Abstract
Inflammatory bowel diseases (IBD) are chronic conditions that primarily affect the gastrointestinal tract, with a complex pathogenesis; they are characterized by a significant heterogeneity of clinical presentations and of inflammatory pathways that sustain intestinal damage. After the introduction of the first biological therapies, the pipeline of therapies for IBD has been constantly expanding, and a significant number of new molecules is expected in the next few years. Evidence from clinical trials and real-life experiences has taught us that up to 40% of patients do not respond to a specific drug. Unfortunately, to date, clinicians lack a valid tool that can predict each patient’s response to therapies and that could help them in choosing what drug to administer. Several candidate biomarkers have been investigated so far, with conflicting results: clinical, genetic, immunological, pharmacokinetic and microbial markers have been tested, but no ideal marker has been identified so far. Based on recent evidence, multiparametric models seemingly hold the greatest potential for predicting response to therapy. In this narrative review, we aim to summarize the current knowledge on predictors and early markers of response to biological therapies in IBD.
Highlights
Crohn’s disease (CD) and ulcerative colitis (UC) represent the two main forms of inflammatory bowel diseases (IBD)
TREM-1: triggering receptor expressed on myeloid cells 1; CCR2-CCL7: chemokine receptor type 2–chemokine ligand 7; TNF: tumor necrosis factor; mTNF: membrane tumor necrosis factor; PBMC: peripheral blood mononuclear cells; LPS: lipopolysaccharide; OSM: oncostatin M; NK cells: natural killer cells; IL: interleukin; CD40L: ligand of cluster of differentiation 40; IBD: inflammatory bowel disease; CD: Crohn’s disease; UC: ulcerative colitis; MAdCAM-1: mucosal vascular addressin cell adhesion molecule 1; VCAM-1: vascular cell adhesion molecule 1; ICAM-1: intercellular adhesion molecule 1
The only tool of personalized medicine that has been widely incorporated in IBD clinical practice in regard to biotechnological therapies is represented by Therapeutic drug monitoring (TDM) for secondary non-response to infliximab and adalimumab
Summary
Crohn’s disease (CD) and ulcerative colitis (UC) represent the two main forms of inflammatory bowel diseases (IBD). While the armamentarium treatment is constantly expanding—with new drugs targeting different pat pathways—there is still a significant proportion of patients who do not respon apy: data from clinical trials and real life report clinical efficacy of 2aosfi2n0gle dru 60% of patients [9,10]. Whether these patients would respond to another agent i sible to foretell, but there is strong evidence that second- and third-line agents expandfeincgti—veweitvhenneiwn dthruegcsatsaergoeftipnrgimdifafreyrefnatipluartheo, gaeltnheotiucgphatthowaayles—ssethreerextiesnsttil[l1a1].
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