Dietary phosphilipids and sterols protective against peptic ulceration.

The prevalence of duodenal ulceration in regions of developing countries with a stable diet is related to the staple food(s) in that diet. A higher prevalence occurs in areas where the diet is principally milled rice, refined wheat or maize, yams, cassava, sweet potato or green bananas, and a lower prevalence in areas where the staple diet is based on unrefined wheat or maize, soya, certain millets or certain pulses. Experiments using animal peptic ulcer models showed that the lipid fraction in foods from the staple diets of low prevalence areas gave protection against both gastric and duodenal ulceration, including ulceration due to non-steroidal anti-inflammatory drugs (NSAIDs), and also promoted healing of ulceration. The protective activity was found to lie in the phospholipid, sterol and sterol ester fractions of the lipid. Amongst individual phospholipids present in the phospholipid fraction, phosphatidyl ethanolamine (cephalin) and phosphatidyl choline (Lecithin) predominated. The sterol fraction showing activity contained ß-sitosterol, stigmasterol and an unidentified isomer of ß-sitosterol. The evidence shows that dietary phytosterols and phospholipids, both individually and in combination, have a protective effect on gastroduodenal mucosa. These findings may prove to be important in the prevention and management of duodenal and gastric ulceration including ulceration due to NSAIDs.

How labile is gastric infection with H pylori?

It is known that patients infected with H pylori can spontaneously become free from infection, and that the reverse change can occur. The time-scale of these conversions is expressed as percentages per year. Since they have been investigated in terms of serology, the changes are called sero-reversion and sero-conversion respectively. Using serological evidence to investigate these phenomena is open to the criticisms that positive serology can be present in the absence of all other evidence of infection, and that a time-lag of 6-12 mo or longer can occur between eradication of the infection and sero-reversion. Investigations using direct evidence of current infection are sparse. The few that exist suggest that some individuals can seroconvert or sero-revert within six to twelve weeks. If these findings are confirmed, it means that some patients have an ability that is variable in time to resist, or spontaneously recover from, H pylori infection. Evidence suggests that the deciding factor of susceptibility is the level of gastric secretion of acid.

Differences in mucosal appearances and in relapse rates in duodenal ulceration treated with sucralfate or cimetidine.

A total of 46 patients with duodenal ulcer were randomly assigned, without the knowledge of the investigators, to treatment with cimetidine 200 mg three times daily and 400 mg at night or sucralfate 1 g four times daily followed by one year of maintenance treatment with cimetidine 400 mg at night or sucralfate 1 g twice daily, respectively, in those patients with healed ulcers. The endoscopic healing rates and relapse rates during the maintenance period were similar, four relapses occurring in each group. All four relapses in the sucralfate group occurred at 12 months and only two were symptomatic. All the cimetidine relapses were symptomatic, two occurring at six months, one at nine months, and one at 12 months. Following the one year maintenance period, 13 cimetidine patients and 11 sucralfate patients were followed up for 36 months. During the first two years, nine of 13 (69 percent) cimetidine-treated and two of 11 (18 percent) sucralfate-treated patients had relapses. During the third year, three more sucralfate-treated patients and one more cimetidine-treated patient had relapses, making a total of 10 of 13 (77 percent) and five of 11 (45 percent) in the cimetidine and sucralfate groups, respectively. Duodenal biopsy specimens obtained before and after healing and after one year of maintenance were examined by light and electron microscopy. The sucralfate group showed greater improvement after one year of maintenance therapy than did the cimetidine group, although the appearances in either group were not predictive of subsequent relapse. The results show that relapses are less frequent and occur later after sucralfate therapy and also that the morphologic appearances are more normal after treatment with sucralfate than after treatment with cimetidine.

Possible absence of Helicobacter pylori in the early stages of duodenal ulceration.

BACKGROUND: Helicobacter pylori is thought to be a cause of duodenal ulceration, but there is some evidence that it is found less often in early than in later disease. AIM: To assess the presence of H. pylori in patients undergoing endoscopy for dyspepsia, with respect to their duration of symptoms. DESIGN: Retrospective case note review. METHODS: Patients were categorized as having a history greater or less than 6 months, and as H. pylori-positive or -negative, using biopsy rapid urease, culture and PCR tests. RESULTS: Thirty-two duodenal ulcer patients with a history >6 months were all H. pylori-positive according to the PCR test; the five with a shorter history were H. pylori-negative. No patient H. pylori-negative by PCR was positive by the other tests. DISCUSSION: H. pylori was (at least) less commonly present before 6 months. It is possible that H. pylori, although nearly always present after 6 months, is not present at the onset of the disease. Confirmation of this finding would imply that infection with the organism is not the cause of duodenal ulceration, but a factor producing recurrence and chronicity.

The protective effect of Meciadanol (O-methyl-3(+)-catechin) on experimental ulceration.

Meciadanol, (O-methyl-3(+)-catechin), a histidine decarboxylase inhibitor was shown to have a marked protective action against experimental peptic ulceration in three rat models. The three methods used to induce ulceration were the instillation of absolute alcohol, pyloric ligation following an ulcerogenic South Indian diet and the instillation of rice bran oil into the stomach after pyloric ligation. Meciadanol was shown to reduce incidence, numbers and areas of ulceration and protected mast cells against degranulation and to preserve a normal vascular patterns. Furthermore, Meciadanol reduced gastric acid output and concentration in the pylorus ligation model. These results indicate that Meciadanol may be useful for the treatment of peptic ulcers in humans.