- Email: [email protected]
184 MicroRNAs Are Differentially Expressed in Crohn's Disease
AGA Abstracts
of L-Try) or those fed with L-Try depleted (0 g/kg of L-Try) and L-Try rich-diet (4 g/kg of L-Try) without or with: 1) removed pineal gland (pinealectomy) or 2) blockade of melatonin Mel2 receptors with luzindole (20 mg/kg-d i.p.) on healing of gastric ulcers induced by acetic acid (ulcer area=28 mm2). At 9 days after ulcer induction, gastric lesions and ulcers were measured by planimetry, gastric blood flow (GBF) was determined by H2-gas clearance technique and plasma L-Try, melatonin and gastrin levels were determined by RIA and HPLC and gastric mucosal PGE2 concentrations and expression of mRNA for COX-1 and COX-2 and hypoxia inducible factor-1alpha (HIF-1α) by RT-PCR were determined. Ulcer healing was significantly accelerated in rats fed with L-Try rich diet while raising GBF at ulcer margin, plasma L-Try, melatonin and gastrin levels and mucosal generation of PGE2. This increase in ulcer healing effect was mimicked by exogenous administration of melatonin (20 mg/kg-d i.g.) or L-Try (200 mg/kg-d). In L-Try free diet the plasma levels of L-Try and melatonin levels were significantly diminished and ulcer healing was significantly delayed with the extent similar to that caused by pinealectomy. Indomethacin and rofecoxib, which attenuated PGE2 biosynthesis by ~90% and 75%, respectively, or luzindole, an antagonist of Mel2 receptors, significantly attenuated L-Try rich diet-induced acceleration of ulcer healing and the rise in the GBF. HIF-1α was downregulated but COX-1 and COX-2 mRNAs were upregulated in L-Try rich diet and melatonin-treated gastric mucosa. We conclude that endogenous melatonin synthesized from L-Try accelerates ulcer healing via interaction with Mel2 receptors, an enhancement of gastric microcirculation, probably mediated by PGE2 derived from COX-1 and COX-2 overexpression and activity and increase in gastrin which exerts trophic influence on gastric mucosa.
necessary to determine the roles of each of these microRNAs in the pathogenesis of inflammatory bowel disease (IBD). These findings may result in the development of microRNA-based therapies and diagnostic tests for IBD. 185 An Exploratory Investigation of the Utility of the Immunknow™ Assay in Inflammatory Bowel Disease Louis Cohen, Rui Wang, Hang Lee, Joshua R. Korzenik Background and Aims Current methods for measuring disease activity and monitoring therapy in Inflammatory Bowel Disease (IBD) are inadequate. The Immuknow® assay was developed to measure CD4 cell ATP levels as a surrogate for immune cell function. This assay is used in the transplant population to monitor immunosuppressive therapy, independent of the particular medication utilized. The primary aim of this cross sectional pilot study is to assess if the Immuknow® assay is a clinically useful measure of disease activity, immune system function and therapeutic efficacy in patients with IBD. Methods Consecutive patients with IBD were enrolled at the Massachusetts General Hospital IBD Center. Patients were stratified according to disease activity - Harvey Bradshaw Index (HBI) for Crohn's Disease (CD) and Simple Colitis Activity Index (SCAI) for Ulcerative Colitis (UC). Erythrocyte sedimentation rate (ESR) and c reactive protein (CRP) were drawn in addition to CD4 cell ATP levels. Results 70 patients were enrolled in the study - 35 with active disease and 35 with inactive disease as defined by disease activity indices. A significant association was observed with both CD and UC clinical indexes of activity. The Immuknow® score was significantly correlated by spearman rank test with both the HBI (r 0.4 p 0.004) and SCAI (r 0.5 p 0.03), the primary specific endpoint of the study. No significant correlation was identified between CRP or ESR and either SCAI or HBI. Immuknow® did correlate with CRP (r 0.4 p 0.007) but not with ESR. Conclusion This pilot study revealed a significant correlation between the Immuknow® score and clinical disease activity indices in IBD, where traditional markers of inflammation (ESR,CRP) did not. Immuknow® may offer a novel measure of disease activity while providing greater insight into a patient's immune status. Larger studies are warranted to fully investigate the use of the Immuknow® score as an inflammatory marker in IBD and potentially to monitor response to therapy.
183 Altered Expression of a Stem Cell Marker DCAMKL1 in the Gastric Epithelium with Regeneration, Metaplasia and Dysplasia Miho Kikuchi, Hiroshi Nagata, Toshifumi Hibi Lineages in the fundic mucosa arise from a stem cell zone in the isthmus of glands. Tumorigenesis is thought to arise in the stem cell. Intestinal-type gastric adenocarcinoma progresses through atrophic gastritis, intestinal metaplasia and dysplasia. Recent studies indicated that Doublecortin calcium/calmodulin-dependent protein kinase-like-1 (DCAMKL1) can mark stem cells in the normal gastrointestinal mucosa. The purpose of this study was to elucidate behavior of the cells specifically expressed for DCAMKL1 during the process of mucosal regeneration, intestinal metaplasia and dysplasia. METHODS: We employed immunohistochemical analysis to visualize DCAMKL1-expressing cells in the acetic acid-induced chronic ulcer, irradiation-induced intestinal metaplasia and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced dysplasia of the rat stomach. RESULTS: In the normal fundic mucosa, DCAMKL1 cells lied above mucous neck cells. In the mucosa surrounding the ulcer, parietal cells and mucous neck cells were lost, while hyperplasia of foveolar cells was evident. Trefoil factor family 2 (TFF2)/ spasmolytic polypeptide (SP)-stained cells were present at the base of the fundic glands and displayed more intense staining, consistent with the SP-expressing metaplasia (SPEM). DCAMKL1-positive cells were dispersedly present between foveolar cells and juxtaposed to SPEM cells. PCNA cells were also distributed in the vicinity of SPEM, and some PCNA cells were coexpressed in SPEM. In the process of regeneration, the TFF2 cell population expanded in the gland, and PCNA cells and DCAMKL1 cells were repopulated above and beneath the TFF2 cells. In the irradiated rat, SPEM was present below the mucosa showing intestinal metaplasia, and DCAMKL1 expression was observed at the base of the metaplastic epithelium. In the rat treated with MNNG, cystic dilation of glands with dysplasia was elicited around SPEM. The dysplastic cells were stained with TFF2, DCAMKL1and PCNA, while they were expressed in different dysplastic cells. CONCLUSIONS: DCAMKL1 shows distinct expression profiles during the process of ulcer healing, intestinal metaplasia and dysplasia, and its expression is associated with TFF2. In the regenerative mucosa, SPEM emerges, and the stem cell zone is repositioned downward to the gland base. The stem cell zone is present above and below TFF2 cells, and this may support bidirectional lineage reconstruction. In the mucosa showing intestinal metaplasia, DCAMKL1 is expressed in the cells, compatible with the crypt. This indicates that DCAMKL1 is a common stem cell marker in the gastrointestinal tract. Furthermore, DCAMKL1 is a putative marker for gastric precancer cells.
186 Ulcerative Colitis: Fecal Calprotectin Correlates Closely with the Endoscopically Assessed Disease Activity Alain Schoepfer, Christoph Beglinger, Alex Straumann, Pietro Renzulli, Frank Seibold Background: There is a necessity for a reliable non-invasive marker to track the activity of Ulcerative Colitis (UC). The Rachmilewitz score, consisting of an endoscopic and a clinical part, is a validated instrument for activity assessment. Fecal calprotectin is a marker reflecting the neutrophil migration to the intestinal mucosa. The correlation of the extent of inflammatory mucosal lesions in UC with fecal calprotectin levels is so far unknown. With the purpose to evaluate a reliable non-invasive activity marker, we determined the correlations between endoscopical-assessed disease activity and four - fecal calprotectin, clinical activity index, Creactive protein (CRP) and blood leukocytes - candidate-markers. Methods: We prospectively included UC patients undergoing colonoscopy and healthy controls. UC patients were scored endoscopically and clinically according the Rachmilewitz index. Patients and controls provided fecal samples for calprotectin measurements (cutoff for positive >50μg/mL) and blood samples for measuring CRP and leukocytes. Correlation analysis was performed using the Spearman's rank correlation coefficient. Results: Baseline values in UC patients (n= 108) compared to controls (n=48): Calprotectin: 449±351 vs 9.1±3μg/mL (P<0.001), CRP 11.8±14.3 vs <3mg/L (P<0.001), blood leukocytes 9.2±3.2 vs 5.4±1.6G/L (P<0.001). Fecal calprotectin correlated closest with endoscopic disease activity (Spearman's correlation coefficient r = 0.885), followed by clinical disease activity score (r = 0.712), then CRP (r = 0.619), and blood leukocytes (r = 0.503). The overall accuracy for detection of endoscopically active disease (score ≥4) was 89% for calprotectin, 75% for clinical activity index, 70% for blood leukocytosis, and 66% for elvevated CRP. Calprotectin levels were significantly different in UC patients with inactive disease (endoscopic score 0-3, mean calprotectin 46±19μg/mL), from patients with mild (score 4-6, calprotectin 203±124μg/mL, P<0.001), moderate (score 7-9, calprotectin 586±163μg/mL, P<0.001), and severe disease (score 10-12, calprotectin 843±259μg/mL, P<0.001) Conclusions: Among non-invasive markers, fecal calprotectin correlates best with endoscopically-assessed activity index, followed by the Rachmilewitz clinical activity index, CRP, and blood leukocytes. Fecal calprotectin is therefore a valuable instrument for assessment of disease activity in UC.
184 MicroRNAs Are Differentially Expressed in Crohn's Disease Feng Wu, Simin Zhang, Yuriko Mori, Theodore M. Bayless, Stephen J. Meltzer, John H. Kwon Background: MicroRNAs, a group of small, non-coding RNAs encoded in the human genome, are increasingly recognized as major negative regulators of gene expression in many processes, including development, cancer and inflammation. We previously demonstrated that microRNAs are differentially expressed in ulcerative colitis and regulate epithelial cell chemokine expression. However, the expression of microRNAs in Crohn's disease (CD) has not been studied. Aim: To determine whether microRNAs are differentially expressed in ileal and colonic CD. Methods: Endoscopic pinch biopsies were obtained from the terminal ileum, cecum, transverse colon, sigmoid colon and rectum of normal, healthy subjects and patients with active Crohn's ileitis and colitis. MicroRNA microarrays were performed on small RNA fractions isolated from each biopsy. Differentially expressed microRNAs were validated by quantitative RT-PCR. Results: Our microarray data demonstrate that different colon regions have only slight variability in overall microRNA expression. However, 18 microRNAs are differentially expressed in the terminal ileum, when compared to other colon regions. In the terminal ileum, four microRNAs are significantly increased (miR-16, miR-21, miR-223 and miR-594) in CD, while no microRNAs are decreased. In the sigmoid colon, seven microRNAs are significantly increased (miR-20a, miR-23b, miR-106a, miR-107, miR-150, miR-191 and miR-200c) and three microRNAs are significantly decreased (miR-19b, miR422b and miR-629) in CD. The pattern of expression of these microRNAs in patients with active Crohn's ileitis and colitis is distinct from normal, healthy subjects. Conclusions: MicroRNAs are differentially expressed in active CD and these microRNAs differ by disease location. These findings further expand the possible roles of microRNAs by demonstrating the differential expression of microRNAs in Crohn's ileitis and colitis. Further studies are
AGA Abstracts
187 Comparative Evaluation of a New Semi-Quantitative, Rapid, Office-Based Strip Test with An ELISA-Based Assay for Measuring Fecal Calprotectin to Assess Intestinal Inflammation: Prospective Multicenter Clinical Study Yogesh Shastri, Oliver Schröder, Jurgen Stein INTRODUCTION: Estimation of fecal neutrophil derived protein calprotectin has been used as a non invasive marker to assess intestinal inflammation. Tests for detecting fecal calprotectin (FC) are Enzyme Linked Immunosorbent Assay (ELISA) based. They require well equipped laboratory (e.g. ELISA reader, trained technician), limiting their widespread use because of logistics and high costs. There is need for simple, rapid and cheap test to determine FC levels. Performance of a new rapid office-based strip test device and an ELISA-based assay for assessing FC were compared. AIMS & METHODS: 527 consecutive subjects [306 females] (99 with UC, 233 with CD, 107 with IBS, and 88 healthy controls)underwent 1286 stool tests [Crohn's disease (CD)-690, ulcerative colitis (UC)-401, irritable bowel syndrome-107, and healthy controls-88] for estimating FC using a commercial ELISA and the new, officebased test, which is a semi-quantitative immunochromatographic rapid strip device using monoclonal antibodies at 4 tertiary referral centers across the Rhein-Main region of Germany. Activity of inflammatory bowel disease was assessed using combination of clinical, laboratory
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of L-Try) or those fed with L-Try depleted (0 g/kg of L-Try) and L-Try rich-diet (4 g/kg of L-Try) without or with: 1) removed pineal gland (pinealectomy) or 2) blockade of melatonin Mel2 receptors with luzindole (20 mg/kg-d i.p.) on healing of gastric ulcers induced by acetic acid (ulcer area=28 mm2). At 9 days after ulcer induction, gastric lesions and ulcers were measured by planimetry, gastric blood flow (GBF) was determined by H2-gas clearance technique and plasma L-Try, melatonin and gastrin levels were determined by RIA and HPLC and gastric mucosal PGE2 concentrations and expression of mRNA for COX-1 and COX-2 and hypoxia inducible factor-1alpha (HIF-1α) by RT-PCR were determined. Ulcer healing was significantly accelerated in rats fed with L-Try rich diet while raising GBF at ulcer margin, plasma L-Try, melatonin and gastrin levels and mucosal generation of PGE2. This increase in ulcer healing effect was mimicked by exogenous administration of melatonin (20 mg/kg-d i.g.) or L-Try (200 mg/kg-d). In L-Try free diet the plasma levels of L-Try and melatonin levels were significantly diminished and ulcer healing was significantly delayed with the extent similar to that caused by pinealectomy. Indomethacin and rofecoxib, which attenuated PGE2 biosynthesis by ~90% and 75%, respectively, or luzindole, an antagonist of Mel2 receptors, significantly attenuated L-Try rich diet-induced acceleration of ulcer healing and the rise in the GBF. HIF-1α was downregulated but COX-1 and COX-2 mRNAs were upregulated in L-Try rich diet and melatonin-treated gastric mucosa. We conclude that endogenous melatonin synthesized from L-Try accelerates ulcer healing via interaction with Mel2 receptors, an enhancement of gastric microcirculation, probably mediated by PGE2 derived from COX-1 and COX-2 overexpression and activity and increase in gastrin which exerts trophic influence on gastric mucosa.
necessary to determine the roles of each of these microRNAs in the pathogenesis of inflammatory bowel disease (IBD). These findings may result in the development of microRNA-based therapies and diagnostic tests for IBD. 185 An Exploratory Investigation of the Utility of the Immunknow™ Assay in Inflammatory Bowel Disease Louis Cohen, Rui Wang, Hang Lee, Joshua R. Korzenik Background and Aims Current methods for measuring disease activity and monitoring therapy in Inflammatory Bowel Disease (IBD) are inadequate. The Immuknow® assay was developed to measure CD4 cell ATP levels as a surrogate for immune cell function. This assay is used in the transplant population to monitor immunosuppressive therapy, independent of the particular medication utilized. The primary aim of this cross sectional pilot study is to assess if the Immuknow® assay is a clinically useful measure of disease activity, immune system function and therapeutic efficacy in patients with IBD. Methods Consecutive patients with IBD were enrolled at the Massachusetts General Hospital IBD Center. Patients were stratified according to disease activity - Harvey Bradshaw Index (HBI) for Crohn's Disease (CD) and Simple Colitis Activity Index (SCAI) for Ulcerative Colitis (UC). Erythrocyte sedimentation rate (ESR) and c reactive protein (CRP) were drawn in addition to CD4 cell ATP levels. Results 70 patients were enrolled in the study - 35 with active disease and 35 with inactive disease as defined by disease activity indices. A significant association was observed with both CD and UC clinical indexes of activity. The Immuknow® score was significantly correlated by spearman rank test with both the HBI (r 0.4 p 0.004) and SCAI (r 0.5 p 0.03), the primary specific endpoint of the study. No significant correlation was identified between CRP or ESR and either SCAI or HBI. Immuknow® did correlate with CRP (r 0.4 p 0.007) but not with ESR. Conclusion This pilot study revealed a significant correlation between the Immuknow® score and clinical disease activity indices in IBD, where traditional markers of inflammation (ESR,CRP) did not. Immuknow® may offer a novel measure of disease activity while providing greater insight into a patient's immune status. Larger studies are warranted to fully investigate the use of the Immuknow® score as an inflammatory marker in IBD and potentially to monitor response to therapy.
183 Altered Expression of a Stem Cell Marker DCAMKL1 in the Gastric Epithelium with Regeneration, Metaplasia and Dysplasia Miho Kikuchi, Hiroshi Nagata, Toshifumi Hibi Lineages in the fundic mucosa arise from a stem cell zone in the isthmus of glands. Tumorigenesis is thought to arise in the stem cell. Intestinal-type gastric adenocarcinoma progresses through atrophic gastritis, intestinal metaplasia and dysplasia. Recent studies indicated that Doublecortin calcium/calmodulin-dependent protein kinase-like-1 (DCAMKL1) can mark stem cells in the normal gastrointestinal mucosa. The purpose of this study was to elucidate behavior of the cells specifically expressed for DCAMKL1 during the process of mucosal regeneration, intestinal metaplasia and dysplasia. METHODS: We employed immunohistochemical analysis to visualize DCAMKL1-expressing cells in the acetic acid-induced chronic ulcer, irradiation-induced intestinal metaplasia and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced dysplasia of the rat stomach. RESULTS: In the normal fundic mucosa, DCAMKL1 cells lied above mucous neck cells. In the mucosa surrounding the ulcer, parietal cells and mucous neck cells were lost, while hyperplasia of foveolar cells was evident. Trefoil factor family 2 (TFF2)/ spasmolytic polypeptide (SP)-stained cells were present at the base of the fundic glands and displayed more intense staining, consistent with the SP-expressing metaplasia (SPEM). DCAMKL1-positive cells were dispersedly present between foveolar cells and juxtaposed to SPEM cells. PCNA cells were also distributed in the vicinity of SPEM, and some PCNA cells were coexpressed in SPEM. In the process of regeneration, the TFF2 cell population expanded in the gland, and PCNA cells and DCAMKL1 cells were repopulated above and beneath the TFF2 cells. In the irradiated rat, SPEM was present below the mucosa showing intestinal metaplasia, and DCAMKL1 expression was observed at the base of the metaplastic epithelium. In the rat treated with MNNG, cystic dilation of glands with dysplasia was elicited around SPEM. The dysplastic cells were stained with TFF2, DCAMKL1and PCNA, while they were expressed in different dysplastic cells. CONCLUSIONS: DCAMKL1 shows distinct expression profiles during the process of ulcer healing, intestinal metaplasia and dysplasia, and its expression is associated with TFF2. In the regenerative mucosa, SPEM emerges, and the stem cell zone is repositioned downward to the gland base. The stem cell zone is present above and below TFF2 cells, and this may support bidirectional lineage reconstruction. In the mucosa showing intestinal metaplasia, DCAMKL1 is expressed in the cells, compatible with the crypt. This indicates that DCAMKL1 is a common stem cell marker in the gastrointestinal tract. Furthermore, DCAMKL1 is a putative marker for gastric precancer cells.
186 Ulcerative Colitis: Fecal Calprotectin Correlates Closely with the Endoscopically Assessed Disease Activity Alain Schoepfer, Christoph Beglinger, Alex Straumann, Pietro Renzulli, Frank Seibold Background: There is a necessity for a reliable non-invasive marker to track the activity of Ulcerative Colitis (UC). The Rachmilewitz score, consisting of an endoscopic and a clinical part, is a validated instrument for activity assessment. Fecal calprotectin is a marker reflecting the neutrophil migration to the intestinal mucosa. The correlation of the extent of inflammatory mucosal lesions in UC with fecal calprotectin levels is so far unknown. With the purpose to evaluate a reliable non-invasive activity marker, we determined the correlations between endoscopical-assessed disease activity and four - fecal calprotectin, clinical activity index, Creactive protein (CRP) and blood leukocytes - candidate-markers. Methods: We prospectively included UC patients undergoing colonoscopy and healthy controls. UC patients were scored endoscopically and clinically according the Rachmilewitz index. Patients and controls provided fecal samples for calprotectin measurements (cutoff for positive >50μg/mL) and blood samples for measuring CRP and leukocytes. Correlation analysis was performed using the Spearman's rank correlation coefficient. Results: Baseline values in UC patients (n= 108) compared to controls (n=48): Calprotectin: 449±351 vs 9.1±3μg/mL (P<0.001), CRP 11.8±14.3 vs <3mg/L (P<0.001), blood leukocytes 9.2±3.2 vs 5.4±1.6G/L (P<0.001). Fecal calprotectin correlated closest with endoscopic disease activity (Spearman's correlation coefficient r = 0.885), followed by clinical disease activity score (r = 0.712), then CRP (r = 0.619), and blood leukocytes (r = 0.503). The overall accuracy for detection of endoscopically active disease (score ≥4) was 89% for calprotectin, 75% for clinical activity index, 70% for blood leukocytosis, and 66% for elvevated CRP. Calprotectin levels were significantly different in UC patients with inactive disease (endoscopic score 0-3, mean calprotectin 46±19μg/mL), from patients with mild (score 4-6, calprotectin 203±124μg/mL, P<0.001), moderate (score 7-9, calprotectin 586±163μg/mL, P<0.001), and severe disease (score 10-12, calprotectin 843±259μg/mL, P<0.001) Conclusions: Among non-invasive markers, fecal calprotectin correlates best with endoscopically-assessed activity index, followed by the Rachmilewitz clinical activity index, CRP, and blood leukocytes. Fecal calprotectin is therefore a valuable instrument for assessment of disease activity in UC.
184 MicroRNAs Are Differentially Expressed in Crohn's Disease Feng Wu, Simin Zhang, Yuriko Mori, Theodore M. Bayless, Stephen J. Meltzer, John H. Kwon Background: MicroRNAs, a group of small, non-coding RNAs encoded in the human genome, are increasingly recognized as major negative regulators of gene expression in many processes, including development, cancer and inflammation. We previously demonstrated that microRNAs are differentially expressed in ulcerative colitis and regulate epithelial cell chemokine expression. However, the expression of microRNAs in Crohn's disease (CD) has not been studied. Aim: To determine whether microRNAs are differentially expressed in ileal and colonic CD. Methods: Endoscopic pinch biopsies were obtained from the terminal ileum, cecum, transverse colon, sigmoid colon and rectum of normal, healthy subjects and patients with active Crohn's ileitis and colitis. MicroRNA microarrays were performed on small RNA fractions isolated from each biopsy. Differentially expressed microRNAs were validated by quantitative RT-PCR. Results: Our microarray data demonstrate that different colon regions have only slight variability in overall microRNA expression. However, 18 microRNAs are differentially expressed in the terminal ileum, when compared to other colon regions. In the terminal ileum, four microRNAs are significantly increased (miR-16, miR-21, miR-223 and miR-594) in CD, while no microRNAs are decreased. In the sigmoid colon, seven microRNAs are significantly increased (miR-20a, miR-23b, miR-106a, miR-107, miR-150, miR-191 and miR-200c) and three microRNAs are significantly decreased (miR-19b, miR422b and miR-629) in CD. The pattern of expression of these microRNAs in patients with active Crohn's ileitis and colitis is distinct from normal, healthy subjects. Conclusions: MicroRNAs are differentially expressed in active CD and these microRNAs differ by disease location. These findings further expand the possible roles of microRNAs by demonstrating the differential expression of microRNAs in Crohn's ileitis and colitis. Further studies are
AGA Abstracts
187 Comparative Evaluation of a New Semi-Quantitative, Rapid, Office-Based Strip Test with An ELISA-Based Assay for Measuring Fecal Calprotectin to Assess Intestinal Inflammation: Prospective Multicenter Clinical Study Yogesh Shastri, Oliver Schröder, Jurgen Stein INTRODUCTION: Estimation of fecal neutrophil derived protein calprotectin has been used as a non invasive marker to assess intestinal inflammation. Tests for detecting fecal calprotectin (FC) are Enzyme Linked Immunosorbent Assay (ELISA) based. They require well equipped laboratory (e.g. ELISA reader, trained technician), limiting their widespread use because of logistics and high costs. There is need for simple, rapid and cheap test to determine FC levels. Performance of a new rapid office-based strip test device and an ELISA-based assay for assessing FC were compared. AIMS & METHODS: 527 consecutive subjects [306 females] (99 with UC, 233 with CD, 107 with IBS, and 88 healthy controls)underwent 1286 stool tests [Crohn's disease (CD)-690, ulcerative colitis (UC)-401, irritable bowel syndrome-107, and healthy controls-88] for estimating FC using a commercial ELISA and the new, officebased test, which is a semi-quantitative immunochromatographic rapid strip device using monoclonal antibodies at 4 tertiary referral centers across the Rhein-Main region of Germany. Activity of inflammatory bowel disease was assessed using combination of clinical, laboratory
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