SUMMARY To investigate factors which predispose to relapse in patients with ulcerative colitis, we conducted a survey to compare the events occurring in the four weeks preceding the clinic attendance of 62 outpatients in remission with those taking place in the same period before the onset of relapse in 21 patients attending with active disease. The only event which occurred significantly more often in patients who subsequently relapsed was ingestion of paracetamol and other inhibitors of prostaglandin synthesis (76% (16/21) relapse vs 39% (24/62) remission, p
An elevated platelet count is well recognized as a marker of inflammatory bowel disease activity. There is an increased incidence of systemic thromboembolism in this disease. Recent work indicates that platelets exhibit several proinflammatory properties including release of inflammatory mediators, and recruitment, chemotaxis and modulation of the activity of other inflammatory cells. Furthermore there is evidence that microvascular thrombosis and a procoagulant state may play a role in the pathogenesis of inflammatory bowel disease.
These observations prompted recent studies of platelet activity in inflammatory bowel disease, which indicate enhanced platelet aggregation in vivo and in vitro, and increased platelet activation as measured by increased release of intracellular proteins into plasma and expression of platelet surface markers, including P‐selectin and GP53. These abnormalities could contribute to the pathogenesis of inflammatory bowel disease by enhancing inflammation and promoting microinfarction. Aminosalicylates reduce platelet activity although they also have many other additional properties to explain their efficacy in inflammatory bowel disease. There are however several specific anti‐platelet drugs now available which may provide new therapeutic possibilities in the management of this disease.
SUMMARY In iii'o rectal dialysis was used to study rectal mucosal release of immunoreactive prostaglandin E2-like material and its relation to disease activity, rectal electrical potential difference (PD), and treatment in 24 patients with ulcerative colitis. In untreated colitics in remission and in relapse, median values for apparent mucosal prostaglandin E2 (PGE2) release were increased three-fold (P <0.05) and 13-fold (P <0-002) respectively over that found in control subjects. In patients in remission during treatment with sulphasalazine and/or corticosteroids, median apparent PGE2 release was similar to that of controls, but in colitics in relapse, despite treatment, it was greatly increased (p < 0.002). Ulcerative colitis in relapse was associated with a significant reduction in rectal PD (p < 0.002); in patients with quiescent ulcerative colitis, a smaller reduction was found (p <0.05). In nine patients studied serially before and during treatment, there were associations between changes in disease activity assessed sigmoidoscopically, in PD and in apparent mucosal PGE2 release. Furthermore, rectal mucosal PGE2 release and PD were linearly correlated (p < 00 1). These findings indicate that mucosal PGE2 release is markedly enhanced in active ulcerative colitis, and they confirm the value of rectal PD as a guide to disease activity. In addition, they suggest that rectal dialysis may be a useful way of studying rectal prostaglandin metabolism in man.
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