Nathalie Broutet

cagA Status and Eradication Treatment Outcome of Anti-Helicobacter pylori Triple Therapies in Patients with Nonulcer Dyspepsia

ABSTRACT The differences in eradication rates reported in clinical trials aiming to cure Helicobacter pylori infection cannot be entirely explained by the type of regimen, bacterial resistance, or lack of compliance. Using data from a clinical trial, a logistic regression model was constructed to determine whether cagAstatus, assessed by PCR, affects the outcome of eradication. Resistance to clarithromycin (10% of the strains) predicted failure perfectly. In the model (n = 156), a cagA-lacking strain (odds ratio [OR] = 2.2; 95% confidence interval [CI], (1.1 to 4.7), tobacco smoking OR = 3.1; 95% CI, 1.3 to 7.0), and a double dose of proton pump inhibitor in the treatment regimen (OR = 0.3; 95% CI, 0.2 to 0.7) were associated with the treatment outcome. The exact role of cagA in the outcome of H. pylorieradication therapy has not been explored. However, the type of histological lesions which it causes in the gastric mucosa may be implicated. Regardless of the mechanism involved, cagAstatus is a good predictive marker of eradication outcome.

Long-term effects of Helicobacter pylori eradication on gastric antral mucosa in duodenal ulcer patients.

Objectives The aim of this study was to assess the consequences of prolonged Helicobacter pylori eradication on gastric antral mucosa in duodenal ulcer patients. Patients and methods Forty‐three duodenal ulcer patients with confirmed H. pylori eradication after one year of follow‐up were included in this retrospective study. Before H. pylori eradication and during the follow‐up, four antral prepyloric biopsy samples were taken for histopathological examination and culture. Histopathological lesions were graded semi‐quantitatively according to the updated Sydney System for activity, chronic inflammation, glandular atrophy and intestinal metaplasia (IM), as well as presence of lymphoid follicles. Results After a mean follow‐up of 43 ± 23 months, H. pylori eradication statistically improved all gastritis scores, including the atrophy score and the lymphoid follicle score but excluding the IM score. H. pylori eradication resulted in normalization of gastric mucosa in 51.2% of patients and a significantly lower proportion of patients with non‐atrophic gastritis and atrophic gastritis without IM. Atrophy totally disappeared in 16/29 patients (55.2%) in whom IM was absent. No predictive factor for regression of atrophy or normalization of gastric mucosa was identified. Conclusion In duodenal ulcer patients, prolonged absence (more than one year) of H. pylori can lead to normalization of the antral mucosa and the disappearance of mucosaassociated lymphoid tissue, as well as the regression of antral atrophy. Long‐term studies involving selected patients with atrophy and IM which persist after H. pylori eradication are needed to determine the potential benefits of treating H. pylori gastritis with regard to gastric cancer prevention. Eur J Gastroenterol Hepatol 12:719‐725

Helicobacter pylori: from the stomach to the heart.

A surprising number of extra-gastrointestinal diseases have been reported to be associated with Helicobacter pylori infection, including coronary heart disease and stroke. Since coronary heart disease is the principal cause of death in western countries, and since the known risk factors cannot fully explain the pathogenic mechanisms of the disease, the exploration of the role of possible causal agents has stimulated intense research. Infectious agents have been linked to coronary heart disease on epidemiological and pathogenic grounds. In 1994, H. pylori infection was reported to be one of them. Since then, a number of studies have been published with controversial results. Studies performed thus far show a high degree of heterogeneity in the selection of patients and also in the type of disease studied, i.e. coronary heart disease in general or acute myocardial infarction. Since the pathogenic development is most likely different for each of these two conditions (one chronic and the other acute) they should be studied separately. H. pylori infection can cause platelet aggregation and induces a procoagulant activity. H. pylori can also contribute to atherosclerosis, through increased concentration of homocysteine in the blood, caused by decreased levels of folic acid and cobalamin, or to an autoimmune process. Prospective cohort studies and interventional trials focusing separately on the chronic and acute phases of coronary heart disease and H. pylori infection should be performed in order to provide firm epidemiological data for a causal relationship.

Detecting Helicobacter pylori infection in hospitalized frail older patients: The challenge

OBJECTIVES: Helicobacter pylori infection has not been well studied in older people, especially in hospitalized, frail patients. The aim of our study was to evaluate the prevalence of the infection in this population using five H. pylori diagnostic tests.

Helicobacter pylori infection in patients consulting gastroenterologists in France : prevalence is linked to gender and region of residence

Background Because of limited data on the epidemiology of Helicobacter pylori in France, the prevalence of this infection by region and its associated risk factors were studied between 1995 and 1997 among patients consulting a representative sample of gastroenterologists by region. Method A cross-sectional study was performed. Patients consulting gastroenterologists for whatever reason were screened for H. pylori infection determined by specific salivary IgG. A questionnaire was filled out by the gastroenterologist. A multivariate analysis was performed with all relevant variables. Results 3153 patients were included. The mean age was 48.5 years; 51.8% were women. After stratification by patients consulting for upper digestive tract (UDT) and non-UDT symptoms, H. pylori infection was found to be more prevalent, in both groups, for characteristics such as being born in a developing country, overcrowding during childhood, and primary educational level. Interestingly, gender (odds ratio ORUDT for women = 0.7 [95% CI 0.5–0.8] and ORnon−UDT for women = 0.6 [95% CI 0.5–0.8]) and living in a region other than the south-west (ORUDT varying from 1.5 to 2.0 and ORnon−UDT varying from 1.3 to 2.1, depending on the region) was associated with the odds of prevalent infection. Conclusion These findings show (1) that gender deserves more attention in the epidemiology of H. pylori and (2) a regional disparity in France regarding H. pylori infection.

Association of serum pepsinogen with atrophic body gastritis in Costa Rica.

Individuals with atrophic gastritis (AG), especially atrophic body gastritis (ABG), are at increased risk of developing gastric cancer. Serum concentrations of pepsinogens (PG) have been proposed as markers for ABG. The aim of this study was to determine the risk factors for AG and ABG and the potential of using serum PG concentrations to detect ABG in a dyspeptic population in Costa Rica, which is one of the countries with the highest incidence and mortality rates of gastric cancer in the world. Seven biopsy specimens, a fasting blood sample and a questionnaire concerning sociodemographic factors were obtained from 501 consecutive dyspeptic patients. The serum PGI level and the PGI/PGII ratios were significantly lower in patients with ABG than in other groups (P<0.000). A cut-off point of 3.4 led to a sensitivity of 91.2% in identifying ABG, a negative predictive value of 98.1%, but a positive predictive value of only 11.2%. Helicobacter pylori were present in 93% of the patients and all those with peptic ulcers were positive. AG was associated with increased age, lower body mass index, high alcohol intake and low fruit consumption. ABG was associated with age, alcohol consumption and PGI/PGII<3.4. In dyspeptic patients with a high prevalence of H. pylori infection, serum PG levels provide an assessment of ABG but it is necessary to introduce other serological and genetic markers in order to achieve a better specificity. Those markers could be serum antibodies to H. pylori-CagA, cytokine gene polymorphisms or others.

Lewis Antigen Expression and Other Pathogenic Factors in the Presence of Atrophic Chronic Gastritis in a European Population

To study the relationship between Helicobacter pylori cagA and vacA status and the expression of Lewis (Le) antigens and between these characteristics and atrophic chronic gastritis (ACG), H. pylori infection was assessed by culture and by histologic and serologic tests, cagA and vacA were assessed by a polymerase chain reaction--based reverse hybridization assay, and bacterial Le expression was assessed by immunoblotting. ACG was any form of antral or fundic atrophy with or without intestinal metaplasia. Of the 215 isolates, 64% were cagA(+) and 100% were vacA(+) (s1m1, 42%; s1m2, 29%; s2m2, 29%; and s2m1, 0). Le typing of 155 isolates showed that 6 (4%) were Le(x), 31 (20%) were Le(y), 87 (56%) were Le(x,y), and 31 (20%) were neither Le(x) nor Le(y). Two main clusters of isolates were identified by multiple correspondence analysis: s1a/m1/cagA(+)/Le(x)+/Le(y)+ (n=44; 29.7%) and s2/m2a/cagA(-)/Le(y)+ or Le(x)-/Le(y)- (n=29; 19.7%). Among patients with ACG, 54% of their isolates were from cluster s1m1/cagA(+)/Le(x)+/Le(y)+, which was associated with the presence of ACG (odds ratio, 7.4; 95% confidence interval, 1.5-37.0).

Phenotypic Variation of Helicobacter pylori Isolates from Geographically Distinct Regions Detected by Lectin Typing

ABSTRACT A total of 309 Helicobacter pylori isolates from 18 different countries were analyzed with a previously developed lectin typing system. The system was developed by using a proteolytic pretreatment to enhance the carbohydrate fraction of the sample. Four lectins from Ulex europaeus, Lotus tetragonolobus, Erythrina cristigali, and Triticum vulgaris were used to type the strains. The lectins were chosen for their specificities for sugars commonly encountered in the lipopolysaccharide of H. pylori. The isolates were received from their parent institutions as pellets of biomass and were typed at one of three centers (in Ireland, Sweden, and Estonia). All 16 possible lectin reaction patterns were observed in the study, with the isolates with the predominant pattern exhibiting reactions with all the lectins in the panel. For European patients suffering from gastritis, an association was noted between lectin reaction pattern MH4 and atrophic chronic gastritis; isolates with lectin reaction pattern MH4 were isolated from patients with atrophic chronic gastritis, whereas isolates with this pattern were not isolated from patients with chronic gastritis (P = 0.0006). In addition, statistically significant relationships were noted between the lectin reaction pattern and the associated pathology of isolates from the Swedish population. Isolates with patterns MH13 and MH16, which had low lectin reactivities, correlated with nonulcer disease (P = 0.0025 and P = 0.0002, respectively), and all four isolates from adenocarcinoma patients were characterized as possessing reaction pattern MH16. In contrast, isolates with lectin reaction patterns MH1 and MH10, which had high lectin reactivities, were associated with ulcer disease (P = 0.046 and P = 0.0022, respectively).

Saliva specimens for diagnosis of Helicobacter pylori obtained in remote areas of Nepal.

A surprising low prevalence rate of Helicobacter pylori infection was found in Dolpo, Nepal, leading the authors to demonstrate the importance of IgG conservation. The interest of studying the genetics of the bacteria in these remote infected populations is also emphasised.