Aims: Previous studies have found a positive association between Helicobacter pylori infection and colorectal adenomas. The aim of the present study was to examine this association while taking possible confounding factors into account. Methods: 98 serum samples were available from 182 patients with colorectal adenomas who entered a case-control study of colorectal adenomas and diet. The H. pylori status in patients was compared with a hospital control group and a population control group. Results: H. pylori IgG antibodies were more common in colorectal polyp patients compared with either control group, the prevalence being 79% in cases compared with 62% in both control groups. The corresponding RR was 1.4 (0.76–2.6) compared with hospital controls and 2.1 (1.1–3.9) compared with population controls. After adjusting for possible confounding variables the association between H. pylori status and adenoma risk was even more marked. There was an RR of 1.6 (0.80–3.4) compared with hospital controls and an RR of 2.6 (1.3–5.4) compared with population controls, the latter association being statistically significant. Conclusion: These findings suggest a statistically significant association between H. pylori infection and colorectal polyps. A possible mechanism might be increased gastrin levels in H. pylori-infected subjects which exhibit a trophic effect on colonic mucosa.

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Aims: Previous studies have suggested that the regular use of NSAIDs reduces the risk of colorectal adenomas. The aim of this study was to examine this association while taking possible confounding factors into account. Methods: The intake of drugs including NSAID intake during the last 20 years was assessed by means of a case-control study in 184 cases and matched hospital and community controls. Results: Overall, there were few individuals with a relevant drug intake for more than 5 years. NSAID intake for more than five years was associated with decreased risk in comparison with both control groups. The RR was 0.20 (0.04–1.04) compared with hospital and 0.21 (0.04–0.99) compared with population controls, the latter association being statistically significant. Subgroup analysis by type of drug revealed a significant protective effect only for long-term aspirin intake in relation to hospital controls, the RR being 0.09 (0.01–0.82). Conclusion: Our data support the hypothesis that there is a protective effect of NSAID intake of more than 5 years against the development of colorectal polyps.

1. The role of prostaglandins in mediating bile salt-induced diarrhoea was investigated with a colonic perfusion technique in vivo in rats either untreated or pretreated with the prostaglandin (PG) synthesis inhibitor, indomethacin. 2. Colonic perfusion with sodium deoxycholate (1 and 2 mmol/l) reduced net water and sodium absorption, whereas at a concentration of 5 mmol/l it caused net fluid secretion. Deoxycholate dose-dependently increased protein and deoxyribonucleic acid (DNA) output into the perfusion fluid and, at a concentration of 5 mmol/l, produced histological evidence of colonic mucosal damage (mucus release, goblet cell depletion, patchy epitheliolysis and inflammatory cell infiltration); histological change was less with deoxycholate at 2 mmol/l and did not occur at 1 mmol/l. 3. Output of immunoreactive prostaglandin E2 (PGE2) into the colonic perfusion fluid rose eight-, 10- and 270-fold after deoxycholate at 1, 2 and 5 mmol/l respectively. 4. Colonic perfusion with added PGE2, in concentrations 10 times lower (2.8 nmol/l) and 10 times higher (0.28 μmol/l) than those found in the perfusate after deoxycholate at 5 mmol/l did not alter mucosal function or structure. However, PGE2 in much higher concentration (0.28 mmol/l) reduced net absorption of water and sodium, increased protein output threefold and, as seen with light microscopy, produced excess surface mucus with minimal goblet cell depletion and no tissue damage. 5. Pretreatment with indomethacin reduced the colonic PGE2 output of rats perfused with deoxycholate at 2 and 5 mmol/l by 56 and 87% respectively, but the bile salt-induced changes in net water and sodium transport and DNA output were not significantly affected. The PG synthesis inhibitor reduced protein loss, goblet cell depletion and surface mucus seen after perfusion with deoxycholate at 2 mmol/l, although it did not prevent the more marked structural changes caused by deoxycholate at 5 mmol/l. 6. These results suggest that in rats prostaglandins (i) are not important mediators of the deoxycholate-induced impairment of colonic water and electrolyte transport, (ii) may contribute to the mucus secretion and goblet cell depletion produced by perfusion with deoxycholate in concentrations below those causing gross tissue damage, and that (iii) overt mucosal damage is not an essential prerequisite for prostaglandin release.

The fecal bile acid excretion pattern was investigated in 25 cholecystectomized and 26 noncholecystectomized patients as a measure for the exposure of the colonic mucosa to bile acids. Separation of free, conjugated, and sulfated bile acids was achieved by liquid-gel chromatography using DEAP Sephadex LH-20 and quantification of individual bile acids by gas-liquid chromatography. Total bile acid concentration was higher in cholecystectomized (5.33 +/- 0.71 mg/g) than in noncholecystectomized patients (3.69 +/- 0.65 mg/g). Deoxycholic acid excretion was elevated in cholecystectomized patients in three aspects: the concentration of deoxycholic acid was higher (2.92 +/- 0.39 mg/g and 1.71 +/- 0.35 mg/g, respectively), its percentage proportion of total bile acids was increased (53.9 +/- 2.8% and 41.4 +/- 3.1%, respectively), and its daily output was twice as large as that in patients without previous cholecystectomy (63.2 +/- 11.5 and 32.9 +/- 5.9 mg/day, respectively).