P174 Capsule endoscopy findings and faecal calprotectin levels predict clinical relapse in patients with quiescent small bowel Crohn’s disease
S. Ben-Horin1, U. Kopylov*2, A. Lahat1, D. Yablecovitch1, S. Neuman1, N. Levhar1, E. Klang3, B. Avidan2, B. Weiss4, H. Yanai5, I. Dotan5, Y. Chowers6, M. M. Amitai3, R. Eliakim2
1Chaim Sheba Medical Centre, Gastroenterology, Ramat Gan, Israel, 2Sheba Medical Centre, Gastroenterology, Tel Hashomer, Israel, 3Sheba Medical Centre, Department of Diagnostic Imaging, Tel Hashomer, Israel, 4Edmond and Lily Safra Children’s Hospital, Gastroenterology, Tel Hashomer, Israel, 5Tel Aviv Medical Centre, IBD Centre, Department of Gastroenterology and Liver Diseases, Tel Aviv, Israel, 6Rambam Health Care Campus, Haifa, Israel; Bruce & Ruth Rappaport School of Medicine, Technion Israel Institute of Technology, Gastroenterology, Haifa, Israel
There is increasing recognition of the need for better monitoring of Crohn’s disease patients to identify patients at risk of development of clinical exacerbations and long-term complications. Frequently, clinical exacerbation or disease complications may follow a period of complete remission. Early identification of factors associated with such imminent risk of relapse may allow for early intervention and possible reduction of both short and long-term complications.
The study aim was to identify predictors of clinical relapse in patients with quiescent small bowel disease using non-invasive monitoring modalities such as small bowel capsule endoscopy (CE), magnetic resonance enterography (MRE) and inflammatory biomarkers.
Patients with known quiescent small bowel Crohn’s disease (CD) for at least 3 months (CDAI < 220) were prospectively recruited, and they underwent MRE, followed by Agile patency capsule. If patency was proven, CE was performed. C-reactive protein (CRP) and faecal calprotectin (FC) were evaluated for their association with clinical activity, MRE and CE findings. The Lewis score (LS) was calculated for each tertile. Significant small bowel (SB) inflammation was defined as LS > 790. Patients were followed by serial assessment of CRP and FCP (every 3 months), CE (biannually), and MRE (annually). The main study endpoint was the development of clinical relapse
In total, 62 patients were recruited; 1 patient was excluded from the study after a failure to excrete the first capsule; 2 patients left the study because of pregnancy, and 3 withdrew consent. Moreover, 12 out of the enrolled 56 patients developed a relapse after a mean follow-up duration of 6.6 ± 5 months. Baseline parameters predicting later clinical relapse were the presence of significant endoscopic inflammation (LS > 790) (odds ratio [OR] 10.9, 95% confidence interval (CI) 2.5–47.8), p = 0.002), significant proximal small bowel disease (LS > 790 in the proximal small bowels) (OR 14.3, 95% CI 1.4–154.3, p = 0.03), and elevated initial FC (336 ± 494 µg/g vs 87 ± 84 µg/g, p = 0.02). At follow-up evaluations, aggravation of the small bowel inflammation (mean LS of 1 434 ± 1 253 vs 13 ± 513, p = 0.006), and further elevation of FC levels (1 444 ± 1 276 µg/g vs -35 ± 449 µg/g) were found as additional predicting factors. Other clinical, imaging or laboratory parameters such as the Montreal classification, elevated CRP, active disease on MRE, or choice of medical treatment, were not predictive of clinical relapse.
Monitoring CD patients with quiescent disease with faecal calprotectin and capsule endoscopy can identify CD patients at risk of clinical relapse. The benefit of early therapeutic intervention in these patients merits evaluation in future prospective studies.