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P240. Faecal lactoferrin and calprotectin level in evaluation of disease phenotype in Crohn's disease

M. Manelska1, L. Paradowski1, 1Medical University in Wroclaw Poland, Clinic of Gastroenterology and Hepatology, Wroclaw, Poland

Background

Crohn's Disease phenotype depends on the natural history of the disease and is an important factor in the assessement of response to treatmeant, complications or need of surgery. Lactoferrin and calprotectin are the neutrophil-derived proteins released into mucosa and intestine lumen in the case of inflammation. Their concentration reflects local inflammation and due to predict mucosal deep healing. The aim of the study was to evaluate the clinical usefulness of determining the faecal lactoferrin and calprotectin concentration of each specific Crohn's disease phenotypes based on Montreal Classification.

Methods

70 patients with Crohn's Disease were divided into 3 groups depending on the disease phenotype defined on the basis Montreal Classification (the “B” criterion – behaviour). Patients performed laboratory, endoscopic (gastroscopy, ileocolonoscopy) and radiological (CT/MRI enterography) tests. Group B1-enrolled patients with non-stricturing, non-penetrating disease phenotype consisted of 31 patients (44.3%). The second group (B2) included patients with stricturing CD phenotype was composed of 17 (24.3%). The B3 (penetrating phenotype) included 22 patients (31.4%). Stool samples were analysed with the ELISA for assessement of lactoferrin and calprotectin concentration. Patients after extensive bowel resections or during glucocorticoid and non-steroidal anti-inflammatory drugs therapy were exluded.

Results

We found lactoferrin concentration exeeding the norm in 20/22 patients (91%) with penetrating, 10/17 (59%) in stenosing and 10/31 (32.2%) non-stricturing, non-penetrating disease. Statistically significant positive correlation was found for B1/B2 (p = 0.03) and B2/B3 (p = 0.02) groups. No correlation was found for B1/B2 group (p = 0.59). Faecal lactoferrin concentration was also evaluated in whole group fistula-presenting CD patients in relation to its concentration in stool of non-fistula presenting group. Calprotectin concentration exeeding the norm was found in 14/22 (63.5%) penetrating disease group, 13/17 (76.5%) in stricturing group and 12/31 (39%) in non-stricturing, non-penetrating group. It has been shown no correlation between the calprotectin concentration in B1 and B2 group.

Conclusion

We conclude that faecal lactoferrin concentration is valuable tool to evaluate CD phenotype, especially in differentiation penetrating disease from other types. It is dependent on higer inflammation activity in patients with fistulas. There was no evidence of such close relationship for faecal calprotectin concentration.