rheumatoid arthritis poorly responding to methotrexate treated with etanercept?
RCT (n=42)
Randomized
Does azilsartan improve clinical outcomes in patients with active rheumatoid arthritis poorly responding to methotrexate treated with etanercept?
Adding azilsartan to etanercept may improve clinical and inflammatory markers in patients with active rheumatoid arthritis who respond poorly to methotrexate.
Azilsartan add-on may enhance etanercept response in methotrexate-refractory RA; hypothesis-generating pilot data require larger confirmatory trials.
BACKGROUND AND AIM: Much evidence has emerged documenting the involvement of the renin-angiotensin system (RAS) in inflammatory processes. The objective of this study was to evaluate the effects of blocking RAS with azilsartan (Azil) on the clinical efficacy of etanercept (Etan) in patients with active rheumatoid arthritis (RA). PATIENTS AND METHODS: Forty-two patients diagnosed with active RA and poorly responding to methotrexate were enrolled in this pilot clinical study. They were randomly allocated into two groups, and treated with either Etan (50 mg/week) and placebo or the same dose of Etan with Azil (20 mg/day) for 90 days. The clinical outcome was evaluated using the Disease Activity Score-28 joint (DAS-28), simplified disease activity index (SDAI), clinical disease activity index (CDAI) and the health assessment questionnaire disease index (HAQ-DI). Blood samples were obtained for the assessment of C-reactive protein and erythrocyte sedimentation rate at baseline and after 90 days. RESULTS: The markers of pain and disease activity, C-reactive protein and erythrocyte sedimentation rate were significantly improved when Azil was used, as an adjuvant with Etan, compared with the use of Etan and placebo. CONCLUSION: Blocking RAS with azilsartan may improve the effects of etanercept on the clinical markers of pain and disease severity of patients with active RA not responding to methotrexate.
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Mahmood et al. (2018) conducted an RCT in Active rheumatoid arthritis (n=42). Azilsartan and Etanercept vs. Placebo and Etanercept 50 mg/week was evaluated on Clinical outcome evaluated using DAS-28, SDAI, CDAI, HAQ-DI, C-reactive protein, and erythrocyte sedimentation rate. Azilsartan as an adjuvant to etanercept significantly improved markers of pain, disease activity, CRP, and ESR compared with etanercept and placebo in patients with active rheumatoid arthritis.
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