Childhood gastrointestinal dysfunction has been recognized as the triggering elements of multiple organ failure. The causes of gastrointestinal dysfunction include: injury of intestinal barrier, release of inflammatory mediators, translocation of intestinal bacteria, gastro-intestinal mucosal ischemia and anoxia injury caused by abnormal intestinal blood flow perfusion, and apoptosis of gastrointestinal epithelial cells. To prevent and treat this disease, the mechanism of gastrointestinal mucosal protection should be clarified in various aspects. Prostaglandins (PGs) and nitric oxide (NO) have a protective effect on gastrointestinal mucosa by inhibiting acid secretion, increasing mucus and bicarbonate ion secretion and by increasing mucosal blood flow as well as inhibiting mast cell and leukocyte adhesion. Many peptides participate in the process of gastrointestinal mucosal protection and injury repair differently with transforming growth factor, pancreatic secretory trypsin inhibitor (PSTI), glucagon-like peptides-2 (GLPs-2), basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF), and epithelial growth factor (EGF). Phase II enzymes form a super-family of detoxification enzymes involving in the protection of cells from potentially harmful compounds and oxidation injury. In the trifoil peptide family, the stable structure of each peptide gives a characteristic three-loop shape and provides for exceptional resistance to proteolytic degradation. The peptides participate in mucosal repair by epithelial restitution and reconstitute the integrity of mucosa barrier. Intestinal trifoil factor (ITF) is also an endogenous peptide which could inhibit the apoptosis of epithelial cells through the NF-κB cascade regulation. Glutamine protects mucosa via three aspects: maintenance of mucosal barrier, regulation of the enteric immune function, and protection of mucosa from oxidization injury. Clinical manifestations of the disease and possible intervention approaches are also described.

Key words: gastrointestinal dysfunctions; children; pathogenesis; mucosal protection; clinical feature; diagnosis