Title of article :
Serum calprotectin levels correlate with biochemical and histological markers of disease activity in TNBS colitis
Author/Authors :
Cury، نويسنده , , Didia Bismara and Mizsputen، نويسنده , , Sender Jankiel and Versolato، نويسنده , , Clara and Miiji، نويسنده , , Luciana Odashiro and Pereira، نويسنده , , Edson and Delboni، نويسنده , , Maria Aparecida and Schor، نويسنده , , Nestor and Moss، نويسنده , , Alan C.، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2013
Pages :
5
From page :
66
To page :
70
Abstract :
AbstractBackground and aim calprotectin is elevated in patients with inflammatory bowel disease (IBD). Whether it correlates other markers of disease activity is unknown. The aim of this study was to correlate serum calprotectin with biochemical and histological measures of intestinal inflammation. als and methods olitis was induced in wistar rats, and serial blood samples were collected at 0, 3, and 12 days. Animals were subsequently sacrificed for pathological evaluation at day 12. Serum calprotectin and cytokines were measured by ELISA. Pathologic changes were classified at the macroscopic and microscopic levels. s olitis induced elevated serum calprotectin, TNF and IL-6 within 24 h. Levels of serum calprotectin remained elevated in parallel to persistence of loose stool and weight loss to day 12. Serum calprotectin levels correlated with serum levels of TNF-α and IL6 (p < 0.001), but not CRP. Animals with liquid stool had significantly higher levels of serum calprotectin than control animals. There was a correlation between macroscopic colitis scores, and levels of serum calprotectin. sion calprotectin levels correlate with biochemical and histological markers of inflammation in TNBS colitis. This biomarker may have potential for diagnostic use in patients with IBD.
Keywords :
TNBS , C-reactive protein , Inflammatory marker , Mucosal scores , Serum calprotectin
Journal title :
Cellular Immunology
Serial Year :
2013
Journal title :
Cellular Immunology
Record number :
1862480
Link To Document :
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