Elevated Calprotectin Levels Reveal Loss of Vascular Pattern and Atrophy of Villi in Ileum by Digital Chromoendoscopy and Magnification Colonoscopy in Patients with Spondyloarthritis Without Having Inflammatory Bowel Disease
View abstract on PubMed
Summary
This summary is machine-generated.Fecal calprotectin (FC) levels are elevated in spondyloarthritis (SpA) patients, correlating with intestinal inflammation and ileal damage. High FC indicates potential gut involvement, suggesting FC as a biomarker for SpA management.
Area Of Science
- Gastroenterology
- Rheumatology
- Immunology
Background
- Spondyloarthritis (SpA) is a group of inflammatory diseases affecting the spine and joints.
- Intestinal inflammation is common in SpA, but its detection can be challenging.
- Fecal calprotectin (FC) is a marker of intestinal inflammation.
Purpose Of The Study
- To investigate the correlation between fecal calprotectin (FC) levels and intestinal inflammation in SpA patients without inflammatory bowel disease.
- To assess the utility of FC as a biomarker for gut involvement in SpA.
Main Methods
- 180 SpA patients were included in the study.
- Fecal calprotectin (FC), C-reactive protein (CRP), HLA-B*27, and clinical indices were assessed.
- Digital chromoendoscopy (DCE) was performed in a subset of patients.
Main Results
- Elevated FC levels (positive FC: 27.0%, high FC: 16.0%) were observed in SpA patients.
- High FC correlated with higher functional (BASFI) and disease activity (BASDAI) scores.
- Loss of vascular pattern in the ileum (LVPI), indicative of inflammation, was associated with positive FC and symptoms like abdominal bloating and pain.
- Chronic ileal inflammation correlated significantly with high FC, LVPI, and villous atrophy.
Conclusions
- FC levels are significantly elevated in SpA patients, particularly those with ileal inflammation (LVPI).
- FC shows potential as a valuable biomarker for managing SpA, especially when joint manifestations coincide with ileal villous atrophy.
- The findings suggest a shared immune pathway contributing to chronic gut damage in SpA.
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