The Use of Fecal Calprotectin in Inflammatory Bowel Disease.
نویسنده
چکیده
IB Calprotectin is a calciumand zinc-binding protein, which for practical purposes can be considered to be neutrophil-specific, although low levels are found in other phagocytic cells. Calprotectin accounts for approximately 60% of total soluble proteins in the cytosol fraction of neutrophils. Neutrophils are the common effector cells that define acute inflammation in response to a number of factors. Once the neutrophil migrates to a site of chemoattraction, the contact sets off a cascade of events leading to a respiratory burst, oxygen radical generation, and disintegration of the neutrophil with the release of its cytosolic granules (and calprotectin), which contain a variety of hydrolytic and proteolytic enzymes. In this way, the neutrophil deals with the chemoattractant but at the same time causes indiscriminate damage to its surroundings. The amount of calprotectin reflects the number of participating neutrophils in this inflammation. This has been amply confirmed in intestinal inflammatory diseases by the significant correlation between fecal calprotectin levels and other measures of acute inflammation, be it with 111indium-labeled white cell excretion or quantitative histopathologic assessment of inflammation in colonic biopsies in controls and individuals with ulcerative colitis. The correlation with histology in Crohn’s disease is somewhat less satisfactory, not because of a problem with calprotectin, but due to the patchy nature of Crohn’s disease and the fact that the small bowel is not assessed histologically. The crucial points with calprotectin are that it is highly resistant to degradation by intestinal pancreatic secretions, intestinal proteases, and bacterial degradation and that it is stable in feces at room temperature for at least a week. In short, the amount of calprotectin in feces provides a noninvasive quantitative measure of neutrophil flux to the intestine.
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ورودعنوان ژورنال:
- Gastroenterology & hepatology
دوره 13 1 شماره
صفحات -
تاریخ انتشار 2017