Helicobacter pylori and perturbations in acid secretion: The end of the beginning

doi:10.1053/gast.1996.v110.agast961647

Gastroenterology

Volume 110, Issue 5, May 1996, Pages 1647-1649

https://doi.org/10.1053/gast.1996.v110.agast961647 Get rights and content

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Cited by (21)

Chromoendoscopy points the way to understanding recovery of gastric function after Helicobacter pylori eradication
2006, Gastrointestinal Endoscopy
Noninvasive versus histologic detection of gastric atrophy in a hispanic population in North America
2006, Clinical Gastroenterology and Hepatology
Background & Aims: Cancer risk is directly correlated with the severity and extent of mucosal atrophy, making identification of atrophy a goal in cancer prevention programs. The aim of this study was to compare targeted histology with noninvasive testing for the identification of antral and/or corpus atrophy in North America. Methods: In a cross-sectional study of a random sample of households, 8 gastric biopsy specimens were obtained from defined locations in the antrum and corpus. Biopsies were scored for the presence of Helicobacter pylori and gastric atrophy (defined as loss of normal glandular components). Atrophy was scored by using the Sydney system and a system based on the number and location of corpus biopsies with atrophy. Patients’ sera were examined for pepsinogen I, pepsinogen II, and gastrin-17 (fasting and stimulated). Results: One hundred eighty volunteers, approximately 30 per age group and ranging in age from 18–82 years, participated. There were 76 men. The overall weighted prevalence of a corpus atrophy was 4.7% (95% confidence interval, 2.3–7.0). There was a significant inverse relationship between the grade of corpus atrophy and the pepsinogen I/pepsinogen II ratio (R = −0.31, P < .01). We failed to confirm the usefulness of the proposed algorithm by using gastrin-17, H pylori serology, and serum pepsinogens to categorize the gastric histology. The Sydney system underestimated the prevalence of corpus atrophy by approximately 25%. Conclusion: Noninvasive testing is both possible and practical by using pepsinogen assays for the identification of the precancerous condition of moderate to severe corpus atrophy in North American Hispanic patients.
Pathogenesis of duodenal ulcer disease: The rest of the story
2000, Bailliere's Best Practice and Research in Clinical Gastroenterology
Although several duodenal ulcer disease-specific abnormalities in gastric function have been described (e.g. exaggerated gastrin releasing peptide-stimulated acid secretion and an abnormal sensitivity of the parietal cells to gastrin), none has withstood careful examination. We describe here the critical nature of the duodenal acid load in precipitating and washing out bile salts, which inhibit the growth of Helicobacter pylori(H. pylori) in the development of duodenal ulcer disease. The risk of duodenal ulcer is enhanced by infection with pro-inflammatory H. pylori(e.g. with an intact cag pathogenicity island). Progressive damage to the duodenum promotes gastric metaplasia, resulting in sites for H. pylori growth and more inflammation. This cycle results in an increasing inability of the duodenal bulb to neutralize acid entering from the stomach until changes in duodenal bulb structure and function are sufficient for an ulcer to develop. Cure of the H. pylori infection results in a sustained fall in duodenal acid load as well as a marked (and continuing) reduction in inflammation, which results in the cure of chronic ulcer disease.
H. pylori in the pathogenesis of duodenal ulcer: Interaction between duodenal acid load, bile, and H. pylori
2000, American Journal of Gastroenterology
Citation Excerpt :
The duodenal acid load has at least two components: acid secretion by the stomach, and neutralization of acid in the duodenum (39–42). There are a number of factors that are reversed after cure of H. pylori infection and that promote an increase in duodenal acid load, such as an H. pylori-associated inhibition of the effect of antral distention on acid secretion and impaired duodenal bicarbonate secretion (43–45). Duodenal ulcer disease is also associated with a reduction in size and motility of the duodenal bulb, as well as replacement of normal villous architecture by gastric metaplasia; and areas of gastric metaplasia in the duodenal bulb have also been shown to be capable of local acid secretion (5, 46).
OBJECTIVE:
Helicobacter pylori (H. pylori) growth is inhibited by bile yet it can grow in the duodenal bulb and cause ulcer disease. The aim of this study was to test the effect of bile on H. pylori viability and growth and to determine whether acidification of bile reduces its inhibitory activity.
METHODS:
Fresh human bile was collected at laparotomy and tested for inhibitory activity of H. pylori using broth dilution assays. Six clinical isolates of H. pylori obtained from patients with duodenal ulcer were used for each experiment. The bile was diluted from 1:3 to 1:192; its inhibitory effect on H. pylori was tested before and after acidification, treatment with cholestyramine, or chloroform. Bile was acidified to a pH of 2–6, centrifuged at 8000 rpm for 20 min to remove precipitated bile acids, and the supernatant pH readjusted. Controls included BHI broth without bile (positive control) and bile that was acidified to pH 2 and neutralized without centrifugation.
RESULTS:
Human bile inhibited H. pylori growth in a dose dependent manner. Growth of all strains was supported for all strains only at a dilution of 1:192. In contrast, after acidification to pH ≤5 and centrifugation to remove precipitated bile acids, all strains grew at a bile dilution of 1:12. Neither chloroform extraction of lipids, nor acidification without centrifugation removed the inhibitory action of bile. In contrast, cholestyramine sequestration of bile acids completely removed all inhibitory activity.
CONCLUSIONS:
The duodenal acid load may be the critical factor to explain the ability of H. pylori to colonize the duodenal bulb by precipitating glycine-conjugated bile salts. The combination of a high duodenal acid load and H. pylori infection is likely the critical event in the pathogenesis of H. pylori-related duodenal ulcer disease.
Relationship between antral lymphocyte density and basal gastrin levels in patients with Helicobacter pylori infection
2000, Digestive and Liver Disease
Background. The mechanism by which Helicobacter pylori causes hypergastrinaemia is not completely understood.
Aim. To evaluate whether antral lymphocyte density could play a role in this alteration.
Methods. A total of 12 patients with active duodenal ulcer and 10 with non-ulcer dyspepsia were enrolled upon detection of Helicobacter pylori infection at endoscopy. Enrolled as controls were 7 matched dyspeptic patients without Helicobacter pylori infection. Biopsy specimens were collected for Helicobacter pylori and histological assessments, and for antral lymphocyte density assessment by a histomorphometric method. A blood sample was obtained from each patient to determine basal gastrin levels. All patients were controlled by a further endoscopy 4 weeks after the end of Helicobacter pylori treatment.
Results. Antral lymphocyte density (5464±1328 and 5635±1186 vs 2267±557 lymphocytes/mm²; p<O. 001 and p<O. 001, respectively) and gastrin levels (66.7±14.1 and 60.4±21.7 vs 40:7±7.8 pg/dl, p=0:004 and p=0:02, respectively) were higher in duodenal ulcer and non-ulcer dyspepsia patients than in controls, while no significant differences emerged between duodenal ulcer and nonulcer dyspepsia patients. There was a significant direct correlation between antral lymphocyte density and gastrin levels both in duodenal ulcer (r=0:77; p=0:003) and in non-ulcer dyspepsia (r=0. 75; p=0.03) patients, while no correlation was found in controls (r=0: 12; p=0:8). After treatment, this correlation persisted in 10 eradication failure patients (r=0.68; p=0:027), but disappeared in those successfully cured.
Conclusions. These data suggest that lymphocyte density in the antral mucosa could play a role in the impaired gastrin production occurring in patients with Helicobacter pylori infection.
The role of the host versus the environment in duodenal ulcer disease
1999, Journal of Physiology Paris
Gastric functions can be understood only in the context of a network including the brain gut axis, neuro-endocrine and paracrine mechanisms and growth factors. These host factors including parietal cell sensitivity (PCS) may well interact with an important environmental factor, Helicobacter pylori (Hp), and help to explain its actions. The aim of this study was to investigate PCS related to Hp status and duodenal ulcer (DU). PCS was assessed by constructing dose-response curves after pentagastrin and calculating the D₅₀. Five groups of patients were studied: I) active DU, Hp pos. (8); II) history of DU, Hp pos. (8); III) asymptomatic Hp pos. (8); IV) asymptomatic Hp neg. (10); V) DU on maintenance H₂ blocker therapy, Hp pos. (20). PCS was repeated after Hp eradication. PCS was lowest in group IV, and in Hp pos. groups, was significantly higher, with insignificant differences among them, irrespective of DU. PCS declined significantly after Hp eradication. Group V showed an insignificant decline in PCS during treatment, not preventing recurrence. A higher PCS in Hp infection irrespective of DU, declining after eradication, suggests that this may be a reversible epiphenomena related to Hp infection. This may offer an explanation as to why DU develops only in some subjects with Hp, suggesting the importance of the host in the pathogenesis of DU.

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