Published online Apr 14, 2019. doi: 10.3748/wjg.v25.i14.1764
Peer-review started: November 12, 2018
First decision: January 30, 2019
Revised: February 26, 2019
Accepted: March 1, 2019
Article in press: March 1, 2019
Published online: April 14, 2019
Tumor necrosis factor (TNF) inhibitors are one of the most effective therapies for induction and maintenance of remission in patients with Crohn’s disease (CD), however, to date, no observational prospective studies have been specifically designed to identify predictors of mucosal healing (MH), which should be the therapeutic target.
Improve knowledge about the predictive factors of response to TNF inhibitors and try to provide more tools to perform a personalized treatment.
The aim of this study was to identify predictors of MH after one year of treatment with TNF-α inhibitors.
Prospective observational single center study. Consecutive patients with clinically active CD requiring treatment with a TNF-α inhibitor were included. Clinical, biological and endoscopic data were obtained at baseline, weeks 14 and 46.
Endoscopic response to induction therapy, defined as 80% reduction in global CD Endoscopic Index of Severity (CDEIS), is a robust predictor of long-term MH. Endoscopic response is a predictor of MH. Achievement endoscopic response after induction may be considered as a therapeutic target for anti-TNF-α therapy. None, it was a observational study to identify predictors. After induction of remision with a TNF inhibitor perform a colonoscopy should be considered to predict long-term outocomes. Endoscopic response predict long-term outcomes. There were no hypotheses. After induction of remision with a TNF inhibitor perform a colonoscopy should be considered to predict long-term outocomes in patients with CD.
Clinical and biomarker data are not useful predictors of response to TNF-α inhibitors in CD, whereas endoscopic response to induction therapy, defined as 80% reduction in global CDEIS, is a robust predictor of long-term MH. Achievement of this endoscopic endpoint may be considered as a therapeutic target for anti-TNF-α therapy.