51.   In the past, autoantibodies that have been most consistently detected in inflammatory bowel disease are those reactive to colonic cells and lymphocytes.

52.   In particular, no patients with inflammatory bowel disease or cancer were studied.

53.   To test this, biliary epithelium of inflammatory bowel disease patients without PSC needs to be examined.

54.   One potential source for the increased values of reactive oxygen species in inflammatory bowel disease is the neutrophil.

55.   This reaction has been implicated in the generation of reactive oxygen species in ischemic reperfusion injury, a mechanism which has been recently postulated for inflammatory bowel disease.

56.   It is well known that products of the cyclo-oxygenase reaction, prostaglandins, and of the lipoxygenase reaction, leukotrienes, are increased in inflammatory bowel disease.

57.   Also the specificity of our results needs to be verified as we did not study patients with other inflammatory bowel diseases.

58.   Many of the circulating moncytes in patients with inflammatory bowel disease are activated.

59.   These findings suggested that superoxide is involved in the pathogenesis of inflammatory bowel disease.

60.   Although the aetiology of inflammatory bowel disease remains unknown, its pathogenesis is gradually being unravelled.