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.

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.

Dietary factors in relation to the distribution of duodenal ulcer in India as assessed by studies in rats.

BACKGROUND: The prevalence of duodenal ulcer is less in the northern wheat-eating regions of India and China than in the southern rice-eating areas. METHODS AND RESULTS: Experiments were conducted on rat peptic ulcer models in which controls were fed on either known ulcerogenic rice or rice plus tapioca diets or on non-ulcerogenic stock diet. By using an ulcerogenic diet and pyloric ligation, unrefined wheat, wheat bran and their respective oils were protective against ulceration. Refined wheat, wheat germ and its oil were not protective. Freshly milled rice and unmilled rice were protective, but stored rice bran and its oil increased the ulceration. Fresh rice bran oil was not ulcerogenic, but on storage, it became ulcerogenic. By using stock diet and alcohol-induced ulceration, the findings with whole wheat oil, wheat bran and wheat germ oil were confirmed. Rats fed on the stock diet subjected to pyloric ligation developed ulcers following intragastric injection of stored rice bran oil. This ulcerogenicity was counteracted by whole wheat oil. CONCLUSION: These results suggest that the factor of diet may well explain the regional differences in the prevalence of duodenal ulceration between North and South India and China where other etiologic factors are similar.

Is Helicobacter pylori the primary cause of duodenal ulceration?

Helicobacter pylori infection may not be the primary cause of duodenal ulceration in cases not associated with non-steroidal anti-inflammatory drugs, but may be a secondary complication. In developing countries with a uniformly high prevalence of H. pylori infection there are marked regional differences in the prevalence of duodenal ulcer (DU). In some countries, especially those with a low prevalence of H. pylori, 30-40% or more patients with DU may be H. pylori negative. The absence of H. pylori infection in early cases of DU is also reported. In DU patients with antral H. pylori infection, duodenal colonization by H. pylori may often be absent. After complete H. pylori eradication, recurrence of DU within 6 months in some reports is as high as 20%. The evidence suggests that high acidity and reduced duodenal mucosal resistance remain the primary causes of DU and that H. pylori infection, when present, results in chronicity. Reduced mucosal resistance results in duodenal gastric metaplasia which permits colonization of the duodenum with H. pylori from the antrum. Therefore, whatever causes reduced mucosal resistance may be the primary factor and evidence suggests that this cause may be diet related. This would explain the enigma of regional variations in DU prevalence unrelated to H. pylori prevalence.

Counting apples with oranges: a limitation of the discrimination index.

OBJECTIVES: Three consecutive diets of the Professional and Linguistic Assessment Board's multiple choice question examination in Medicine were analysed in two different ways, taking into account the responses of the candidates to the three separate specialities within medicine. DESIGN: First, discrimination indices were obtained from calculations involving all 60 questions, each with five completions. Then, the 60 questions were analysed separately in the three constituent disciplines of Surgery (15 questions), Obstetrics and Gynaecology (12 questions) and Medicine (33 questions). SETTING: Professional and Linguistic Assessment Board. RESULTS: By the first analysis, performed by considering the whole paper to be a single entity, discrimination indices for medicine were greater than for the other two disciplines: one candidate obtained a random score, i.e. one that was no better than could have arisen, with 95% confidence, by chance as predicted by the hypergeometric distribution, and reliability coefficients were high (0.87). In the second analysis, the paper was considered as three separate components and discrimination indices calculated for each discipline separately. Discrimination indices were similar in all three disciplines, there were 26 random scores, and reliability coefficients were reduced-moderately in Medicine, considerably in the other two disciplines. CONCLUSIONS: These findings emphasize the importance of defining the territory of the subject and ensuring that all the items are drawn from that territory, as well as of using a sufficiently large number of items.

Helicobacter pylori: the mouth, stomach, and gut axis.

The aim of this study was to identify the natural reservoir and route of transmission of Helicobacter pylori infection. Two hundred eight (208) dyspeptic patients (114 males, 94 females; peak age of cohort, 50-59.9) were recruited. Specimens were collected from saliva, supra- and subgingival dental plaque, tongue scrapings, and oropharyngeal swabs. At subsequent endoscopy, gastric antral biopsy was performed for the rapid urease test (RUT), microbiological culture, and, in some patients, histology. Gastric juice samples were aspirated, and in 50 patients duodenal aspirate was collected. Polymerase chain reaction (PCR) with primers targeted to the 16S rRNA sequence of H. pylori was also employed for each of the specimens. In those patients where H. pylori was detected from multiple sites (dental plaque, gastric juice, gastric biopsy, and duodenal aspirate), restriction endonuclease digestion with Hae III was performed to determine if they were epidemiologically linked. The results indicated that 15/208 patients (7%) tested positively for H. pylori by PCR in dental plaque; only 2 samples were positive by culture. In none of the other oral sites sampled was H. pylori detected by any test used in the study. Gastric juice and gastric biopsy specimens from 36/ 208 patients (17%) and 114/208 patients (55%), respectively, were positive by PCR. Duodenal aspirate from 6/50 patients (12%) also tested positively by PCR. All specimens tested by restriction endonuclease digestion with Hae III (15/15 patients) were positive in both antral biopsy and gastric juice specimens, as well as 5 specimens from the duodenal aspirate. Four of the dental plaque strains had restriction patterns similar to those of the stomach and duodenal sites, providing evidence that these sites were infected with the same strain of H. pylori. In conclusion, the results suggest that H. pylori selects the gastric mucosa as its preferred site. The detection in dental plaque could indicate that the oral cavity may act as a reservoir or sanctuary for the organism. Whether H. pylori is a resident or transient oral microorganism is still unclear, although it is more likely to be transient in nature.

Oral colonization is unlikely to play an important role in Helicobacter pylori infection.

BACKGROUND: This clinical and microbiological study investigated whether Helicobacter pylori colonizes the mouth en route to the pyloric antrum. It has been suggested that oral colonies are a source of reinfection after eradication of gastric infection. METHODS: Some 208 patients attending for routine diagnostic endoscopy for dyspepsia were recruited. Before endoscopy, samples were collected of saliva, supragingival and infragingival plaque, and swabs were taken from the tongue, mouth and pharynx. At endoscopy, gastric antral biopsies were taken for the rapid urease test, culture and histological examination. Gastric and duodenal juice samples were aspirated. Restriction nuclease digestion with HaeIII was employed on all specimens from patients in whom there was evidence of the organism in the mouth. RESULTS: H. pylori was observed in dental plaque in only 15 patients, all from the 116 who had evidence of the organism in the stomach. Restriction endonuclease digestion demonstrated that in 13 of the 15 patients the strains were identical in mouth and stomach. CONCLUSION: Oral colonization is a rare event, but does occur. Its rarity suggests that it is not an important factor in reinfection.

Quantification of swallowed saliva in aspirated gastric juice.

OBJECTIVE: The aim of this study was to test a new mathematical model of the electrolyte concentrations in basal gastric secretion and to demonstrate whether this model was better than the old formula. Previous evidence suggests that primary gastric acid secretion has an electrolyte composition of [H+] 145, [Na+] 7, [K+] 17 and [Cl] 170 mmol/l, and that this can be modified by an extragastric component consisting of duodenogastric reflux and swallowed saliva. The only quantitative measurement available to date ignores the swallowed saliva. METHOD: Under basal conditions, gastric juice was aspirated and simultaneous sampling of saliva was performed in 60 adult subjects (33 men, 27 women), aged 23-85. Na+, K+, Cl-, phenol red (marker for pyloric loss) and titratable acidity or alkalinity were measured in aspirated gastric juice, and epidermal growth factor (EGF) was measured in saliva and gastric juice. Estimates of the primary gastric acid secretion were made by two methods: (1) V(G) formula which corrects for the duodenogastric reflux and assumes that there is no swallowed saliva: and (2) V(acid) formula, a novel procedure intended to correct for swallowed saliva as well and based on the known concentrations of electrolytes in saliva secreted at varying rates. RESULTS: The mean EGF concentrations were 3.42 ng/ml in saliva, 3.40 ng/ml in gastric juice. From the relationship of EGF output versus calculated primary acid secretion, the concentration of EGF in the extragastric component could be calculated. The V(G) formula gave a zero value of EGF whilst with V(acid), the calculated concentration of salivary EGF was 3.73 ng/ml and showed close correspondence with the measured EGF concentration in spat saliva. CONCLUSION: It is concluded that the new formula is more accurate, and gives a reasonable measurement for the volume of saliva in aspirated gastric juice.

Lessons learned during the INSURRECT project (INteractive SURgical Teaching at REmote CeNtres).

The INSURRECT project began in 1993 as a collaboration between six UK universities in distance teaching of undergraduate surgery. The first year was spent in testing the network and preparing the course material. This was followed by a two-year pilot teaching course. During this phase, 108 teaching sessions were conducted, involving more than 1300 students in all. It was found that successful teaching depended on increasing the amount of audience interaction was much as possible and transmitting high-quality video pictures. Although the time taken to deliver material by interactive video was greater than for conventional lectures, both students and teachers responded favourably to the project.

Epidermal growth factor in saliva and gastric juice: response to histamine.

Epidermal growth factor (EGF) was measured in saliva and in gastric juice under basal conditions and after histamine stimulation (0.04 mg kg-1h-1). Sixty subjects studied comprised 20 normal volunteers, 20 patients with duodenal ulcer (DU), and 20 patients with non-ulcer dyspepsia (NUD). There was no difference in basal salivary EGF concentrations between control and DU or control and NUD subjects, but the EGF concentration in DU patients exceeded that in NUD patients (p < 0.05). Basal gastric juice concentrations of EGF were similar in all three groups. There was no difference between basal salivary and gastric EGF concentrations (p > > 0.05). After histamine stimulation, salivary and gastric EGF concentrations increased in all three groups: the increase was greater in gastric juice than saliva (p < 0.0001). There were no significant differences in the salivary EGF concentrations of controls and NUD patients, or controls and DU patients, but values were significantly higher when DU and NUD patients were compared (p = < 0.05). In the gastric juice, EGF increased more in DU patients than in controls or NUD patients (p < 0.05). This effect was not linked to the greater acid secretion in DU than in the other groups. There was no influence of gender or smoking on the EGF concentration. This evidence suggests that the stomach itself may be able to secrete large amounts of EGF and that histamine is a potent stimulus. It is more likely that the gastric EGF is responding to the presence of a duodenal ulcer than that lack of EGF is responsible for persistence of the ulcer.

Gastric juice epidermal growth factor concentration and Helicobacter pylori in patients with duodenal ulcer.

The level of epidermal growth factor (EGF) was measured in the basal and maximally stimulated gastric juice of 20 control subjects and 20 patients each with duodenal ulcer and non-ulcer dyspepsia. Basal gastric juice was analysed for ammonia and urea concentrations, and the [ammonia]3/[urea] ratio was used to show Helicobacter pylori status, as was the [13C]urea breath test in nine controls. There was complete concordance in the nine controls between the two methods for determining H. pylori status. Twenty-five subjects were H. pylori positive (seven with duodenal ulcer, nine with non-ulcer dyspepsia, nine controls) and 35 H. pylori negative (13, 11 and 11 respectively). In H. pylori-positive subjects, the median EGF concentrations in the stimulated secretion of patients with duodenal ulcer and without (non-ulcer dyspepsia and controls combined) were 46.7 and 18.0 ng/ml (P < 0.001), and in H. pylori-negative subjects were 40.0 and 26.5 ng/ml respectively (P < 0.01). There was no difference in EGF concentration between controls and subjects with non-ulcer dyspepsia irrespective of H. pylori status. Lack of EGF is unlikely to be a cause of duodenal ulcer. The increased EGF concentration in patients with ulcer bore no relationship to the H. pylori status of the individual. If this bacterium causes duodenal ulcer, it is not via a reduction in EGF concentration.

Broadband telemedicine: teaching on the information superhighway.

The INSURRECT project uses the SuperJANET network to link six sites in the UK for interactive teaching and learning in surgery, an area of higher education where visual information is critical to the learning process. Collaboration between the six universities allows students access to a larger pool of surgical expertise and case studies than any single institution could provide. The project expects to improve the time that medical students can devote to surgery by up to 50%, by providing both supervised and unsupervised access to important visual information and case studies. Finally, the reduction in student numbers in operating theatres should reduce the infection risk to patients. A key component of the project is the central image resource, located in London, but allowing students and surgeons access from anywhere on the network. This paper describes the development of the interactive surgical teaching system and our experience with it during the first 18 months. One subjective observation, noticed after just one term's teaching, was the improved quality of the teaching.