Abstract:Background:Anastomotic recurrence is frequent in patients with Crohn’s disease (CD)
following ileocecal resection. The degree of endoscopic recurrence,
quantified by the Rutgeerts score (RS), correlates with risk of clinical and
surgical recurrence. Several studies demonstrate the accuracy of fecal
calprotectin (FC) for detection of endoscopic recurrence, however the
optimal threshold FC value remains to be established. The aim of our
meta-analysis was to evaluate the accuracy of common FC cut-offs for
detecti… Show more
“…Another recent meta-analysis showed that an FC cutoff of 150 μg/g could be used to detect a postoperative endoscopic recurrence of Crohn's disease (pooled sensitivity was 0.70 [95% CI, 0.59 to 0.81], specificity, 0.69 [95% CI, 0.61 to 0.77], and DOR, 5.92 [95% CI, 2.61 to 12.17]). 46 Researchers disagree on whether FC can accurately detect intestinal inflammation in both the small and large bowels. Some studies report that FC can detect Crohn's disease throughout the intestinal tract, 20,47 but others have suggested a lower degree of accuracy for diagnosis in the small intestine.…”
Background/Aims: The diagnosis of small bowel Crohn's disease with negative ileocolonoscopic findings has been challenging. Fecal calprotectin (FC) has been used to detect colonic inflammation, but its efficacy for detecting small bowel inflammation is less established. We performed an updated meta-analysis to evaluate the diagnostic accuracy of FC to detect active small bowel inflammation observed during capsule endoscopy.
Methods:We conducted a systematic literature search for studies that evaluated the correlation between small bowel inflammation and FC in patients with suspected/established Crohn's disease. We calculated the pooled sensitivity, specificity, and diagnostic odds ratios (DORs) and constructed hierarchical summary receiver operating characteristic curves for FC cutoffs of 50, 100, and 200 µg/g.
Results:Fourteen studies were eligible for the final analysis. The DORs of all FC cutoffs were significant. The highest DOR was observed at 100 µg/g (sensitivity, 0.73; specificity, 0.73; and DOR, 7.89) and was suggested as the optimal diagnostic cutoff. If we analyzed only studies that included patients with suspected Crohn's disease, the DOR was 8.96. If we analyzed only studies that included patients with a Lewis score ≥135 as a diagnostic criterion for active disease, the DOR was 10.90.Conclusions: FC has significant diagnostic accuracy for detecting small bowel inflammation, and an FC cutoff of 100 µg/g can be used as a tool to screen for small bowel Crohn's disease.
“…Another recent meta-analysis showed that an FC cutoff of 150 μg/g could be used to detect a postoperative endoscopic recurrence of Crohn's disease (pooled sensitivity was 0.70 [95% CI, 0.59 to 0.81], specificity, 0.69 [95% CI, 0.61 to 0.77], and DOR, 5.92 [95% CI, 2.61 to 12.17]). 46 Researchers disagree on whether FC can accurately detect intestinal inflammation in both the small and large bowels. Some studies report that FC can detect Crohn's disease throughout the intestinal tract, 20,47 but others have suggested a lower degree of accuracy for diagnosis in the small intestine.…”
Background/Aims: The diagnosis of small bowel Crohn's disease with negative ileocolonoscopic findings has been challenging. Fecal calprotectin (FC) has been used to detect colonic inflammation, but its efficacy for detecting small bowel inflammation is less established. We performed an updated meta-analysis to evaluate the diagnostic accuracy of FC to detect active small bowel inflammation observed during capsule endoscopy.
Methods:We conducted a systematic literature search for studies that evaluated the correlation between small bowel inflammation and FC in patients with suspected/established Crohn's disease. We calculated the pooled sensitivity, specificity, and diagnostic odds ratios (DORs) and constructed hierarchical summary receiver operating characteristic curves for FC cutoffs of 50, 100, and 200 µg/g.
Results:Fourteen studies were eligible for the final analysis. The DORs of all FC cutoffs were significant. The highest DOR was observed at 100 µg/g (sensitivity, 0.73; specificity, 0.73; and DOR, 7.89) and was suggested as the optimal diagnostic cutoff. If we analyzed only studies that included patients with suspected Crohn's disease, the DOR was 8.96. If we analyzed only studies that included patients with a Lewis score ≥135 as a diagnostic criterion for active disease, the DOR was 10.90.Conclusions: FC has significant diagnostic accuracy for detecting small bowel inflammation, and an FC cutoff of 100 µg/g can be used as a tool to screen for small bowel Crohn's disease.
“…Nevertheless, this study did not detect a significantly different levels of fecal calprotectin in patients with and without post-operative recurrence while the other studies did ( Table 2 ). A meta-analysis performed by Tham et al on examining the use of fecal calprotectin for detection of post-operative endoscopic recurrence in CD showed that a significant threshold effect was observed for fecal calprotectin values of 50, 100, 150, and 200 μg/g; while the optimal diagnostic accuracy was obtained for fecal calprotectin value of 150 μg/g, with a pooled sensitivity and specificity being 70 and 69%, respectively ( 100 ).…”
Section: Calprotectin Lactoferrin and S100a12 In Predicting Post-opmentioning
Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract mainly comprising two forms including Crohn's disease (CD) and ulcerative colitis (UC). IBD is a lifelong relapsing remitting disease and relapses occur at random patterns which are unpredictable. Fecal biomarkers have been increasingly used to assess disease activity in IBD due to their positive correlations with intestinal inflammation. Recent studies have also assessed the use of fecal biomarkers in predicting relapse and post-operative recurrence. This review provides information from global studies of using fecal calprotectin, lactoferrin and S100A12 to predict relapse in IBD. Strategies for further studies and the use of these fecal biomarkers for personalized management in IBD are also discussed.
“…Importantly, TFH cell frequencies in the peripheral blood were also significantly increased in CD patients with active intestinal inflammation as determined by fecal calprotectin concentrations above 200 mg/kg, a threshold with high sensitivity and specificity to predict the presence of postoperative recurrence ( Figure 1 B ). 19 Figure 1 TFH cell frequencies correlate with CD activity. ( A ) TFH cell frequencies in ileal biopsies of CD patients (n = 15) were significantly increased in patients with active inflammation (Simple Endoscopic Score for Crohn’s Disease [SES-CD] ≥3 points) as compared with patients in endoscopic remission (SES-CD ≤2 points).…”
Background & aims
The pathogenesis of chronic inflammatory bowel diseases (Crohn’s disease [CD] and ulcerative colitis) involves dysregulated TH1 and TH17 cell responses, which can be targeted therapeutically by the monoclonal antibody Ustekinumab directed against the joint p40 subunit of IL-12 and IL-23. These cytokines may also regulate the differentiation of T follicular helper (TFH) cells, which promote B cell function in germinal centers. However, the role of TFH cells in CD pathogenesis and impact of Ustekinumab therapy on TFH cell fate in patients are poorly defined.
Methods
Lymphocytes were isolated from peripheral blood (n=45) and intestinal biopsies (n=15) of CD patients or healthy controls (n=21) and analyzed by flow cytometry to assess TFH cell phenotypes and functions
ex vivo
. In addition, TFH cell differentiation was analyzed in the presence of Ustekinumab
in vitro
.
Results
TFH cell frequencies in the intestine as well as peripheral blood were associated with endoscopic as well as biochemical evidence of CD activity. CD patients with clinical response to Ustekinumab, but not those with response to anti-TNF antibodies, displayed reduced frequencies of circulating TFH cells in a concentration-dependent manner while the TFH phenotype was not affected by Ustekinumab therapy. In keeping with this notion, TFH cell differentiation was inhibited by Ustekinumab
in vitro
while TFH cell maintenance was not affected. Moreover, Ustekinumab therapy resulted in reduced germinal center activity in CD patients
in vivo
.
Conclusions
These data implicate TFH cells in the pathogenesis of CD and indicate that Ustekinumab therapy affects TFH cell differentiation, which may influence TFH-mediated immune functions in UST-treated CD patients.
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