Background: Fecal biomarkers are emerging tools in the assessment of mucosal healing in inflammatory bowel diseases (IBD). Goals: We aimed to evaluate the accuracy of fecal matrix metalloprotease-9 (MMP-9) and fecal lipocalin-2 (LCN-2) compared with calprotectin in detecting endoscopic activity in IBD Study: Overall, 86 IBD adults underwent colonoscopy consecutively and prospectively, with Crohn’s disease Endoscopic Index of Severity (CDEIS) in Crohn’s disease (CD) patients or Mayo endoscopic subscore calculation for ulcerative colitis (UC) patients, and stool collection. Fecal calprotectin was measured using quantitative immunochromatographic testing. Fecal MMP-9 and LCN-2 was quantified by enzyme-linked immunosorbent assay. MMP-9 and LCN-2 thresholds were determined using receiver operating curves. Results: In 54 CD patients, fecal calprotectin, MMP-9 and LCN-2 correlated with CDEIS and were significantly increased in patients with endoscopic ulcerations. MMP-9 >350 ng/g detected endoscopic ulceration in CD with a sensitivity of 90.0% and a specificity of 63.6%, compared with fecal calprotectin >250 μg/g (sensitivity=90.5% and specificity=59.1%). Fecal LCN-2 demonstrated lower performances than the 2 other biomarkers (sensitivity=85.7% and specificity=45.5%). In 32 UC patients, fecal MMP-9, LCN-2, and calprotectin levels were significantly increased in patients with endoscopic activity. In UC patients, fecal MMP-9 >900 ng/g had the best efficacy to detect endoscopic activity (sensitivity=91.0% and specificity=80.0%, compared with fecal calprotectin >250 μg/g (sensitivity=86.4% and specificity=80.0%) and LCN-2 >6700 ng/g (sensitivity=82.0% and specificity=80.0%). Conclusions: Fecal MMP-9 is a reliable biomarker in detecting endoscopic activity in both UC and CD patients.
Aims: Animal studies suggest that in alcohol withdrawal the balance of neurotransmitters gamma aminobutyric acid (GABA) and glutamate is altered. To test this in humans, we aimed to measure plasma levels of glutamate, GABA and glutamate/GABA ratio in alcoholic patients presenting with complicated AWS with the same values in non-alcohol abuser/dependent controls and to determine prognostic factors for severe withdrawal. Methods: 88 patients admitted to the emergency room for acute alcohol intoxication (DSM-IV) were prospectively included. Measurements of GABA and glutamate were performed on admission (Time 1, T1) and after 12 ± 2 h (T2). The experimental group (EG) was composed of 23 patients who presented at T2 with a severe AWS. The control group (CG) consisted of healthy subjects paired with the EG (gender and age). Logistic regression was performed in order to compare associated clinical and biological variables that could predict severe withdrawal. Results: The concentration of GABA in the EG at T1 was significantly lower than that in the CG. The concentration of glutamate in the EG at T1 was significantly higher than that in the CG. The glutamate/GABA ratio in the EG at T1 was significantly higher than the ratio in the CG. With a multivariate logistic regression model, glutamate level at admission remained the only criterion identified as a predictor of AWS at 12 h. Conclusion: Decreased synthesis of GABA and increased synthesis of glutamate might be related to withdrawal symptoms experienced on brutal cessation of chronic alcohol intake.
7 September 2015 in Journal of Crohn's and Colitis
Fecal calprotectin [fcal] is a biomarker of Crohn’s disease [CD] endoscopic activity. Identifying the endoscopic situations in which fcal is less reliable remains unexplored. We aimed to determine the endoscopic factors influencing fcal level in CD. Overall, 53 CD patients consecutively and prospectively underwent colonoscopy, with CD Endoscopic Index of Severity [CDEIS] calculation and stool collection. Fcal was measured using a quantitative immunochromatographic test. Correlation analysis was done with Pearson statistics. Fcal was correlated with CDEIS [0.66, p < 0.001]. In univariate analysis, fcal was correlated with the affected surface [0.65, p < 0.001] and the ulcerated surface [0.47, p < 0.001]. Fcal was significantly associated with ulceration depth, with median fcal of 867.5 µg/g, 1251.0 µg/g, and 1800.0 µg/g, in patients presenting with non-ulcerated lesions, superficial ulcerations [SU], and deep ulcerations [DU], respectively. Lesion locations did not influence fcal. In multivariate analysis, fcal was associated with affected surface [p = 0.04] and the presence of CD lesions. Moreover, fcal increased with the ulceration depth [p = 0.03]. However, ulcerated surface and CD location did not affect fcal. Using a receiver operating characteristic [ROC] curve, we showed that fcal of 400 µg/g was the best compromise between sensitivity [0.76] and specificity [0.77], whereas fcal ≥ 200 µg/g was highly sensitive [0.86] to detect SU or DU. Fcal is a very reliable biomarker to detect endoscopic ulcerations in CD. We suggest repeating measurement in case of intermediary results [200–400µg/g] in daily practice. Fcal level is mostly influenced by the presence of CD lesions [even non-ulcerated], in a depth-related manner and by the affected surface.