Genetic polymorphism associated with non-response to therapy in inflammatory bowel disease patients: a review

Inflammatory bowel disease (IBD) poses a major therapeutic challenge due to its chronic course and variable treatment responses. Genetic polymorphisms significantly influence drug efficacy, prompting this review to analyze their role in treatment non-response. A systematic literature search (PubMed/Scopus) using terms like “genetic polymorphism,” “non-response,” and “IBD” identified 25 relevant studies. Key findings linked TNFα (−308 G > A), TNFRSF1A, and TNFRSF1B polymorphisms to reduced anti-TNFα therapy effectiveness. TPMT variants correlated with thiopurine toxicity, while CYP3A4 and CYP3A5 polymorphisms altered tacrolimus metabolism. These genetic markers could serve as predictive tools for personalized IBD treatment, emphasizing the potential of genetic screening in clinical practice. Future research should integrate multi-omics approaches to refine predictive models and advance precision medicine, ultimately improving patient outcomes through tailored therapeutic strategies. Inflammatory bowel disease (IBD) is a long-term condition that can be hard to treat because patients respond differently to medications. Genetic differences may explain why some treatments work for some people but not others. This review looked at how genes affect how well IBD medicines work. It is found that some people have genetic changes that make certain drugs less effective or cause more side effects. For example, some genes can affect how the body handles common IBD drugs like infliximab, azathioprine, or tacrolimus. Testing a person’s genetic differences might be able to help doctors to choose the treatment that works best and avoid ones that could be harmful. In the future, using genetic information could help make IBD treatment more personal and more effective, leading to better outcomes and fewer side effects.