P111 CORRELATION OF FECAL CALPROTECTIN AND MUCOSAL BIOPSY IN IDENTIFYING SUBCLINICAL INFLAMMATION IN ULCERATIVE COLITIS PATIENTS: A PRELIMINARY STUDY

For years, the gold standard for Ulcerative Colitis (UC) remission was mucosal appearance during endoscopy. However, recent literature suggests histological or “deep” remission is important for preventing flares and maintaining clinical remission. There are now validated histological scoring systems to identify subclinical inflammation, the simplest being the Nancy Histology Index (NHI). Colonoscopy with histological evaluation is the gold standard for UC monitoring, but frequent endoscopy is not always possible. Literature reporting the utility of fecal calprotectin (FC) in detecting subclinical inflammation is limited. We seek to evaluate the correlation of FC and C-reactive protein (CRP) with NHI scores to better assess their role in detecting subclinical UC. We retrospectively evaluated clinical data and pathology slides of 69 UC patients that were collected over 6-months period at university of Kentucky. Pathology slides were scored according to NHI by a trained researcher and verified by an IBD pathologist. Presence of acute activity was defined as NHI>2. Mayo endoscopic scores (MES) were based on endoscopic reports from one expert endoscopist. Endoscopic remission was defined as MES <2. FC and CRP were recorded if collected within a month of endoscopy. FC was defined as elevated (≥120 mcg/g) or borderline (50.1–120 mcg/g). Elevated CRP was defined as (> 0.9 mg/dl). 33 of the 69 (47.8%) patients analyzed were in endoscopic remission. 17 of those 33 (51.5%) patients in endoscopic remission had acute histological activity (NHI >2). 7 (21.2%) patients with acute histological activity completed FC testing. Of the 7 who submitted FC, 4 were elevated, and 1 was borderline. 15 of the 17 NHI positive patients submitted CRP, 4 (26%) were elevated. Finally, among the 17 patients with NHI >2, four patients flared within a year (Table 1). In these 4 flared patients, FC was abnormal in 3 patients. CRP was negative in these three patients. One patient did not complete a FC or CRP. Conversely, of the 16 patients with quiescent UC and NHI <2 only 1 patient flared within a year. FC and CRP were not completed at the time of endoscopy. We successfully identified an important subset of UC patients in clinical and endoscopic remission with active histological activity. Most patients in this subset had elevated fecal calprotectin levels. This suggests fecal calprotectin can be used for disease monitoring to proactively identify subclinical activity before disease flare. Our findings suggest that biopsies should be performed in all UC patients even in the absence of endoscopic abnormality, and fecal calprotectin should be ordered at regular intervals to pre-emptively detect and prevent UC flares.