P-074 Increased Fecal Calprotectin and Penetrating Phenotype Are Strong Predictors of Small Intestinal Bacterial Overgrowth in Crohn's Disease Patients

Background: The relationship of small intestinal bacterial overgrowth (SIBO) with systemic and intestinal inflammation in patients with Crohn's disease (CD) is uncertain. We aimed to determine the prevalence of and predictors of SIBO and to explore the potential relationship between SIBO and intestinal and/or systemic inflammation in adult CD outpatients. Methods: In this cross-sectional study, between June 2013 and January 2015, 92 CD patients (34 males, 58 females, mean age 39.7 ± 12.5 yr) and 97 controls (40 men, 57 women; mean age 37.6 ± 14.2 yr) with non-chronic gastrointestinal complaints were assessed for presence of SIBO using the H2/CH4 glucose breath test (GBT). Multivariate logistic regression was performed to investigate the potential association between SIBO and demographic, disease-related data, systemic markers of inflammation (C-reactive protein and erythrocyte sedimentation rate), and biomarker of intestinal inflammation (fecal calprotectin concentration [FCC]). Results: The Crohn's and control groups were comparable according to demographics. The SIBO rate was significantly higher in CD patients than in the controls (32.6% versus 12.4%, respectively, P = 0.0008). CD patients with positive GBT results did not differ significantly from those with negative results in terms of demographics, BMI, smoking status, CD location, disease duration, previous intestinal resection, treatment with steroids, immunomodulators, or anti-TNF agent. Likewise, there was no statistically significant difference between SIBO-positive and SIBO-negative patients in terms of mean CDAI (159 versus 148, respectively; P = 0.12) and HBI score (4.3 versus 3.8, respectively; P = 0.15). Of subjects with SIBO, 25 (83.3%) had a CDAI score < 150 and 20 (66.7%) an HBI < 5. By comparison, 56 (90.3%) patients without SIBO had a CDAI score < 150 and 48 (77.4%) an HBI <5 (P > 0.05 for both comparisons). In contrast, individuals with SIBO were significantly more likely to have stricturing phenotype than SIBO-negative patients (43.3% versus 19.3%; P = 0.0015). Notably, the proportion of SIBO-positive patients with elevated FCC was significantly higher than in the SIBO-negative CD individuals (63.3% versus 12.9%, respectively; P < 0.0001). Moreover, FCC was significantly higher in SIBO-positive CD patients compared to the SIBO-negative group (median of 485.8 versus 132.7 µg/g, respectively; P = 0.004). While SIBO-positive individuals had significantly increased marker of intestinal inflammation, there was no difference in C-reactive protein or ESR between the groups. Multivariate analysis identified that the patients presenting increased FCC and stricturing disease had an odds of 9.43 (95% CI, 3.04–11.31; P <0.0001) and 3.83 (95% CI, 1.54–6.75; P = 0.025) respectively, for SIBO diagnosis. Conclusions: In CD patients, SIBO is a highly prevalent condition. Stricturing phenotype and increased FCC were strong and independent predictors of SIBO in this setting. SIBO diagnosis was associated with underlying intestinal inflammation but not with systemic inflammation in CD subjects. Clinicians need to be cognizant of this diagnosis, particularly on CD patients with concurrent intestinal inflammation and in those that present stricturing disease. An individualized screening plan followed by the timely treatment for SIBO should be carried out as part of quality of care improvement in CD individuals.