AGA Clinical Practice: Colorectal Dysplasia in Inflammatory Bowel Diseases

SK Murthy et al. Gastroenterol 2021: DOI: Full Text: AGA Clinical Practice Update on Endoscopic Surveillance and Management of Colorectal Dysplasia in Inflammatory Bowel Diseases: Expert Review

Some of the recommendations:

Best Practice Advice 1: Precancerous colorectal lesions in inflammatory bowel disease should be described as either polypoid (≥2.5 mm tall), nonpolypoid (<2.5 mm), or invisible (detected on nontargeted biopsy), using a modified Paris Classification. The older terms dysplasia-associated lesion or massadenoma-like mass, and flat dysplasia (when referring to dysplasia detected in nontargeted biopsies) should be abandoned.

Best Practice Advice 3: Initial colonoscopy screening for dysplasia should be performed at 8–10 years after disease diagnosis in all people with colonic inflammatory bowel disease, and immediately on diagnosis of primary sclerosing cholangitis. Staging biopsies should be taken from multiple colonic segments to assess histologic disease activity and extent and to help guide future surveillance intervals.

Best Practice Advice 8: Extensive nontargeted biopsies (roughly 4 adequately spaced biopsies every 10 cm) should be taken from flat colorectal mucosa in areas previously affected by colitis when white light endoscopy is used without dye spray chromoendoscopy or virtual chromoendoscopy. Additional biopsies should be taken from areas of prior dysplasia or poor mucosal visibility. Nontargeted biopsies are not routinely required if dye spray chromoendoscopy or virtual chromoendoscopy is performed using a high-defintion endoscope, but should be considered if there is a history of dysplasia or primary sclerosing cholangitis.

Expansive View of Endoscopy from Porto IBD Group

The pediatric IBD Porto Group of ESPGHAN has updated endoscopy guidelines: S Oliva et al. JPGN 2018; 67: 414-430.   In total, the authors make 17 recommendations –here are a few of them:

A) In non-emergency situations, the diagnostic evaluation for suspected IBD in children should include a combination of EGD and colonoscopy.  Multiple biopsies from each segment are recommended even in the absence of macroscopic disease.

B) Endoscopic evaluation is recommended for the following:

  • before major treatment changes
  • in symptomatic patients when it is not clear whether the symptoms are inflammation-related
  • in Crohn’s disease(CD) to ensure mucosal healing during clinical remission
  • in Ulcerative colitis (UC) to ensure mucosal healing during clinical remission only if fecal calprotectin is elevated

C) 6-12 months after bowel resection to identify postoperative recurrence

D) Endoscopic surveillance in pediatric UC after 10 years from the onset of disease (as early as 8 years in older children (>16 years) with risk factors like extensive disease and strong family history

E) In patients with concurrent primary sclerosing cholangitis (PSC), surveillance colonoscopy may be considered every 1-2 years, starting from time of PSC diagnosis. However, in children <12 years of age, surveillance could be postponed based on individual risk factors.

In addition to discussions of conventional endoscopy, the authors favor evaluation of small bowel inflammation: “the choice to perform CE [capsule endoscopy], MRE or both, depends on local availability and expertise.”  The authors caution to consider strictures and the potential need for patency capsule prior to CE.

Conclusion of authors: “Endoscopy in pediatric IBD provides a more definitive diagnosis and disease extent evaluation, assesses therapeutic efficacy and leads to targeted therapy, which lessens complications and progression.”

My take: While I agree that endoscopy increases our understanding of disease extent and response to treatment, I do have some concerns about the recommendations (under section B above) regarding assessment of mucosal healing.  Part of the concern is that there is not a single accepted definition of mucosal healing.  Also, as a practical matter, there needs to be a discussion of the costs and more proof that frequent endoscopy will improve outcomes; it is possible that increased use of endoscopy will lead to some detrimental outcomes in some patients based on the interpretation of the results (eg. dropping a therapy that may be helping and replacing with a less effective treatment)..

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications/diets (along with potential adverse effects) should be confirmed by prescribing physician/nutritionist.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

Brief Updates on Colorectal Cancer

“Low-Dose Aspirin Use After Diagnosis of Colorectal Cancer Does Not Increase Survival: A Case-Control Analysis of a Population-Based Cohort”  Gastroenterol 2014; 146: 700-08.  The authors performed a nested case-control analysis of a cohort of 4794 patients diagnosed with colorectal cancer.  “There was no association between low-dose aspirin usage and colon cancer-specific mortality.”  These study findings contradict previous studies.  More trials are underway.

“Reduced Risk of Colorectal Cancer Up to 10 Years After Screening, Surveillance, or Diagnostic Colonoscopy” Gastroenterol 2014; 146: 709-17.  Conclusion: “In a population-based case-control study, the risk of CRC was strongly reduced up to 10 years after colonoscopy for any indication. Risk was particularly low after screening colonoscopy, even for cancer in the right colon.”  The odds ratio for CRC after screening colonoscopy was 0.09.

NEJM 2014; 370: 1287-97.  Multitarget Stool DNA Testing for Colorectal-Cancer Screening.  Among 9989 average-risk participants, this stool DNA assay identified more cancers than a fecal immunochemical test (FIT) but had more false positives.

Related blog posts:

Are you familiar with CMMR-D?

In a recent review, CMMR-D and Lynch syndrome are reviewed (JPGN 2014; 58: 144-52). The term CMMR-D refers to constitutional mismatch repair deficiency.  This occurs when an individual inherits two MMR gene defects (rather than one gene defect in Lynch syndrome). CMMR-D can occur when a different mutation is inherited from each parent. MMR genes include MLH1, MSH2, MSH6 and PMS2.

Unlike Lynch syndrome when screening for colorectal cancer (CRC) usually starts at age 20 years or 5 years before first CRC in family, with CMMR-D screening recommendations include yearly endoscopic evaluation beginning at age 3 years or at diagnosis.  Complete management guidelines are listed in Table 4.