61.   This review examines the evidence that abnormal oxidative metabolism is of central importance to active inflammatory bowel disease.

62.   Several points merit consideration in the evaluation of the pathogenic role of ROM in inflammatory bowel disease.

63.   Firstly, phagocytes are prominent in the mucosa of patients with active inflammatory bowel disease and can produce ROM via both the respiratory burst and prostaglandin and leukotriene metabolism.

64.   In anecdotal reports of exacerbation of inflammatory bowel disease by iron supplementation, this may be mediated by hydroxyl radical production by the Fenton reaction.

65.   Whether these concentrations of ROM resemble those found in the mucosa in inflammatory bowel disease in vivo is unclear.

66.   The aminosalicylates are far less specific agents, and it is not known which of their many pharmacological actions explains their therapeutic effect in inflammatory bowel disease.

67.   It is now clear that ROM are produced in excess in active inflammatory bowel disease.

68.   The study of humoral anc cellular immunopathogenesis of inflammatory bowel disease has received much interest.

69.   The latter has been extensively studied by Stenson, who suggested a two stage pathogenic framework for inflammatory bowel disease.

70.   In inflammatory bowel disease the initial or predisposing event is unknown.