Tumor necrosis factor blockers have a comparatively low infection risk and appear to slow progression in patients with ankylosing spondylitis
Wallis D, Thavaneswaran A, Haroon N, et al. Tumour necrosis factor inhibitor therapy and infection risk in axial spondyloarthritis: results from a longitudinal observational cohort. Rheumatology (2014) doi: 10.1093/rheumatology/keu255 [Online: August 13, 2014]
Haroon N. The effect of tumor necrosis factor-blockade on new bone formation in ankylosing spondylitis: what is the evidence? Current Opinion in Rheumatology (2014) 26:389-394. doi: 10.1097/BOR.0000000000000077.
New data from a longitudinal observational study inankylosing spondylitis (AS) and axial spondyloarthritis (axSpA) patients suggests that the serious infection rate for tumor necrosis factor bockers is low compared with rates in other rheumatic diseases.
Use of tumor necrosis factor inhibitors in AS and axSpA is increasing. This Canadian study is the first to provide information on infections in a real-world setting rather than a clinical trial.
The 440 patients – 423 with AS and 27 with axSpA -- are part of a database at Toronto Western Hospital’s AS clinic. Most of the records involved men in their 40s, covering the equivalent of 1,712 patient-years (mean individual course of treatment: 3.89 years).
Of 259 infections (most of them bacterial) among 185 patients, only 23 were serious. The overall rate of infections over three years in those on TNF drugs was 19/100 patient-years, with a serious infection rate of only 1.5/100 patient-years. The difference was not significantly different than that among patients not on TNF drugs, and around the same as reported in rheumatoid arthritis (RA).
Chief among risk factors for serious infections: use of disease modifying antirheumatic drugs (DMARDs). Not associated with increased risk in multivariate analysis: age, disease duration, smoking status, Bath AS Functional Index (BASFI), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), co-morbidity scores, or hospitalizations.
The second article above, a review of information new bone formation and spinal ankylosing in AS in clinical trials of TNF drugs, suggests that these inflammation blockers may impede the bone growth associated with radiographic disease progression.
It assesses three short-term (18 month) studies, part of the Outcome Assessment in Ankylosing Spondylitis (OASIS) clinical trials of European AS patients initially treated in the pre-biologics era who later received TNF drugs. The review notes that there were no significant differences in progression between the patients.
Additionally, two long-term studies of radiographic progression, with more than 4 years of follow-up, show better outcomes among patients who took TNF inhibitors. One multi-center study of 33 patients in North America shows 35% of patients in the control group progressed, compared to 27% in the TNFi group. A smaller study (56 patients) in Germany had similar results. Both suggest that TNF drugs can clear inflammatory lesions in AS over time.
The review also suggests a window of opportunity for TNFi use: Results are much better among AS patients with mean disease duration shorter 5 years than among those diagnosed 10 or more years before starting treatment.