Elevated calprotectin levels reveal bowel inflammation in spondyloarthritis. Issue 7 (23rd December 2015)

• Record Type: Journal Article
• Authors: Cypers, H; Varkas, G; Beeckman, S; Debusschere, K; Vogl, T; Roth, J; Drennan, M B; Lavric, M; Foell, D; Cuvelier, C A; De Vos, M; Delanghe, J; Van den Bosch, F; Elewaut, D
• Is Part Of: Annals of the rheumatic diseases. Volume 75:Issue 7(2016)
• Page Start: 1357
• Page End: 1362
• Publication Date: 2015-12-23
• Subjects: Spondyloarthritis -- Inflammation -- Disease Activity; Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2015-208025
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Introduction: Microscopic bowel inflammation is present in up to 50% of patients with spondyloarthritis (SpA) and is associated with more severe disease. Currently no reliable biomarkers exist to identify patients at risk. Calprotectin is a sensitive marker of neutrophilic inflammation, measurable in serum and stool. Objectives: To assess whether serum and faecal calprotectin in addition to C-reactive protein (CRP) can be used to identify patients with SpA at risk of microscopic bowel inflammation. Methods: Serum calprotectin and CRP were measured in 125 patients with SpA. In 44 of these patients, faecal samples were available for calprotectin measurement. All 125 patients underwent an ileocolonoscopy to assess the presence of microscopic bowel inflammation. Results: Microscopic bowel inflammation was present in 53 (42.4%) patients with SpA. Elevated serum calprotectin and CRP were independently associated with microscopic bowel inflammation. Faecal calprotectin was also significantly higher in patients with microscopic bowel inflammation. Patients with CRP and serum calprotectin elevated had a frequency of bowel inflammation of 64% vs 25% in patients with low levels of both. When either CRP or serum calprotectin was elevated, the risk was intermediate (40%) and measuring faecal calprotectin provided further differentiation. Hence we suggest a screening approach where initially serum calprotectin and CRP are assessed and, if necessary, faecal calprotectin. The model using this scenario provided an area under the ROC curve of 74.4% for detection of bowel inflammation. Conclusions: Calprotectin measurements in stool and serum, in addition to CRP, may provide a promising strategy to identify patients with SpA at risk of bowel inflammation and could play a role in overall patient stratification.