Anita Afzali, MD, on Biomarkers for the Optimization of IBD: Finding Precision
Dr Afzali reviews her presentation from the Advances in Inflammatory Bowel Disease regional meeting held on August 7 on how the use of biomarkers can help clinicians make the best choice of therapies to optimize outcomes in IBD.
Anita Afzali, MD, is a professor of medicine at The Ohio State University Wexner Medical Center and medical director of The Ohio State University Inflammatory Bowel Disease Center.
TRANSCRIPT:
Dr. Anita Afzali: Hello, my name is Anita Afzali. I'm a professor of medicine at Ohio State University. I'm also the medical director of our Inflammatory Bowel Disease Center there. I'm happy to share a little bit of a summary of what I just presented, which was titled "Biomarkers for the Optimization of Inflammatory Bowel Disease and Specifically Finding Precision with the Use of These Biomarkers."
There's been significant progress in recent years with biomarkers in the field of inflammatory bowel disease. Now, what we know is that an ideal biomarker should be noninvasive. It should be sensitive, disease-specific, easy to perform, and of course, cost-effective.
For us, the use and utilization of biomarkers can help us in making the diagnosis. It can help us in evaluating a disease phenotype. It can help reflect the clinical response to treatment as far as monitoring strategies, as well as help us identify safety concerns.
We have different types of biomarkers, which I presented on. The first type, or class, or subtype of biomarkers are the prognostic biomarkers. These are an example such as gene signatures, which I presented on and where it has helped us identify which of our patients may perhaps have more of a penetrating or structuring disease phenotype.
Another type of biomarkers are the predictive biomarkers. The predictive biomarkers — as an example, TPMT or thiopurine methyltransferase — this enzyme activity level helps us predict which of our patients are at risk for leukopenia.
More recently, the NUDT15 polymorphism has also been found to be strongly associated with patients who are at risk for being treated with a thiopurine but in also developing a thiopurine-induced lymphopenia.
Also, recently, another biomarker here under the predictive biomarkers class is the biomarker based off of the recent genome-wide association study, which found that carriers of HLA-DQA1*05, the allele for that, are at an increased risk of immunogenicity for patients who are treated with the TNF antagonists.
Again, perhaps for these patients, we may want to consider combination therapy. We certainly don't want to consider or place our patients on monotherapy with a TNF antagonist if they are at a carrier of this, knowing that their risk for immunogenicity is higher.
Last is the monitoring biomarkers. This is perhaps the most familiar that you and I are with. For example, C-reactive protein has an inflammatory biomarker, as well as fecal calprotectin.
In fact, our recent treat-to-target stride to consensus guidelines actually recommends monitoring these biomarkers — CRP, fecal calprotectin — as an intermediate target for when we initiate our patients on a treatment strategy, monitoring after you've initiated the treatment to determine whether or not our patients are having a response to therapy.
Overall, the future of high-quality biomarkers for the practice of precision medicine and inflammatory bowel disease is the wave of the future. I hope you found my presentation at AIBD Regionals helpful.
