4.3 Article

Calprotectin in ankylosing spondylitis - frequently elevated in feces, but normal in serum

期刊

SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
卷 47, 期 4, 页码 435-444

出版社

INFORMA HEALTHCARE
DOI: 10.3109/00365521.2011.648953

关键词

ankylosing spondylitis; calgranulin; calprotectin; gut; intestinal inflammation; S100A8; S100A9

资金

  1. Health and Medical Care Executive Board of the Vastra Gotaland
  2. Rune and Ulla Amlovs foundation for Rheumatology Research
  3. Goteborg's Association Against Rheumatism
  4. Medical Society of Goteborg
  5. Region Vastra Gotaland
  6. COMBINE
  7. Margareta Rheumaresearch foundation

向作者/读者索取更多资源

Objectives. To investigate indirectly the prevalence of intestinal inflammation in ankylosing spondylitis (AS) patients by assessing the levels of fecal calprotectin, to study levels of serum calprotectin in AS, and to correlate the concentrations of calprotectin in feces and serum with reported gastrointestinal symptoms, medication, and measures of disease activity. Methods. All patients fulfilling the Modified New York criteria of AS at the study centers were invited to participate. The patients answered questionnaires concerning medication, symptoms, and disease activity. Physical examination was performed, including back mobility tests. Samples of stools and blood were collected and analyzed for fecal and serum calprotectin. Results. Elevated levels of fecal calprotectin (>50 mg/kg) was found in 140 of 205 AS patients (68%). Levels of fecal calprotectin were associated with increasing age, disease duration, ESR, CRP, and serum calprotectin, but not with gastrointestinal symptoms. Fecal calprotectin was higher in patients using NSAIDs, salicylates, and proton pump inhibitors, but lower in patients using methotrexate and infliximab. Serum calprotectin levels were normal or low in 98% of AS patients and not different from the levels in healthy blood donors. Serum calprotectin levels were positively associated with ESR, CRP, WBC, and PLT. Conclusions. Two-thirds of AS patients had elevated levels of fecal calprotectin, without associated gastrointestinal symptoms. Serum calprotectin was mostly normal in AS, in contrast to various other inflammatory rheumatic diseases. We suggest that fecal calprotectin may be a marker for subclinical intestinal inflammation in AS and should be measured after stopping NSAIDs, but further endoscopic studies are needed.

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