Stability of pH gradients in vivo across the stomach in Helicobacter pylori gastritis, dyspepsia, and health.

A layer of water-insoluble mucus gel is secreted by the gastric epithelium, and is believed to form an important barrier to acid injury. It is postulated that Helicobacter pylori can alter pH gradients by damaging the mucus layer, but no data on pH gradients in vivo in patients with H. pylori gastritis have been published. We aimed to construct a map of mucus-bicarbonate layer pH gradients in health and disease. Fourteen healthy asymptomatic volunteers (mean age, 46 yr) and 14 symptomatic patients with non-ulcer dyspepsia (NUD) (mean age, 46 yr) were studied. A flexible pH microelectrode was passed through the biopsy channel of an endoscope; luminal readings and three mucosal surface pH readings were obtained from each of five specific gastric sites (fundus greater curve, body greater curve, antrum greater curve, antrum lesser curve, and antrum anterior wall) using standardized methodology. Gradients at each site were calculated (mean juxta mucosal pH minus luminal pH); pH electrode accuracy was tested in standard buffer solutions. Biopsies were obtained from each site to assess for H. pylori status. Among asymptomatic volunteers, 21% had H. pylori; in NUD, 50% were infected. There was a significant association between H. pylori and histological gastritis at each site. The overall mean (+/- SE) pH gradients in H. pylori-positive and -negative cases were similar, being 5.35 (+/- 0.06) and 5.26 (+/- 0.07), respectively. There was also no significant correlation between the histological gastritis score and the pH gradient at each gastric site. The pH gradients in healthy subjects (mean 5.31) and NUD (mean 5.29) were not significantly different. We conclude that pH gradients appear to remain stable throughout the stomach in healthy subjects and NUD, independent of H. pylori gastritis.

Serodiagnosis of Helicobacter pylori: comparison of enzyme-linked immunosorbent assays.

Enzyme-linked immunosorbent assays (ELISAs) have been developed to diagnose Helicobacter pylori infection. However, the methods are not standardized. We therefore prospectively evaluated the sensitivities and specificities of ELISAs developed in the United States and the United Kingdom in a study population comprising 41 consecutive symptomatic outpatients and 35 volunteers. At endoscopy, multiple biopsies were obtained for histology and culture and stained sections were graded for chronic gastritis, active chronic gastritis, and density of H. pylori. Serum samples were analyzed for H. pylori by ELISA. The first set of assays for immunoglobulin G (IgG) and IgA used a pool of sonicated isolates of H. pylori from five patients in the United States (antigen A). The second set of assays, developed in the United Kingdom, used three different antigens: antigen 1, an acid-extractable surface antigen; antigen 2, an acid-extractable antigen from an aflagellate variant; and antigen 3, a urease-containing fraction. Cutoff scores for positive results were determined a priori on the basis of previous serological studies. There was close agreement between histology and culture. In the study population, 36% of the individuals were H. pylori positive. The diagnostic value of the different ELISAs were highly comparable, and the crude antigens performed as well as the more purified antigens. The antigen A IgG had a sensitivity and specificity of 96 and 94%, respectively; the values for antigen 1 were 93 and 96%, respectively. The antigen A IgA and antigen 3 assays were the least sensitive tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevalence of Helicobacter pylori in specific forms of gastritis. Further evidence supporting a pathogenic role for H. pylori in chronic nonspecific gastritis.

Helicobacter pylori colonization of the gastric mucosa is strongly associated with chronic nonspecific gastritis; moreover, there is evidence to suggest that H. pylori may cause this form of gastritis. However, there is little or no information on the prevalence of H. pylori in specific forms of gastritis. Our hypothesis was that if H. pylori was pathogenic in chronic nonspecific gastritis, organisms would be found frequently in this type of gastritis but infrequently in specific forms of gastritis. Prevalence rates of H. pylori were determined independently in patients with eosinophilic and Crohn's gastritis, Menetrier's disease, and chronic nonspecific gastritis. The prevalence of H. pylori in patients with chronic nonspecific gastritis was 71%, whereas the organism was not identified in patients with any form of specific gastritis. This finding further supports the accumulating evidence that H. pylori is a primary pathogenic factor in chronic nonspecific gastritis.

[14C]urea breath test for diagnosis of Helicobacter pylori.

H. pylori is a potent urease producer, a characteristic that has been exploited in the development of the [14C]- and [13C]urea breath tests. The prevalence of H. pylori infection also is known to increase with advancing age; however, the individual patient's age has not routinely been considered when interpreting urea breath test results. The aim of this study was to validate a short, age-adjusted [14C]urea breath test for use in diagnosing H. pylori infections. Forty-one subjects (28 volunteers, 13 patients) underwent esophagogastroduodenoscopy with biopsies. Subjects were defined as being H. pylori-positive if histology or culture was positive. In addition, all subjects completed a 120-min [14C]urea breath test. A logistic regression analysis adjusting for age was used to estimate the probability of H. pylori positivity as a function of the 14C values generated. Sixteen subjects were H. pylori-positive, and 25 were H. pylori-negative. The 14C values generated between 15 and 80 min were found to be equally predictive in identifying H. pylori-positive subjects. Advancing age was associated with a higher probability of H. pylori-positivity. By taking advantage of the statistical probabilities, older patients could be accurately diagnosed with H. pylori at lower 14C values. We found that [14C]urea breath test to be both a sensitive and specific test that can be abbreviated to a 30-min examination (total test time). Moreover, our mathematical model indicates that a patient's age should be considered in order to optimize interpretation of the [14C]urea breath test, although further observations are needed to confirm this model.

Helicobacter pylori: controversies and an approach to management.

Helicobacter pylori (formerly, Campylobacter pylori) is a gram-negative, spiral-shaped bacterium with a strong affinity for gastric-type epithelium. Convincing evidence indicates that H. pylori plays an etiologic role in the development of chronic, nonspecific gastritis, and it may play an important role in the pathogenesis of duodenal ulcer disease. An etiologic role for this organism in chronic gastric ulceration, nonulcer dyspepsia, and gastric carcinoma is not established. Whereas the diagnosis of H. pylori infection is relatively straightforward, the questions of when and how to treat the infection do not have established answers. A high rate of recrudescence follows most currently used therapeutic interventions. Until the pathogenicity of H. pylori in clinical disease is further supported and additional treatment trials have been completed, a conservative management approach is recommended.

Is antibacterial therapy against Campylobacter pylori useful in the treatment of indigestion and chronic peptic ulceration?

Campylobacter pylori is a spiral Gram-negative rod that was first identified in human gastric mucosa in 1906. Since 1983, interest in the organism has been renewed; it was first cultured, and has since been found to be very strongly associated with the histologic presence of antral gastritis. Further, it has been suggested that this organism may play a role in peptic ulceration. C. pylori is sensitive to many different antibiotics as well as to bismuth. However, recrudescence of infection after treatment is exceedingly common. Nick Talley and JoAnn Ormand advise that further investigation is needed to delineate if C. pylori is truly a clinically important pathogen, before antimicrobial therapy can be recommended; only thereafter will it be appropriate to determine what represents optimal therapy.