Shahukhal, Ravi

ObjectiveTo determine if the efficacy of biologics differ based on magnetic resonance imaging (MRI) and C‐reactive protein (CRP) findings.MethodsWe compared four subgroups (MRI+/CRP+, MRI+/CRP−, MRI−/CRP+, MRI−/CRP−) from randomized controlled trials (RCTs). A comprehensive database search was performed to include axial spondylarthritis (axSpA; both radiographic axSpA [r‐axSpA] and nonradiographic axSpA [nr‐axSpA]) RCTs with treatment efficacy reported by different MRI and CRP subgroups. Study‐specific disease activity scores (at 12‐16 weeks) were pooled using a random‐effects model and compared between the four subgroups.ResultsFive trials (all nr‐axSpA) were included: three with tumor necrosis factor inhibitors (TNFi, N = 729) and two with interleukin‐17 inhibitors (IL‐17i, N = 794). TNFi and IL‐17i showed efficacy based on the Assessment of Spondyloarthritis International Society 40 (ASAS40) and Bath Ankylosing Spondylitis Disease Activity Index 50 (BASDAI50) in all MRI and CRP subgroups, except the CRP−/MRI− subgroup, which had a single study with only 39 patients. There was no statistically significant difference between the four subgroups in terms of patients achieving ASAS40 (P = 0.60, I2 = 0%) or BASDAI50 (P = 0.27, I2 = 23.9%). The number needed to treat was three for the CRP+/MRI+ and CRP+/MRI− subgroups and six for the CRP−/MRI+ and CRP−/MRI− subgroups. All trials had a low risk of bias. Between‐study heterogeneity was low to moderate. Sensitivity analyses comparing TNFi or IL‐17i versus placebo similarly showed no difference between subgroups in terms of ASAS40 (TNFi, P = 0.57; IL‐17i, P = 0.28) and BASDAI50 (TNFi, P = 0.37; IL‐17i, P = 0.18).ConclusionIn this systematic review, there was no statistically significant difference between the four subgroups in terms of efficacy based on ASAS40 or BASDAI50.

Objective To investigate the effect of therapies on radiographic progression in patients with axial spondyloarthritis (SpA). Methods A comprehensive database search for studies assessing radiographic progression in axial SpA (particular treatment versus no treatment of interest) was performed. Study‐specific standardized mean differences in treatment outcomes at 2 and ≥4 years were estimated and combined using random‐effects models. Results Twenty‐four studies in patients with axial SpA were identified, of which 18 involved tumor necrosis factor inhibitors ( TNF i), 8 involved nonsteroidal antiinflammatory drugs ( NSAID s), and 1 involved secukinumab. Spinal radiographic progression, as measured by the modified Stoke Ankylosing Spondylitis Spine Score ( mSASSS ), was not significantly different between TNF i‐treated and biologics‐naive patients at 2 years ( mSASSS difference −0.73 [95% confidence interval (95% CI ) −1.52, 0.12], I 2 = 28%) and ≥4 years ( mSASSS difference −2.03 [95% CI −4.63, 0.72], I 2 = 63%). Sensitivity analyses restricted to studies with a low risk of bias showed a significant difference in spinal radiographic progression between TNF i‐treated and biologics‐naive patients at ≥4 years ( mSASSS difference −2.17 [95% CI −4.19, −0.15]). No significant difference in spinal radiographic progression was observed between NSAID ‐treated and control patients ( mSASSS difference −0.30 [95% CI −2.62, 1.31], I 2 = 71%) or between secukinumab‐treated and biologics‐naive patients ( mSASSS difference −0.34 [95% CI −0.85, 0.17]). With regard to treatment differences in patients with nonradiographic axial SpA or in patients with radiographic progression measured using the sacroiliac joint score, an insufficient number of studies were available for analysis. Conclusion Although no significant protective effect of TNF i treatment on spinal radiographic progression was seen over the course of 2 years or ≥4 years in patients with axial SpA, our analysis restricted to studies with a low risk of bias showed a protective effect of TNF i after ≥4 years. Therefore, long‐term TNF i exposure might confer beneficial effects on spinal radiographic progression in axial SpA. No difference in radiographic progression at 2 years was seen in either the NSAID or secukinumab treatment groups compared to their controls. Future studies should explore the effects of biologic treatment on radiographic progression, as well as the effects of long‐term biologics exposure, in patients with early axial SpA or those with nonradiographic axial SpA.