(SD). Overall, release values were greater in ulcerative colitis than Crohn's disease (p<0O01). In Crohn's disease, cells obtained from histologically inflamed mucosa released significantly more 5tCr [9.7 (2.5%) n= 11] than those from non-inflamed mucosa [6-4 (1.5%) n=7, p<002] whereas, in ulcerative colitis, abnormal release values were found in 8 of 13 cell populations isolated from mucosa showing no histological evidence of active disease. In five patients with distal ulcerative colitis, cells from mucosa not apparently involved demonstrated normal 11Cr release in four of five studies despite abnormal release from cells from involved mucosa suggesting that a diffuse abnormality of the colonic epithelial cell is not usually present. These data indicate that chronic mucosal inflammation per se is associated with abnormalities of the colonic epithelial cell but that, in ulcerative colitis, the abnormality remains in many patients with quiescent disease. Identification of the local factors responsible for such an abnormality may contribute to an understanding of the pathogenesis of ulcerative colitis.The colonic epithelial cell has an increased turnover in patients with ulcerative colitis. ' The most marked increase is seen in actively inflamed mucosa but increased turnover is also found when the disease is clinically and histopathologically quiescent.4 The underlying pathogenetic mechanisms for these observations are uncertain. Increased cell turnover implies that colonic epithelial cells are being lost from the mucosa at an increased rate. Four possible mechanisms may be involved. First, proliferation per se may, by the pressure of cells migrating up the crypt, force cells from the surface of the mucosa.
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