Abstract

The interleukin-6 family cytokine, oncostatin-M (OSM) has been associated with response to tumor necrosis factor-α antagonists (anti-TNFs) in small cohorts of patients with inflammatory bowel disease (IBD). We aimed to evaluate the association between plasma OSM concentrations and response to anti-TNFs (infliximab and adalimumab) in both ulcerative colitis (UC) and Crohn’s disease (CD). A retrospective cohort study was conducted in patients with IBD with a history of anti-TNF exposure. Blood samples, collected prior to anti-TNF exposure, were analyzed by enzyme-linked immunosorbent assay for the presence and quantity of OSM. Clinical remission was assessed at 1-year post anti-TNF exposure in addition to the occurrence of surgery, hospitalization, corticosteroid use, and adverse drug events. Lastly the threshold OSM plasma concentration associated with anti-TNF non-response was assessed by receiver operator characteristic (ROC) curve analysis. Patients with IBD (CD, n = 82; UC, n = 40) were assessed. In both UC and CD, mean pre-treatment OSM concentrations were significantly lower in those who achieved clinical remission at 1-year (p < 0.0001). A threshold plasma OSM concentration of 168.7 pg/ml and 233.6 pg/ml respectively separated those who achieved clinical remission at 1-year on an anti-TNF from those who did not in CD and UC respectively (CD: area under the receiver operator characteristic curve, AUROC = 0.880, 95% CI 0.79–0.96; UC: AUROC = 0.938, 95% CI 0.87–1.00). High OSM concentrations were associated with anti-TNF discontinuation and use of rescue steroids in CD and UC. High pre-treatment OSM concentrations identify IBD patients at-risk of anti-TNF non-response at 1-year as well as other deleterious clinical outcomes.

Details

Title
High oncostatin M predicts lack of clinical remission for patients with inflammatory bowel disease on tumor necrosis factor α antagonists
Author
Guo, Angela 1 ; Cameron, Ross 2 ; Chande Nilesh 3 ; Gregor, Jamie 3 ; Ponich Terry 3 ; Khanna Reena 3 ; Sey, Michael 3 ; Beaton, Melanie 3 ; Yan, Brian 3 ; Kim, Richard B 4 ; Wilson Aze 5 

 Western University, Department of Physiology and Pharmacology, London, Canada (GRID:grid.39381.30) (ISNI:0000 0004 1936 8884) 
 Western University, Division of Clinical Pharmacology, Department of Medicine, London, Canada (GRID:grid.39381.30) (ISNI:0000 0004 1936 8884) 
 Western University, Division of Gastroenterology, Department of Medicine, London, Canada (GRID:grid.39381.30) (ISNI:0000 0004 1936 8884) 
 Western University, Department of Physiology and Pharmacology, London, Canada (GRID:grid.39381.30) (ISNI:0000 0004 1936 8884); Western University, Division of Clinical Pharmacology, Department of Medicine, London, Canada (GRID:grid.39381.30) (ISNI:0000 0004 1936 8884) 
 Western University, Department of Physiology and Pharmacology, London, Canada (GRID:grid.39381.30) (ISNI:0000 0004 1936 8884); Western University, Division of Clinical Pharmacology, Department of Medicine, London, Canada (GRID:grid.39381.30) (ISNI:0000 0004 1936 8884); Western University, Division of Gastroenterology, Department of Medicine, London, Canada (GRID:grid.39381.30) (ISNI:0000 0004 1936 8884) 
Publication year
2022
Publication date
2022
Publisher
Nature Publishing Group
e-ISSN
20452322
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2622385018
Copyright
© The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.