Faecal markers in the assessment of activity in inflammatory bowel disease

Poullis, Andrew; Foster, Russell G.; Northfield, T. C.; Mendall, Michael A.

doi:10.1046/j.1365-2036.2002.01196.x

Cited by 106 publications

(72 citation statements)

References 41 publications

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“…Moreover, the monomers S100A8 and S100A9 have been detected in urine and renal epithelial cells as well (8,9). In neutrophil cytoplasm it adds up to 60% of the cytosolic proteins (10). Calprotectin is an activator of the innate immune system.…”

Section: Discussionmentioning

confidence: 99%

“…First, it is a measure of local inflammatory activity that seems to be unaffected by a variety of conditions that result in an elevation of systemic inflammation (13,18). Second, calprotectin shows an excellent stability at room temperature for up to as long as 1 week (10,19,20). The quantification is done using the inexpensive and easy ELISA technique.…”

Section: Discussionmentioning

confidence: 99%

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Urinary Calprotectin and the Distinction between Prerenal and Intrinsic Acute Kidney Injury

Heller¹,

Frischmann²,

Grünbaum³

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives To date there is no reliable marker for the differentiation of prerenal and intrinsic acute kidney injury (AKI). We investigated whether urinary calprotectin, a mediator protein of the innate immune system, may serve as a diagnostic marker in AKI.Design, setting, participants, & measurements This was a cross-sectional study with 101 subjects including 86 patients with AKI (34 prerenal, 52 intrinsic including 23 patients with urinary tract infection) and 15 healthy controls. Assessment of urinary calprotectin concentration was by ELISA and immunohistochemistry of kidney biopsy specimens using a calprotectin antibody. Inclusion criteria were: admission to hospital for AKI stage 1 to 3 (Acute Kidney Injury Network); exclusion criteria were: prior renal transplantation and obstructive uropathy.Results Median urinary calprotectin was 60.7 times higher in intrinsic AKI (1692 ng/ml) than in prerenal AKI (28 ng/ml, p Ͻ0.01). Urinary calprotectin in prerenal disease was not significantly different from healthy controls (45 ng/ml, p ϭ 0.25). Receiver operating curve curve analysis revealed a high accuracy of calprotectin (area under the curve, 0.97) in predicting intrinsic AKI. A cutoff level of 300 ng/ml provided a sensitivity of 92.3% and a specificity of 97.1%. Calculating urinary calprotectin/creatinine ratios did not lead to a further increase of accuracy. Immunostainings of kidney biopsies were positive for calprotectin in intrinsic AKI and negative in prerenal AKI.Conclusions Accuracy of urinary calprotectin in the differential diagnosis of AKI is high. Whereas calprotectin levels in prerenal disease are comparable with healthy controls, intrinsic AKI leads to highly increased calprotectin concentrations.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Urinary Calprotectin and the Distinction between Prerenal and Intrinsic Acute Kidney Injury

Heller¹,

Frischmann²,

Grünbaum³

et al. 2011

Clinical Journal of the American Society of Nephrology

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“…6,7 Calprotectin has antimicrobial 8 -14 and antiproliferative 15 -17 properties and appears to play a regulatory role in the inflammatory process. 18 -20 Faecal calprotectin (f-Cp) concentrations are raised in patients with intestinal mucosal inflammation, 21 whereas levels in patients with IBS are similar to those in healthy individuals. 22 -24 F-Cp measurement, therefore, provides a non-invasive marker for distinguishing IBD from IBS, thereby reducing the number of unnecessary endoscopic and radiological investigations in patients presenting with chronic diarrhoea.…”

Section: Introductionmentioning

confidence: 99%

Between-assay variability of faecal calprotectin enzyme-linked immunosorbent assay kits

et al. 2012

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Background: Faecal calprotectin (f-Cp), a marker of intestinal inflammation, can be used to distinguish between functional and organic bowel disease. F-Cp, following extraction, is commonly quantified using enzyme-linked immunosorbent assays (ELISAs) but there are no data comparing the different f-Cp assays or sample extraction devices. We, therefore, evaluated and compared the performance of the Immunodiagnostik, Bü hlmann and Eurospital f-Cp ELISA assays as well as the Roche, Immunodiagnostik and ScheBo Biotech commercial faecal extraction devices. We also briefly report results from a pilot f-Cp external quality assurance (EQA) scheme. Methods: Imprecision, linearity, recovery, drift and limit of quantitation of the f-Cp assays were evaluated and between-assay variability assessed. The three commercial sample extraction devices were compared with the manual weighing method. Four faecal samples were distributed as part of a pilot EQA scheme to 15 laboratories using quantitative ELISA f-Cp assays. Results: The three f-Cp assays demonstrated adequate intra-/interbatch imprecision, linearity and recovery. The crosscomparison study and EQA data demonstrated that, for the same sample, the Bü hlmann assay reports up to 3.8 times higher f-Cp concentrations than the Immunodiagnostik and Eurospital assays. On average, the commercial extraction devices led to a 7.8-28.1% under-recovery of f-Cp in comparison to the manual weighing method. Conclusions: Laboratories should be aware of the lack of the assay standardization, as demonstrated by the between-assay variability. A comparison between f-Cp concentrations reported by these assays and clinical markers of disease severity is required in order to determine their diagnostic accuracy. The EQA scheme represents the first available programme for f-Cp.

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“…Blood and faecal markers could fulfil these criteria and may be a good diagnostic alternative. CRP, Tumour Necrosis Factor Alpha (TNFα) and microalbuminuria have been identified as useful markers of disease activity in human patients with IBD (Poullis et al, 2002;McCann et al, 2007). Nevertheless, McCann et al (2007) reported that there was no Correlation Between those parameters and clinical symptoms (CIBDAI) and his to pathological findings.…”

Section: Diagnosismentioning

confidence: 99%

“…The criteria have been developed for qualitative evaluation of endoscopic mucosal appearances Table 3 (Slovak et al, 2014). In addition, his to pathological analysis is another method for the diagnosis of IBD and objective criteria are established in dogs Table 4 (Poullis et al, 2002;McCann et al, 2007;Magro et al, 2013).…”

Section: Diagnosismentioning

confidence: 99%

Inflammatory Bowel Disease and Current Treatment Options in Dogs

Arslan¹

2017

American Journal of Animal and Veterinary Sciences

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Inflammatory Bowel Disease (IBD) is an idiopathic and chronic gastrointestinal failure of cats, dogs and some farm animals such as horses. Since the long and difficult classical therapy of the disease has various side effects such as malignancy and lymphoma, new therapeutic methods are needed. However, a safe and standardized treatment protocol has not been developed, yet. Therefore, IBD treatment is still a big dilemma for both veterinary and human medicine. In this review, IBD and new possible therapeutic alternatives were evaluated for dogs.

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Faecal markers in the assessment of activity in inflammatory bowel disease

Cited by 106 publications

References 41 publications

Urinary Calprotectin and the Distinction between Prerenal and Intrinsic Acute Kidney Injury

Urinary Calprotectin and the Distinction between Prerenal and Intrinsic Acute Kidney Injury

Between-assay variability of faecal calprotectin enzyme-linked immunosorbent assay kits

Inflammatory Bowel Disease and Current Treatment Options in Dogs

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