Issue: April 2017
March 03, 2017
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High Fecal Calprotectin Levels in Patients With Ankylosing Spondylitis Linked with IBD

Issue: April 2017
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Fecal calprotectin was linked with disease activity in patients with ankylosing spondylitis and could serve as a biomarker for the development of inflammatory bowel disease, according to recently published data.

Eva Klingberg, MD, PhD, in the Department of Rheumatology and Inflammation Research at the University of Gothenburg in Sweden, and colleagues assessed fecal calprotectin levels in 204 patients at baseline and again at 5 years. They performed ileocolonoscopy in patients with a fecal calprotectin level of at least 500 mg/kg at baseline and in patients with a level of at least 200 mg/kg after 5 years.

At both timepoints, two-thirds of patients had a fecal calprotectin level of at least 50 mg/kg. In 80% of patients, fecal calprotectin levels changed by less than 200 mg/kg between the two timepoints. Investigators found baseline fecal calprotectin was positively associated with C-reactive protein disease activity score, bath ankylosing spondylitis (AS) disease activity index, bath AS functional index, C-reactive protein, erythrocyte sedimentation rate and fecal calprotectin at 5 years. Use of NSAIDs was associated with higher levels of fecal calprotectin and tumor necrosis factor (TNF) inhibitor use was associated with lower fecal calprotectin at both timepoints. However, patients who used TNF receptor fusion proteins had significantly higher calprotectin at 5 years. In addition, 1.5% of patients had Crohn’s disease after 5 years and this was associated with baseline fecal calprotectin levels.

“On the basis of these results, we propose that fecal calprotectin may be a potential biomarker to identify patients with AS at risk of developing [inflammatory bowel disease] IBD,” the researchers wrote. “Thus, fecal calprotectin quantification should be considered, especially in patients with high disease activity and gastrointestinal symptoms.” – by Will Offit

 

Disclosure: The researchers report that the work was supported by grants from the Health and Medical Care Executive Board of the Västra Götaland, Rune and Ulla Amlövs Foundation for Rheumatology Research, Göteborg Association against Rheumatism, the Swedish Association Against Rheumatism, the Medical Society of Göteborg, and the Region Västra Götaland (agreement concerning research and education of doctors), Controlling Chronic Inflammatory Diseases with Combined Efforts (COMBINE), the Margareta Rheuma Research Foundation and the Swedish Society of Medicine.