Introduction. Crohn's disease (CD) is a chronic inflammatory bowel disease (IBD) with periods of remission and exacerbation. Numerous studies have been conducted in order to identify the ideal marker when it comes to the inflammatory bowel diseases. In the literature, fecal calprotectin is mentioned as a marker of inflammation. Elevated levels of calprotectin can be detected in stool and they indicate the migration of neutrophils to the intestinal mucosa that occurs with intestinal inflammation. The aim. The main goal of this study was to examine the concentration of fecal calprotectin and CRP depending on the clinical, endoscopic and histological characteristics of patients with Crohn's disease and whether there is a correlation of these markers with disease activity. Methods. The research was conducted in the period from January 2015 to January 2016. The study included subjects who had been diagnosed with Crohn's disease. The study involved 45 respondents, aged 20 - 58 years. All subjects included in the study underwent a colonoscopic examination with biopsy and pathohistological analysis. Fecal calprotectin was determined in one stool sample in all subjects, and that was done quantitatively by a commercial ELISA assay. Determination of serum CRP concentrations was performed in the Central Biochemical Laboratory by standard methods. Results. Fecal concentrations of calprotectin are elevated in all three forms of the disease, while they are significantly higher in moderately severe (545 vs. 218, p ˂ 0.001) and severe forms of the disease (1000 vs. 218, p ˂ 0.001) compared to the mild form. Fecal concentrations of calprotectin are significantly higher at endoscopic grade 3 compared to the other three endoscopic grades (765.3 vs. 314, p ˂ 0.001), (765.3 vs. 392.8, p ˂ 0.001), (765.3 vs. 448.2, p ˂ 0.001). Fecal concentrations of calprotectin are significantly higher in extensive pathological findings compared to normal epithelial surface (1000 vs. 21, p ˂ 0.001) as well as in extensive pathological findings compared to focal pathological findings (1000 vs. 309, p ˂ 0.001). Conclusion. The more severe form of clinical disease activity is accompanied by higher fecal values of calprotectin and higher endoscopic grade, and a more severe histological grade of disease is accompanied by higher fecal values of calprotectin.
References
1.
Fagerhol MK, Dale I, Andersson T. A RADIOIMMUNOASSAY FOR A GRANULOCYTE PROTEIN AS A MARKER IN STUDIES ON THE TURNOVER OF SUCH CELLS. Biochemistry, Pathology and Genetics of Pulmonary Emphysema. 1981. p. 273–82.
2.
Langhorst J, Elsenbruch S, Koelzer J, Rueffer A, Michalsen A, Dobos GJ. Noninvasive Markers in the Assessment of Intestinal Inflammation in Inflammatory Bowel Diseases: Performance of Fecal Lactoferrin, Calprotectin, and PMN-Elastase, CRP, and Clinical Indices. The American Journal of Gastroenterology. 2008;103(1):162–9.
3.
Schoepfer AM, Beglinger C, Straumann A, Safroneeva E, Romero Y, Armstrong D, et al. Fecal Calprotectin More Accurately Reflects Endoscopic Activity of Ulcerative Colitis than the Lichtiger Index, C-reactive Protein, Platelets, Hemoglobin, and Blood Leukocytes. Inflammatory Bowel Diseases. 2013;19(2):332–41.
4.
Linskens RK, Van Bodegraven AA, Schoorl M, Tuynman HARE, Bartels P. Predictive Value of Inflammatory and Coagulation Parameters in the Course of Severe Ulcerative Colitis. Digestive Diseases and Sciences. 2001;46(3):644–8.
5.
Moran A, Jones A, Asquith P. Laboratory Markers of Colonoscopic Activity in Ulcerative Colitis and Crohn’s Colitis. Scandinavian Journal of Gastroenterology. 1995;30(4):356–60.
6.
Solem CA, Loftus EV, Tremaine WJ, Harmsen WS, Zinsmeister AR, Sandborn WJ. Correlation of C-Reactive Protein With Clinical, Endoscopic, Histologic, and Radiographic Activity in Inflammatory Bowel Disease. Inflammatory Bowel Diseases. 2005;11(8):707–12.
7.
Schoepfer AM, Beglinger C, Straumann A, Trummler M, Vavricka SR, Bruegger LE, et al. Fecal Calprotectin Correlates More Closely With the Simple Endoscopic Score for Crohn’s Disease (SES-CD) than CRP, Blood Leukocytes, and the CDAI. American Journal of Gastroenterology. 2010;105(1):162–9.
8.
Sipponen T, Savilahti E, Kolho KL, Nuutinen H, Turunen U, Färkkilä M. Crohnʼs disease activity assessed by fecal calprotectin and lactoferrin: Correlation with Crohnʼs disease activity index and endoscopic findings. Inflammatory Bowel Diseases. 2008;14(1):40–6.
9.
Brignola C, Campieri M, Bazzocchi G, Farruggia P, Tragnone A, Lanfranchi GA. A laboratory index for predicting relapse in asymptomatic patients with Crohn’s disease. Gastroenterology. 1986;91(6):1490–4.
10.
Gaya DR, Lyon TDB, Duncan A, Neilly JB, Han S, Howell J, et al. Faecal calprotectin in the assessment of Crohn’s disease activity. QJM: An International Journal of Medicine. 2005;98(6):435–41.
11.
Alibrahim B, Aljasser MI, Salh B. Fecal Calprotectin Use in Inflammatory Bowel Disease and Beyond: A Mini-Review. Canadian Journal of Gastroenterology and Hepatology. 2015;29(3):157–63.
12.
Brophy MB, Nolan EM. Manganese and Microbial Pathogenesis: Sequestration by the Mammalian Immune System and Utilization by Microorganisms. ACS Chemical Biology. 2015;10(3):641–51.
13.
Marshall W, Marta L, Andrew D, Ruth A. Clinical Biochemistry: Metabolic and Clinical Aspects. 2014.
14.
Ramesh G. Biomarkers in toxicology. 2014.
15.
Torres J, Mehandru S, Colombel JF, Peyrin-Biroulet L. Crohn’s disease. The Lancet. 2017;389(10080):1741–55.
16.
Odink K, Cerletti N, Brüggen J, Clerc RG, Tarcsay L, Zwadlo G, et al. Two calcium-binding proteins in infiltrate macrophages of rheumatoid arthritis. Nature. 1987;330(6143):80–2.
17.
SCHRÖDER O, NAUMANN M, SHASTRI Y, POVSE N, STEIN J. Prospective evaluation of faecal neutrophil‐derived proteins in identifying intestinal inflammation: combination of parameters does not improve diagnostic accuracy of calprotectin. Alimentary Pharmacology & Therapeutics. 2007;26(7):1035–42.
18.
Podolsky DK. Inflammatory Bowel Disease. New England Journal of Medicine. 2002;347(6):417–29.
19.
Lehmann FS, Burri E, Beglinger C. The role and utility of faecal markers in inflammatory bowel disease. Therapeutic Advances in Gastroenterology. 2015;8(1):23–36.
20.
Nielsen OH, Vainer B, Madsen SM, Seidelin JB, Heegaard NHH. Clinical Reviews. American Journal of Gastroenterology. 2000;95(2):359–67.
21.
Vermeire S, Van Assche G, Rutgeerts P. C-Reactive Protein as a Marker for Inflammatory Bowel Disease. Inflammatory Bowel Diseases. 2004;10(5):661–5.
22.
Ikhtaire S, Shajib MS, Reinisch W, Khan WI. Fecal calprotectin: its scope and utility in the management of inflammatory bowel disease. Journal of Gastroenterology. 2016;51(5):434–46.
23.
Benitez JM, Meuwis MA, Reenaers C, Van Kemseke C, Meunier P, Louis E. Role of endoscopy, cross-sectional imaging and biomarkers in Crohn’s disease monitoring. Gut. 2013;62(12):1806–16.
24.
Gomollón F, Dignass A, Annese V, Tilg H, Van Assche G, Lindsay JO, et al. 3rd European Evidence-based Consensus on the Diagnosis and Management of Crohn’s Disease 2016: Part 1: Diagnosis and Medical Management. Journal of Crohn’s and Colitis. 2017;11(1):3–25.
25.
Peyrin-Biroulet L, Loftus EV, Colombel JF, Sandborn WJ. The Natural History of Adult Crohn’s Disease in Population-Based Cohorts. American Journal of Gastroenterology. 2010;105(2):289–97.
26.
Tarabar D. Inflamatornebolesticreva. 2011.
27.
Matsuoka K, Kobayashi T, Ueno F, Matsui T, Hirai F, Inoue N, et al. Evidence-based clinical practice guidelines for inflammatory bowel disease. Journal of Gastroenterology. 2018;53(3):305–53.
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