101.   A defect in the barrir function of the intestinal mucosa has been proposed as important in both the pathogenesis and systemic mainifestations of inflammatory bowel disease.

102.   A defect in the barrier function of the intstinal mucosa has been proposed as an important factor in the pathogenesis of chronic inflammatory bowel disease.

103.   Indeed it has been proposed thatany increase in permeability in patients with inflammatory bowel disease results from polymorphonuclear transmigration through the intestinal mucosa.

104.   Control epithelial cells failed to respond to CaI, while cells from both forms of inflammatory bowel disease augmented their PAF activity.

105.   In control subjects, as well as in patients with inflammatory bowel disease, basal PAF generation by epithelial cells is similar to that of lamina propria mononuclear cells.

106.   In this context, an altered plasma pattern of polyunsaturated fatty acids has been described in inflammatory bowel disease.

107.   The data base for inflammatory bowel diseases established in our hospital has allowed us to review our experience.

108.   All patients were followed up for a minimum of two years through the inflammatory bowel diseases clinic.

109.   Because height centiles before illness were not often available, however, the impact of inflammatory bowel disease on their genetically determined growth potential cannot be completely assessed.

110.   Recent publications indicate a variety of settings -- the assessment of inflammatory bowel disease, detection of sepsis, and prognosis of acute pancreatitis being the most prominent.