SUMMARYThe role of arachidonic acid metabolites and the mode of action of 5-aminosalicylic acid, the active moiety of sulphasalazine and disodium azodisalicylate, in ulcerative colitis remain obscure. Therefore, experiments were performed in which the effects of medication on immunoreactive prostaglandin (PG) E2 concentrations in free faecal water were assessed using the equilibrium in vivo dialysis of faeces. Colonic PGE2 concentrations in patients with active ulcerative colitis (n= 11) ranged from 2035-18 000 pg/ml to be compared with a range of 103-188 pg/ml in healthy volunteers (n=10; p<0.001). In all healthy volunteers PGE2 concentrations decreased slightly (p<005) after disodium azodisalicylate intake 2 g/day, whereas low dose disodium azodisalicylate (0.25 g/day) caused no change. In patients with ulcerative colitis in complete clinical, sigmoidoscopic, and histologic remission withdrawal of sulphasalazine (2 g/day; n=6) increased PGE2 concentrations to values above normal levels (p<005) which returned to pretrial values (p<005) on disodium azodisalicylate (2 g/day; n=7). In conclusion, increased PGE2 in free faecal water indicates an abnormality in the colonic mucosa, even in the absence of conventional signs of inflammation. We could not confirm the hypothesis that sulphasalazine and 5-aminosalicylic acid exert their therapeutic effect through promotion of endogenous cytoprotective prostaglandins. In contrast, the observation that raised PGE2 concentrations were normalised by disodium azodisalicylate in patients with inactive ulcerative colitis suggests that subclinical disease activity was decreased by 5-aminosalicylic acid.Both cyclooxygenase and lipoxygenase products of arachidonic acid metabolism have been implicated in the pathogenesis of ulcerative colitis. The findings of increased amounts of prostanoids in faeces and rectal mucosa of patients with ulcerative colitisl-3 provided the hypothesis that prostaglandins may mediate the inflammatory response. The therapeutic effect of 5-aminosalicylic acid which is proved to be the major, though not necessarily the only active component of sulphasalazine,4 may be related to the anti-inflammatory activity of the substance which is a salicylate and a weak prostaglandin
In the nephrotic syndrome the renal loss of albumin is often insufficient to explain the hypoalbuminaemia. Studies with labelled albumin have in many cases revealed an increased ‘endogenous’ catabolism of albumin. In the present investigations the significance of abnormal gastrointestinal protein loss as a source of endogenous hypercatabolism was assessed by means of the 51Cr-albumin test. Thirteen patients were examined. In 4 a slight increase of faecal 51Cr-output was observed, in the remaining 9 faecal 51Cr-excretion was normal. It is concluded that gastrointestinal protein loss at most plays a contributory role for the endogenous hypercatabolism. Other intestinal function tests, histological and radiological examination of the small intestine were performed. The results of these investigations were normal in the majority of the patients.
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