Serum or Plasma Oncostatin M for Predicting Primary Non-Response to Tumor Necrosis Factor-α Antagonist Therapy in Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis.

Abstract

Background: Over 30% of patients with inflammatory bowel disease (IBD) experience primary non-response to tumor necrosis factor-α antagonists (anti-TNFs). Oncostatin M (OSM), a TNF-α-independent pro-inflammatory signaling cytokine, is emerging as a potential predictive biomarker of treatment response. Through a systematic review and meta-analysis, we assessed the utility of baseline serum or plasma OSM for predicting anti-TNF response in IBD patients. Methods: We searched PubMed, Embase, Cochrane Library, and Web of Science through March 2026 for studies reporting associations between baseline serum/plasma OSM and endoscopic or clinical response to anti-TNF therapy in adult IBD patients. We used a bivariate random-effects model to estimate pooled sensitivity, specificity, diagnostic odds ratio (DOR), and area under the receiver operating characteristic (ROC) curve (AUC). Quality was assessed using QUADAS-2. Results: Data from four studies (n = 441 patients) were pooled. We estimated a pooled sensitivity of 82.8% (95% CI 71.4-90.3%) and a specificity of 88.4% (95% CI 82.7-92.4%) for predicting anti-TNF non-response. The pooled AUC was 0.899 (95% CI 0.858-0.940), with low heterogeneity (I² = 16.0%). The pooled DOR was 36.7 (95% CI 15.7-85.8), with a positive likelihood ratio of 7.1 and a negative likelihood ratio of 0.19. Risk of bias was low across the studies. Conclusions: Higher serum OSM was associated with treatment failure in IBD patients receiving anti-TNF therapy, with a pooled AUC of 0.899 in assay-stratified analysis and 0.820 when all studies were included. However, the small number of available studies, substantial variability in OSM cutoffs (14-233.6 pg/mL) and assay heterogeneity limit the robustness and generalizability and call for additional prospective data to more-robustly characterize the clinical utility of OSM.