This transcript has been edited for clarity.
I'm Jordan Axelrad, co-director of the Inflammatory Bowel Disease Center at NYU Langone Health. I'm going to be discussing risk stratification in Crohn's disease.
Assessing disease activity, severity, and risk stratification in Crohn's disease is essential to guide early and effective therapy, reduce complications, and improve long-term outcomes. Two commonly used systems for assessing disease activity are the Crohn's Disease Activity Index (CDAI), and the Harvey-Bradshaw Index (HBI). They correlate with each other, but the Crohn's disease activity scoring systems rely on subjective symptoms.
In addition to the clinical parameters just mentioned, societies such as the American Gastroenterological Associations (AGA) recommend stratifying patients into either a low-risk or a moderate/high-risk group for those who may be at risk for a more complicated disease course, such as the future development of stricturing, penetrating, or perianal disease.
By identifying high-risk patients at their Crohn's diagnosis or during disease monitoring, we can tailor treatments to prevent disease progression and optimize care.
Today, I'll cover three main aspects of risk stratification in Crohn's disease, including clinical and demographic factors, tools for assessment, and treatment strategies based on risk.
Turning to clinical and demographic risk factors, certain patient characteristics are associated with high risk of more complicated disease. Those factors include age of onset. Early-onset disease, such as at younger than 30 years of age, is associated with a more severe, aggressive course of Crohn's disease. Pediatric-onset Crohn's disease, in particular, carries a very high risk of progression.
In terms of disease location and behavior, ileal and ileocolonic involvement are also linked with a higher risk of stricturing and penetrating disease compared to colonic disease in Crohn's. Perianal disease is also a major predictor of complications and often requires early biologic therapy, which we'll be discussing in a bit. Other factors include upper gastrointestinal involvement, such as the duodenum and the stomach, and a large distribution of bowel inflammation.
Family history and genetics may also play a role. A strong family history of Crohn’s increases the risk of a more severe disease course, although genetics alone do not determine the disease. Certain genes that have been associated with a more severe course include the NOD2, ATG16L1, and IL23R genes.
In addition to genetics, smoking has been strongly associated with a more severe disease course, including an increased risk of future surgery and decreased response to our medical therapies. The last important clinical factor is, of course, the history of having a previous surgery for Crohn's disease. These are the most important clinical and demographic factors for assessing risk.
Turning to how to assess for these factors, including the use of biomarkers, endoscopy, and radiography, we can use these tools to further risk stratify our patients. Stool and serum biomarkers are critically important for this, and we all have familiarity using C-reactive protein and fecal calprotectin.
Endoscopy can be also used to assess for markers of a more severe disease, including deep ulcers on colonoscopy, the presence of anatomic abnormalities such as strictures, and we often will use the Simple Endoscopic Score for Crohn's Disease (SES-CD) to quantify disease activity, and of course, measure response to treatment.
We just mentioned biomarkers and endoscopy. What about imaging? Imaging is also a critical aspect of risk stratification. We often use cross-sectional axial imaging, such as magnetic resonance enterography and computed tomography enterography, to help us detect transmural inflammation and anatomic complications we were discussing such as strictures, fistulae, and other penetrating complications.
Imaging can be also used to assess bowel thickening and other complications, including intra-abdominal abscess, which can help indicate a more severe phenotype that requires early medical or surgical intervention.
Now that we've discussed the important factors that are associated with the risk stratification and how to measure it, how do we tailor treatment based on this assessment?
Treatment should be individualized to prevent disease progression and complications, again, based on how we have stratified our patients into low- or moderate/high-risk, and of course, disease activity based on these tools.
To remind everyone, low-risk patients are those who have Crohn's with isolated colonic disease, no deep ulcers, low or normal biomarkers, and no perianal disease. These are patients, particularly whom have moderate or mild disease activity, who could be considered for more of a step-up approach. Early initiation of advanced therapy would be required for any refractoriness or evidence of progression.
High-risk patients include those of a young age at diagnosis, with ileal or ileocolonic disease, deep ulcers on colonoscopy, the presence of perianal disease, high biomarkers, and imaging findings demonstrating anatomic abnormalities of severe activities such as stricturing and penetrating disease.
These are patients who we need to be very aggressive with early. These patients should be considered for top-down therapy, so starting with our most effective therapies for these individual patients. These include biologics, and then for refractoriness, considering small molecules, specifically JAK inhibitors.
These are also patients who fit in the high-risk group who could be considered for a proactive therapeutic drug monitoring to optimize treatment response when initiating biologic therapies, specifically anti-TNF agents.
There are some special considerations here. Patients with perianal disease should be given anti-TNF therapy early, with possible surgical intervention if required. Those with fibrostenotic disease may require endoscopic dilation and/or surgery as well, early, to prevent longer-term complications.
In conclusion, risk stratification in Crohn's disease integrates clinical, biomarker, endoscopic, and radiographic findings to guide personalized treatment. Early identification of high-risk patients allows for timely initiation of effective therapies, helps us reduce complications, and improves long-term outcomes for our patients with Crohn's disease.
Thank you.
COMMENTARY
Crohn’s Risk Stratification: Optimizing Patient Care
DISCLOSURES
| March 05, 2025This transcript has been edited for clarity.
I'm Jordan Axelrad, co-director of the Inflammatory Bowel Disease Center at NYU Langone Health. I'm going to be discussing risk stratification in Crohn's disease.
Assessing disease activity, severity, and risk stratification in Crohn's disease is essential to guide early and effective therapy, reduce complications, and improve long-term outcomes. Two commonly used systems for assessing disease activity are the Crohn's Disease Activity Index (CDAI), and the Harvey-Bradshaw Index (HBI). They correlate with each other, but the Crohn's disease activity scoring systems rely on subjective symptoms.
In addition to the clinical parameters just mentioned, societies such as the American Gastroenterological Associations (AGA) recommend stratifying patients into either a low-risk or a moderate/high-risk group for those who may be at risk for a more complicated disease course, such as the future development of stricturing, penetrating, or perianal disease.
By identifying high-risk patients at their Crohn's diagnosis or during disease monitoring, we can tailor treatments to prevent disease progression and optimize care.
Today, I'll cover three main aspects of risk stratification in Crohn's disease, including clinical and demographic factors, tools for assessment, and treatment strategies based on risk.
Turning to clinical and demographic risk factors, certain patient characteristics are associated with high risk of more complicated disease. Those factors include age of onset. Early-onset disease, such as at younger than 30 years of age, is associated with a more severe, aggressive course of Crohn's disease. Pediatric-onset Crohn's disease, in particular, carries a very high risk of progression.
In terms of disease location and behavior, ileal and ileocolonic involvement are also linked with a higher risk of stricturing and penetrating disease compared to colonic disease in Crohn's. Perianal disease is also a major predictor of complications and often requires early biologic therapy, which we'll be discussing in a bit. Other factors include upper gastrointestinal involvement, such as the duodenum and the stomach, and a large distribution of bowel inflammation.
Family history and genetics may also play a role. A strong family history of Crohn’s increases the risk of a more severe disease course, although genetics alone do not determine the disease. Certain genes that have been associated with a more severe course include the NOD2, ATG16L1, and IL23R genes.
In addition to genetics, smoking has been strongly associated with a more severe disease course, including an increased risk of future surgery and decreased response to our medical therapies. The last important clinical factor is, of course, the history of having a previous surgery for Crohn's disease. These are the most important clinical and demographic factors for assessing risk.
Turning to how to assess for these factors, including the use of biomarkers, endoscopy, and radiography, we can use these tools to further risk stratify our patients. Stool and serum biomarkers are critically important for this, and we all have familiarity using C-reactive protein and fecal calprotectin.
Endoscopy can be also used to assess for markers of a more severe disease, including deep ulcers on colonoscopy, the presence of anatomic abnormalities such as strictures, and we often will use the Simple Endoscopic Score for Crohn's Disease (SES-CD) to quantify disease activity, and of course, measure response to treatment.
We just mentioned biomarkers and endoscopy. What about imaging? Imaging is also a critical aspect of risk stratification. We often use cross-sectional axial imaging, such as magnetic resonance enterography and computed tomography enterography, to help us detect transmural inflammation and anatomic complications we were discussing such as strictures, fistulae, and other penetrating complications.
Imaging can be also used to assess bowel thickening and other complications, including intra-abdominal abscess, which can help indicate a more severe phenotype that requires early medical or surgical intervention.
Now that we've discussed the important factors that are associated with the risk stratification and how to measure it, how do we tailor treatment based on this assessment?
Treatment should be individualized to prevent disease progression and complications, again, based on how we have stratified our patients into low- or moderate/high-risk, and of course, disease activity based on these tools.
To remind everyone, low-risk patients are those who have Crohn's with isolated colonic disease, no deep ulcers, low or normal biomarkers, and no perianal disease. These are patients, particularly whom have moderate or mild disease activity, who could be considered for more of a step-up approach. Early initiation of advanced therapy would be required for any refractoriness or evidence of progression.
High-risk patients include those of a young age at diagnosis, with ileal or ileocolonic disease, deep ulcers on colonoscopy, the presence of perianal disease, high biomarkers, and imaging findings demonstrating anatomic abnormalities of severe activities such as stricturing and penetrating disease.
These are patients who we need to be very aggressive with early. These patients should be considered for top-down therapy, so starting with our most effective therapies for these individual patients. These include biologics, and then for refractoriness, considering small molecules, specifically JAK inhibitors.
These are also patients who fit in the high-risk group who could be considered for a proactive therapeutic drug monitoring to optimize treatment response when initiating biologic therapies, specifically anti-TNF agents.
There are some special considerations here. Patients with perianal disease should be given anti-TNF therapy early, with possible surgical intervention if required. Those with fibrostenotic disease may require endoscopic dilation and/or surgery as well, early, to prevent longer-term complications.
In conclusion, risk stratification in Crohn's disease integrates clinical, biomarker, endoscopic, and radiographic findings to guide personalized treatment. Early identification of high-risk patients allows for timely initiation of effective therapies, helps us reduce complications, and improves long-term outcomes for our patients with Crohn's disease.
Thank you.
Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.
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