Management of Helicobacter pylori infection is evolving and in this 4th edition of the Maastricht consensus report aspects related to the clinical role of H pylori were looked at again in 2010. In the 4th Maastricht/Florence Consensus Conference 44 experts from 24 countries took active part and examined key clinical aspects in three subdivided workshops: (1) Indications and contraindications for diagnosis and treatment, focusing on dyspepsia, non-steroidal anti-inflammatory drugs or aspirin use, gastro-oesophageal reflux disease and extraintestinal manifestations of the infection. (2) Diagnostic tests and treatment of infection. (3) Prevention of gastric cancer and other complications. The results of the individual workshops were submitted to a final consensus voting to all participants. Recommendations are provided on the basis of the best current evidence and plausibility to guide doctors involved in the management of this infection associated with various clinical conditions.

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Management of Helicobacter pylori infection—the Maastricht IV/ Florence Consensus Report

ContextRecent reports suggest an increasing occurrence and severity of Clostridium difficile–associated disease. We assessed whether the use of gastric acid–suppressive agents is associated with an increased risk in the community.ObjectiveTo determine whether the use of gastric acid–suppressive agents increases the risk of C difficile–associated disease in a community population.Design, Setting, and PatientsWe conducted 2 population-based case-control studies using the United Kingdom General Practice Research Database (GPRD). In the first study, we identified all 1672 cases of C difficile recorded between 1994 and 2004 among all patients registered for at least 2 years in each practice. Each case was matched to 10 controls on calendar time and the general practice. In the second study, a subset of these cases defined as community-acquired, that is, not hospitalized in the prior year, were matched on practice and age with controls also not hospitalized in the prior year.Main Outcome MeasuresThe incidence of C difficile and risk associated with gastric acid–suppressive agent use.ResultsThe incidence of C difficile in patients diagnosed by their general practitioners in the General Practice Research Database increased from less than 1 case per 100 000 in 1994 to 22 per 100 000 in 2004. The adjusted rate ratio of C difficile–associated disease with current use of proton pump inhibitors was 2.9 (95% confidence interval [CI], 2.4-3.4) and with H2-receptor antagonists the rate ratio was 2.0 (95% CI, 1.6-2.7). An elevated rate was also found with the use of nonsteroidal anti-inflammatory drugs (rate ratio, 1.3; 95% CI, 1.2-1.5).ConclusionsThe use of acid-suppressive therapy, particularly proton pump inhibitors, is associated with an increased risk of community-acquired C difficile. The unexpected increase in risk with nonsteroidal anti-inflammatory drug use should be investigated further.

https://jamanetwork.com/journals/jama/articlepdf/202048/JOC50155.pdf

Use of gastric acid-suppressive agents and the risk of community-acquired Clostridium difficile-associated disease

ContextReduction of gastric acid secretion by acid-suppressive therapy allows
pathogen colonization from the upper gastrointestinal tract. The bacteria
and viruses in the contaminated stomach have been identified as species from
the oral cavity.ObjectiveTo examine the association between the use of acid-suppressive drugs
and occurrence of community-acquired pneumonia.Design, Setting, and ParticipantsIncident acid-suppressive drug users with at least 1 year of valid database
history were identified from the Integrated Primary Care Information database
between January 1, 1995, and December 31, 2002. Incidence rates for pneumonia
were calculated for unexposed and exposed individuals. To reduce confounding
by indication, a case-control analysis was conducted nested in a cohort of
incident users of acid-suppressive drugs. Cases were all individuals with
incident pneumonia during or after stopping use of acid-suppressive drugs.
Up to 10 controls were matched to each case for practice, year of birth, sex,
and index date. Conditional logistic regression was used to compare the risk
of community-acquired pneumonia between use of proton pump inhibitors (PPIs)
and H2-receptor antagonists.Main Outcome MeasureCommunity-acquired pneumonia defined as certain (proven by radiography
or sputum culture) or probable (clinical symptoms consistent with pneumonia).ResultsThe study population comprised 364 683 individuals who developed
5551 first occurrences of pneumonia during follow-up. The incidence rates
of pneumonia in non–acid-suppressive drug users and acid-suppressive
drug users were 0.6 and 2.45 per 100 person-years, respectively. The adjusted
relative risk for pneumonia among persons currently using PPIs compared with
those who stopped using PPIs was 1.89 (95% confidence interval, 1.36-2.62).
Current users of H2-receptor antagonists had a 1.63-fold increased
risk of pneumonia (95% confidence interval, 1.07-2.48) compared with those
who stopped use. For current PPI users, a significant positive dose-response
relationship was observed. For H2-receptor antagonist users, the
variation in dose was restricted.ConclusionCurrent use of gastric acid–suppressive therapy was associated
with an increased risk of community-acquired pneumonia.

https://jamanetwork.com/journals/jama/articlepdf/199672/joc41159.pdf

Risk of community-acquired pneumonia and use of gastric acid-suppressive drugs.

It is increasingly perceived that gut host–microbial interactions are important elements in the pathogenesis of functional gastrointestinal disorders (FGID) The most convincing evidence to date is the finding that functional dyspepsia and irritable bowel syndrome (IBS) may develop in predisposed individuals following a bout of infectious gastroenteritis There has been a great deal of interest in the potential clinical and therapeutic implications of small intestinal bacterial overgrowth in IBS However, this theory has generated much debate because the evidence is largely based on breath tests which have not been validated The introduction of culture-independent molecular techniques provides a major advancement in our understanding of the microbial community in FGID Results from 16S rRNA-based microbiota profiling approaches demonstrate both quantitative and qualitative changes of mucosal and faecal gut microbiota, particularly in IBS Investigators are also starting to measure host–microbial interactions in IBS The current working hypothesis is that abnormal microbiota activate mucosal innate immune responses which increase epithelial permeability, activate nociceptive sensory pathways and dysregulate the enteric nervous system While we await important insights in this field, the microbiota is already a therapeutic target Existing controlled trials of dietary manipulation, prebiotics, probiotics, synbiotics and non-absorbable antibiotics are promising, although most are limited by suboptimal design and small sample size In this article, the authors provide a critical review of current hypotheses regarding the pathogenetic involvement of microbiota in FGID and evaluate the results of microbiota-directed interventions The authors also provide clinical guidance on modulation of gut microbiota in IBS

https://gut.bmj.com/content/gutjnl/62/1/159.full.pdf

Intestinal microbiota in functional bowel disorders: a Rome foundation report

https://www.journal-of-hepatology.eu/article/S0168-8278(13)00602-8/pdf

Pathological bacterial translocation in liver cirrhosis.

BACKGROUND: Gastric and duodenal bacterial overgrowth frequently occurs in conditions where diminished acid secretion is present. Omeprazole inhibits acid secretion more effectively than cimetidine and might therefore more frequently cause bacterial overgrowth. AIM: This controlled prospective study compared the incidence of gastric and duodenal bacterial overgrowth in patients treated with omeprazole or cimetidine. METHODS: 47 outpatients with peptic disease were randomly assigned to a four week treatment regimen with omeprazole 20 mg or cimetidine 800 mg daily. Gastric and duodenal juice were obtained during upper gastrointestinal endoscopy and plated for anaerobic and aerobic organisms. RESULTS: Bacterial overgrowth (> or = 10(5) cfu/ml) was present in 53% of the patients receiving omeprazole and in 17% receiving cimetidine (p < 0.05). The mean (SEM) number of gastric and duodenal bacterial counts was 6.0 (0.2) and 5.0 (0.2) respectively in the omeprazole group and 4.0 (0.2) and 4.0 (0.1) in the cimetidine group (p < 0.001 and < 0.01; respectively). Faecal type bacteria were found in 30% of the patients with bacterial overgrowth. Basal gastric pH was higher in patients treated with omeprazole compared with cimetidine (4.2 (0.5) versus 2.0 (0.2); p < 0.001) and in patients with bacterial overgrowth compared with those without bacterial overgrowth (5.1 (0.6) versus 2.0 (0.1); p < 0.0001). The nitrate, nitrite, and nitrosamine values in gastric juice did not increase after treatment with either cimetidine or omeprazole. Serum concentrations of vitamin B12, beta carotene, and albumin were similar before and after treatment with both drugs. CONCLUSIONS: These results show that the incidence of gastric and duodenal bacterial overgrowth is considerably higher in patients treated with omeprazole compared with cimetidine. This can be explained by more pronounced inhibition of gastric acid secretion. No patient developed signs of malabsorption or an increase of N-nitroso compounds. The clinical significance of these findings needs to be assessed in studies with long-term treatment with omeprazole, in particular in patients belonging to high risk groups such as HIV infected and intensive care units patients.

https://gut.bmj.com/content/gutjnl/39/1/54.full.pdf

Bacterial overgrowth during treatment with omeprazole compared with cimetidine: a prospective randomised double blind study.

The extent of duodenal bacterial overgrowth during the pronounced inhibition of acid secretion that occurs with omeprazole treatment is unknown. The bacterial content of duodenal juice of patients treated with omeprazole was therefore examined in a controlled prospective study. Duodenal juice was obtained under sterile conditions during diagnostic upper endoscopy. Aspirates were plated quantitatively for anaerobic and aerobic organisms. Twenty five outpatients with peptic ulcer disease were investigated after a 5.7 (0.5) weeks (mean (SEM)) treatment course with 20 mg (nine patients) or 40 mg (16 patients). The control group consisted of 15 outpatients referred for diagnostic endoscopy without prior antisecretory treatment. No patient in the control group had duodenal bacterial overgrowth. In the omeprazole group bacterial overgrowth (> or = 10(5) cfu/ml) was found in 14 (56%) patients (p = 0.0003). The number of bacteria (log10) in duodenal juice in patients treated with omeprazole was distinctly higher (median 5.7; range < 2-8.7) when compared with the control group (median < 2; range < 2-5.0; p = 0.0004). As well as orally derived bacteria, faecal type bacteria were found in seven of 14 and anaerobic bacteria in three of 14 patients. Bacterial overgrowth was similar with the two doses of omeprazole. These results indicate that duodenal bacterial overgrowth of both oral and faecal type bacteria occurs often in ambulatory patients treated with omeprazole. Further studies are needed to determine the clinical significance of these findings, particularly in high risk groups during long term treatment with omeprazole.

https://gut.bmj.com/content/gutjnl/35/1/23.full.pdf

Duodenal bacterial overgrowth during treatment in outpatients with omeprazole.

We describe the case of a young woman with Cogan's syndrome and associated Crohn's disease. Systemic disease was manifested by oligoarthritis and valvular involvement. Crohn's disease has previously been described in two cases of Cogan's syndrome. We suggest therefore that Crohn's disease is pathogenetically related to Cogan's syndrome. For both, systemic involvement is characteristic, and immune-mediated mechanisms and vasculitis are thought to play a major pathogenetic role. Furthermore, both respond to treatment with corticosteroids.

J Thorens

Papers

Bacterial overgrowth during treatment with omeprazole compared with cimetidine: a prospective randomised double blind study.

Duodenal bacterial overgrowth during treatment in outpatients with omeprazole.

Association of Crohn's Disease and Cogan's Syndrome

Gastric and duodenal bacterial colonization in HIV-infected patients without gastrointestinal symptoms.