Fecal calprotectin is a useful screening parameter for hepatic encephalopathy and spontaneous bacterial peritonitis in cirrhosis

Gundling, Felix; Schmidtler, F.; Hapfelmeier, Alexander; Schulte, Benjamin; Schmidt, Thomas; Pehl, C.; Schepp, Wolfgang; Seidl, H.

doi:10.1111/j.1478-3231.2011.02577.x

Cited by 50 publications

(20 citation statements)

References 29 publications

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“…Interestingly, in Child-Pugh A patients, HOMA index was independently associated with higher rate of overt HE, supporting the hypothesis that insulin resistance syndrome could promote inflammation and increased risk of overt HE. Indeed, fecal calprotectin correlated with critical flicker frequency and HE grading [16].…”

Section: Discussionmentioning

confidence: 97%

Metformin Inhibits Glutaminase Activity and Protects against Hepatic Encephalopathy

et al. 2012

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AimTo investigate the influence of metformin use on liver dysfunction and hepatic encephalopathy in a retrospective cohort of diabetic cirrhotic patients. To analyze the impact of metformin on glutaminase activity and ammonia production in vitro.MethodsEighty-two cirrhotic patients with type 2 diabetes were included. Forty-one patients were classified as insulin sensitizers experienced (metformin) and 41 as controls (cirrhotic patients with type 2 diabetes mellitus without metformin treatment). Baseline analysis included: insulin, glucose, glucagon, leptin, adiponectin, TNFr2, AST, ALT. HOMA-IR was calculated. Baseline HE risk was calculated according to minimal hepatic encephalopathy, oral glutamine challenge and mutations in glutaminase gene. We performed an experimental study in vitro including an enzymatic activity assay where glutaminase inhibition was measured according to different metformin concentrations. In Caco2 cells, glutaminase activity inhibition was evaluated by ammonia production at 24, 48 and 72 hours after metformina treatment.ResultsHepatic encephalopathy was diagnosed during follow-up in 23.2% (19/82): 4.9% (2/41) in patients receiving metformin and 41.5% (17/41) in patients without metformin treatment (logRank 9.81; p = 0.002). In multivariate analysis, metformin use [H.R.11.4 (95% CI: 1.2–108.8); p = 0.034], age at diagnosis [H.R.1.12 (95% CI: 1.04–1.2); p = 0.002], female sex [H.R.10.4 (95% CI: 1.5–71.6); p = 0.017] and HE risk [H.R.21.3 (95% CI: 2.8–163.4); p = 0.003] were found independently associated with hepatic encephalopathy. In the enzymatic assay, glutaminase activity inhibition reached 68% with metformin 100 mM. In Caco2 cells, metformin (20 mM) decreased glutaminase activity up to 24% at 72 hours post-treatment (p<0.05).ConclusionsMetformin was found independently related to overt hepatic encephalopathy in patients with type 2 diabetes mellitus and high risk of hepatic encephalopathy. Metformin inhibits glutaminase activity in vitro. Therefore, metformin use seems to be protective against hepatic encephalopathy in diabetic cirrhotic patients.

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Section: Discussionmentioning

confidence: 97%

Metformin Inhibits Glutaminase Activity and Protects against Hepatic Encephalopathy

et al. 2012

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“…Other conventional markers of gut inflammation, such as FCAL, 20 have also been shown to be non-specifically elevated in decompensated cirrhosis. 25 , 54 , 55 A relative limitation of FCAL, however, is that it is representative of mainly neutrophil activity and not of the other critical innate ( e.g. innate lymphoid cells) and adaptive ( e.g.…”

Section: Discussionmentioning

confidence: 99%

Faecal cytokine profiling as a marker of intestinal inflammation in acutely decompensated cirrhosis

et al. 2020

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Background & Aims: Gut dysbiosis and inflammation perpetuate loss of gut barrier integrity (GBI) and pathological bacterial translocation (BT) in cirrhosis, contributing to infection risk. Little is known about gut inflammation in cirrhosis and how this differs in acute decompensation (AD). We developed a novel approach to characterise intestinal immunopathology by quantifying faecal cytokines (FCs) and GBI markers. Methods: Faeces and plasma were obtained from patients with stable cirrhosis (SC; n = 16), AD (n = 47), and healthy controls (HCs; n = 31). A panel of 15 cytokines and GBI markers, including intestinal fatty-acid-binding protein-2 (FABP2), D-lactate, and faecal calprotectin (FCAL), were quantified by electrochemiluminescence/ELISA. Correlations between analytes and clinical metadata with univariate and multivariate analyses were performed. Results: Faecal (F) IL-1b, interferon gamma, tumour necrosis factor alpha, IL-21, IL-17A/F, and IL-22 were significantly elevated in AD vs. SC (q <0.01). F-IL-23 was significantly elevated in AD vs. HC (p = 0.0007). FABP2/D-lactate were significantly increased in faeces in AD vs. SC and AD vs. HC (p <0.0001) and in plasma (p = 0.0004; p = 0.011). F-FABP2 correlated most strongly with disease severity (Spearman's rho: Child-Pugh 0.466; p <0.0001; model for end-stage liver disease 0.488; p <0.0001). FCAL correlated with plasma IL-21, IL-1b, and IL-17F only and none of the faecal analytes. F-cytokines and F-GBI markers were more accurate than plasma in discriminating AD from SC. Conclusions: FC profiling represents an innovative approach to investigating the localised intestinal cytokine microenvironment in cirrhosis. These data reveal that AD is associated with a highly inflamed and permeable gut barrier. FC profiles are very different from the classical innate-like features of systemic inflammation. There is non-specific upregulation of T H 1/T H 17 effector cytokines and those known to mediate intestinal barrier damage. This prevents mucosal healing in AD and further propagates BT and systemic inflammation.

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“…Raia et al studied the concentration of FC in 30 pediatric patients with cystic fibrosis; FC levels were reported to be significantly higher compared to controls (P<0.01) and significantly lower compared to 15 patients with IBD (P<0.001) [38]. Further studies have linked higher levels of FC to small intestinal bacterial overgrowth [39], food allergy, gastroesophageal reflux disease [40], hepatic encephalopathy in patients with liver cirrhosis [41], and iatrogenic causes, such as gastric bypass surgery [42].…”

Section: Role Of Fc In Other Gi Diseasesmentioning

confidence: 99%

Clinical utility of fecal calprotectin: potential applications beyond inflammatory bowel disease for the primary care physician

Mari

Baker

Mahamid

et al. 2019

aog

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Fecal calprotectin (FC) is an inflammatory marker released mainly from gastrointestinal granulocytes measured in stool samples. FC is noninvasive, economical, simple, and acceptable for patients. Levels of FC have proven reliable for intestinal inflammation, with good clinical sensitivity, and are useful in screening and monitoring inflammatory bowel disease (IBD), as well as in the differential diagnosis between IBD and irritable bowel syndrome (IBS). Given its advantages, FC represents an attractive biomarker that could be utilized in various gastrointestinal (GI) diseases apart from IBD, and is currently being studied extensively by many research groups with significant amounts of data emerging. In this current review we aim to provide an outline of the utility of FC in distinguishing between IBS and IBD, as well as an up-to-date summary of the available clinical experience concerning FC in various common conditions of the GI tract commonly encountered by gastroenterology practitioners, such as IBS, microscopic colitis, acute gastroenteritis, Clostridium difficile infection, colorectal cancer, diverticular disease, coeliac disease, and other GI conditions.

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Fecal calprotectin is a useful screening parameter for hepatic encephalopathy and spontaneous bacterial peritonitis in cirrhosis

Abstract: Fecal calprotectin concentrations serve as a screening tool for HE and SBP. Assessment of FCCs may faciliate grading of HE-severity.

Cited by 50 publications

References 29 publications

Metformin Inhibits Glutaminase Activity and Protects against Hepatic Encephalopathy

Metformin Inhibits Glutaminase Activity and Protects against Hepatic Encephalopathy

Faecal cytokine profiling as a marker of intestinal inflammation in acutely decompensated cirrhosis

Clinical utility of fecal calprotectin: potential applications beyond inflammatory bowel disease for the primary care physician

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