Helicobacter pylori produces histamine and spermidine.

The mechanism by which Helicobacter pylori associates with the development of upper gastrointestinal diseases is still not well understood. Toxic metabolites of H. pylori are discussed as possible factors. We were interested to investigate, whether biogenic amines might be involved. Ten monocultures of H. pylori from the antrum of patients with H. pylori associated diseases were analyzed for the content of the biogenic amine histamine. The bacteria were isolated on Columbia blood agar with Skirrow's supplement in a microaerophilic environment. After three passages onto fresh agar plates the bacteria were harvested in their sonicated suspensions analyzed by reversed-phase high-performance liquid chromatography (HPLC) and gas chromatography-mass spectrometry (GC-MS). From the HPLC analysis, histamine was found in six cultures. Analysis with GC-MS, however, revealed the presence of histamine in all the cultures (0.1-1.63 nmol histamine/10(8) bacteria). Additionally to histamine, all cultures were found to contain spermidine in concentrations of 0.010-7.912 nmol/10(8) bacteria. It is discussed that histamine produced by H. pylori may be involved in the pathogenesis of H. pylori associated gastrointestinal diseases.

Conjugation of 1-naphthol in human gastric epithelial cells.

The biotransformation of xenobiotics is essential to the maintenance of the body's integrity. Mucosal biotransformation has been well documented in the small and large intestine of animals and humans but whether the gastric mucosa plays a role in detoxifying ingested compounds remains largely unknown. The conjugation of the model phenolic compounds, 1-naphthol, by human gastric epithelial cells was assessed in vitro. Freshly isolated and cultured epithelial cells were prepared from surgical specimens obtained from patients undergoing total gastrectomy for cancer. Cell preparations were incubated with 1- 14C-naphthol over 1 hour and the glucuronide and sulphate conjugates formed were separated by thin-layer chromatography. Conjugation of 1-naphthol was observed with both freshly isolated and cultured cells. In freshly isolated cells, the 1 hour turnover of 1 microM 1-naphthol to its glucuronide and sulphate conjugates averaged 19% and 10% respectively. At higher 1-naphthol concentrations, both types of conjugate were formed at about the same rate, up to saturation (apparent Vmax = 0.07 nmol/mg protein/minute, and apparent Km = 40 microM). In cultured cells, the 1 hour turnover of 1 microM 1-naphthol to its glucuronide and sulphate conjugates averaged 35% and 8% respectively. These results suggest that the human gastric mucosa is a detoxifying organ, and that its role with regard to chemical carcinogenesis and drug first pass metabolism deserves further assessment.

Evaluation of a monoclonal antibody for detection of Helicobacter pylori in a direct immunofluorescence test.

A monoclonal antibody was developed for detection of Helicobacter pylori in gastric tissue sections in a direct immunofluorescence test. On a comparison of the immunofluorescence test with standard methods for detection of Helicobacter pylori, i.e. culture, the urease activity test and histological examination of tissue sections, using 158 biopsy specimens, 30 specimens were positive in all methods and 64 negative. In the remaining cases comparison was not possible because either immunofluorescence (29 specimens) or the standard methods (16 specimens) gave ambiguous results. The direct immunofluorescence test may have potential as an alternative to standard methods, but further testing in a defined patient population is necessary.

Effect of Helicobacter pylori infection on 24 hour intragastric acidity in patients with gastritis and duodenal ulcer.

Helicobacter pylori status, gastric histology, and 24 hour acidity were studied in 35 gastritis patients, 21 duodenal ulcer patients, and 14 subjects with normal gastric mucosa. H pylori was identified in 21 of 35 patients with chronic active gastritis and in 19 of 21 duodenal ulcer patients, but in none of those with normal gastric mucosa. Mean scores of activity of gastritis were similar in H pylori positive gastritis and duodenal ulcer patients, but were significantly lower in H pylori negative gastritis patients (2.1 (0.8) and 2.3 (0.9) v 1.4 (0.7); p < 0.01, respectively). Median 24 hour hydrogen ion activity (interquartile range) was 21 (8.9-38.0) mmol/l in normal subjects and 23 (11.2-49.0) mmol/l, 19 (7.1-33.1) mmol/l, 44 (25.1-63.1) mmol/l, and 36 (31.6-39.8) mmol/l respectively in gastritis and duodenal ulcer patients with and without H pylori infection. During all predefined time periods, intragastric acidity was significantly higher in patients with H pylori positive duodenal ulcers compared with gastritis patients and normal subjects. However, there was no significant difference in intragastric acidity between the H pylori positive and negative gastritis patients. These results suggest that most of the subjects with chronic H pylori infection have normal gastric acidity.

The role of omeprazole (40 mg) in the treatment of gastric Helicobacter pylori infection.

The efficacy of omeprazole in the elimination of Helicobacter pylori was investigated in a prospective randomized-controlled trial. 50 patients with upper gastrointestinal symptoms and chronic active H. pylori-associated gastritis were allocated to one of the following four therapeutic schedules: 1) omeprazole 40 mg/d for 4 weeks (n = 13); 2) bismuth subsalicylate (BSS) 3 x 600 mg for 4 weeks (n = 12); 3) omeprazole plus BSS for 4 weeks (n = 13); 4) triple therapy (BSS for 4 weeks, amoxicillin 3 x 750 mg and metronidazole 3 x 400 mg for 10 days) (n = 12). Clinical symptoms, endoscopic and histologic findings, and H. pylori status were reassessed immediately after therapy, and 1 and 6 months later. After cessation of therapy bacterial clearance rates were: 1) omeprazole 2/13 (15%); 2) BSS 6/12 (50%); 3) omeprazole plus BSS 5/13 (38%); 4) triple therapy 10/12 (83%). The degree of density of gastric mucosal infestation with H. pylori and the degree of activity of gastritis was reduced in all treatment groups but was most prominent after triple therapy. Clinical symptoms improved in all treatment groups. One and six months after completion of therapy H. pylori eradication rates were: 1) omeprazole 0/13 (0%); 2) BSS 1/12 (8%); 3) omeprazole plus BSS 1/13 (8%); 4) triple therapy 10/12 (83%). Our study shows that 40 mg/d omeprazole is ineffective in eradicating H. pylori. Dual therapy with omeprazole and bismuth subsalicylate does not improve bacterial elimination. Only triple therapy effectively eradicates H. pylori.