| Summary: | BACKGROUND: Pediatric patients with Inflammatory Bowel Disease (IBD) undergo costly and invasive investigations to diagnose and treat their chronic disease. To that end, it is important for researchers and physicians to continue to work to find novel tools to improve diagnosis and treatment processes. One of the main challenges is differentiating between the two main forms of IBD, Crohn disease (CD) and ulcerative colitis (UC). Physicians currently rely on a combination of endoscopic evaluations, mucosal biopsies, radiology studies, and biochemical testing to assess for the presence and extent of inflammation in the gastrointestinal (GI) tract. Serologic biomarkers can be useful to some extent, but changes in these markers do not typically reflect disease specific to the GI tract, or the state of inflammation related to a patient's IBD. In contrast, fecal biomarkers have the unique potential to provide specific information about inflammation in the GI tract. While serum antibody levels have been well studied for use in the diagnosis of patients with IBD, fecal antibody levels and anti-saccharomyces cerevisiae antibody (ASCA) in particular, have not been extensively evaluated. In this study, we will assess the dynamic range of fecal ASCA levels in acute and convalescent fecal samples collected from children and adolescents with CD and UC.
METHODS: We recruited pediatric patients from inpatient and ambulatory settings at the Gastroenterology Program at Boston Children's Hospital. Patients had a diagnosis of either CD or UC. We collected baseline stool samples during a point of active disease, and follow-up samples three to six months later during a point of inactive disease. Samples were analyzed for fecal ASCA as well as lactoferrin (FLA), another marker of inflammation that can be measured in the stool.
RESULTS: In patients with CD, fecal ASCA levels were significantly higher during active disease than during inactive disease. Additionally, fecal ASCA levels were higher in patients with CD than in patients with UC, regardless of disease activity. When compared to FLA, ASCA was shown to differentiate between CD and UC, with greater changes in the level of fecal ASCA (active - inactive) correlating with a diagnosis of CD. In patients with CD, FLA levels were significantly higher in the context of active disease than in inactive disease. However, FLA did not differentiate between CD and UC.
CONCLUSIONS: Our results suggest that fecal ASCA may be a new marker of inflammation in the GI tract. Unlike FLA, changes in fecal ASCA levels appear more dynamic in patients with CD. Future studies are required to further demonstrate both how changes in fecal ASCA may help physicians distinguish between different forms of IBD as well as how measurement of fecal ASCA may help assess disease activity and response to therapy in patients with CD.
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