Microscopic colitis or functional bowel disease with diarrhea: a French prospective multicenter study.

OBJECTIVES: To describe the characteristics of a cohort of patients with microscopic colitis (MC; lymphocytic (LC) or collagenous (CC) colitis) and to compare them with patients with functional bowel disorder with diarrhea (FBD-D). METHODS: Between September 2010 and June 2012, patients fulfilling the following inclusion criteria were prospectively included in 26 centers in France: (i) having at least three bowel movements daily with change in stool consistency; (ii) duration of abnormal bowel habit >4 weeks; and (iii) normal or near-normal colonoscopy. Each patient underwent a colonoscopy and colonic biopsies. We compared the demographic, clinical, biological, and etiological characteristic of patients with MC (CC and LC) with those of control patients with FBD-D. RESULTS: A total of 433 patients were included: 129 with MC (87 LC and 42 CC), 23 with another organic disease, and 278 with FDB-D, including patients with diarrhea and abdominal pain who met the criteria of Rome III (irritable bowel syndrome with diarrhea) and patients with functional diarrhea without abdominal pain. Logistic regression analysis identified the following independent predictors of MC: age >50 years (odds ratio (OR)=3.1, 95% confidence interval (CI)=1.6-5.9), presence of nocturnal stools (OR=2, 95% CI=1.1-3.9), weight loss (OR=2.5, 95% CI=1.3-4.7), duration of diarrhea <12 months (OR=2.0, 95% CI=1.1-3.5), recent introduction of new drugs (OR=3.7, 95% CI=2.1-6.6; P<0.0001), and the presence of a known autoimmune disorder (OR=5.5, 95% CI=2.5-12). CONCLUSIONS: Age >50 years, the presence of nocturnal stools, weight loss, the introduction of a new drug, and the presence of a known autoimmune disease increase the probability of MC and thus the indication for colonoscopy with biopsies.

[Follow-up of patients after Helicobacter pylori eradication]. / Quelle surveillance après éradication d'Helicobacter pylori?

After Helicobacter pylori eradication, the risk of new contamination in adulthood is very low and there is no need for further microbiological surveillance. Helicobacter pylori infection induces alteration of the gastric mucosa, beginning with chronic active gastritis and leading to atrophy, intestinal metaplasia and dysplasia. Chronic active gastritis disappears completely a few months after bacterial eradication while atrophy, intestinal metaplasia or dysplasia remain. Mucosal atrophy and intestinal metaplasia confer a high risk for the development of gastric cancer. The risk of cancer occurring on these premalignant lesions depends on their extension, topography and severity. So their diagnosis and grading is important for cancer prevention and implies that antral and fundic biopsies are systematically done even on endoscopically normal mucosa. Low grade atrophy or intestinal metaplasia limited to the antrum do not require further surveillance. For high grade or fundic lesions reassessment of endoscopic and histologic lesions is recommended every three years. Dysplasia should undergo specialized management.

Comparative evaluation of 29 commercial Helicobacter pylori serological kits.

BACKGROUND: Serology is a noninvasive diagnostic method for the detection of Helicobacter pylori infection. Many commercial kits are now on the market. It is necessary to assess their performances to help the user to choose the most appropriate. MATERIAL AND METHODS: The performances of 29 commercial serological tests detecting antibodies to Helicobacter pylori (17 enzyme-linked immunosorbent assay and 12 near-patient tests) were evaluated using sera from 108 patients prospectively selected from gastroenterology departments of five French hospital centers. These patients were infected (45) or uninfected (47) by H. pylori, or had doubtful results (16), according to the gold standard (culture or histology plus rapid urease test or urea breath test). The tests were evaluated by determining the usual parameters of performance: sensitivity, specificity, positive predictive value, negative predictive value, and accuracy. Two analyzes were performed including or not the 16 patients with doubtful infection as uninfected or not analyzed. RESULTS: Depending on the type of analysis, four or two of the 17 enzyme-linked immunosorbent assay tests presented excellent results with the five performance parameters >90%. Calculation of the Youden index allowed to show significantly better performances for one of the 4. Performances of the 12 near-patient tests were lower with accuracies <90% for all except one test. CONCLUSION: These data should help the users to choose the kit the most appropriate to their goals.

From array-based hybridization of Helicobacter pylori isolates to the complete genome sequence of an isolate associated with MALT lymphoma.

BACKGROUND: Helicobacter pylori infection is associated with several gastro-duodenal inflammatory diseases of various levels of severity. To determine whether certain combinations of genetic markers can be used to predict the clinical source of the infection, we analyzed well documented and geographically homogenous clinical isolates using a comparative genomics approach. RESULTS: A set of 254 H. pylori genes was used to perform array-based comparative genomic hybridization among 120 French H. pylori strains associated with chronic gastritis (n = 33), duodenal ulcers (n = 27), intestinal metaplasia (n = 17) or gastric extra-nodal marginal zone B-cell MALT lymphoma (n = 43). Hierarchical cluster analyses of the DNA hybridization values allowed us to identify a homogeneous subpopulation of strains that clustered exclusively with cagPAI minus MALT lymphoma isolates. The genome sequence of B38, a representative of this MALT lymphoma strain-cluster, was completed, fully annotated, and compared with the six previously released H. pylori genomes (i.e. J99, 26695, HPAG1, P12, G27 and Shi470). B38 has the smallest H. pylori genome described thus far (1,576,758 base pairs containing 1,528 CDSs); it contains the vacAs2m2 allele and lacks the genes encoding the major virulence factors (absence of cagPAI, babB, babC, sabB, and homB). Comparative genomics led to the identification of very few sequences that are unique to the B38 strain (9 intact CDSs and 7 pseudogenes). Pair-wise genomic synteny comparisons between B38 and the 6 H. pylori sequenced genomes revealed an almost complete co-linearity, never seen before between the genomes of strain Shi470 (a Peruvian isolate) and B38. CONCLUSION: These isolates are deprived of the main H. pylori virulence factors characterized previously, but are nonetheless associated with gastric neoplasia.

[Helicobacter pylori resistance: who needs what treatment?]. / Résistance de Helicobacter pylori: qui traiter et comment?

The standard treatment recommended for eradication of Helicobacter pylori is a combination of three drugs for seven days: one proton pump inhibitor at a double dose and two antibiotics. The high risk of failure - on the order of 30% - justifies routine testing to verify eradication after this first treatment. Verification is most often conducted with a urea breath test, more rarely by endoscopy when endoscopy or gastric histology is otherwise necessary. When eradication fails, longer multidrug treatment with different antibiotics is proposed. The failure rate after second-line treatment is 9-10%. If a third treatment is necessary, bacterial culture is recommended to select antibiotics on the basis of the antibiotic susceptibility testing.

[Confirmation of Helicobacter pylori eradication following first line treatment. How and when?]. / Quand et comment contrôler l'éradication de Helicobacter pylori après un traitement de première ligne?

Helicobacter pylori (H. pylori) eradication treatment should always be thought of as a package which includes first and second line therapies together. So, testing of H. pylori eradication following first line treatment should always be performed and should be explained to the patient with the prescription of the triple therapy. For confirmation of H. pylori eradication both the urea breath test and the biopsy based test (when endoscopy is clinically indicated) are recommended. Stool antigen test is also an accurate test although it seems to have a lower diagnostic value after eradication treatment. Testing should be performed at least of 4 weeks after treatment. Serology with pre and 6 months post treatment samples is usually not recommended except in the case of H. pylori eradication campaign in populations at high risk for stomach cancer for instance.

[Cholangiocarcinoma developing in von Meyenburg complexes in haemochromatosis]. / Cholangiocarcinome sur complexes de von Meyenburg au cours d'une hémochromatose génétique.

A 63-year-old man with genetic haemochromatosis underwent resection of a cholangiocarcinoma that developed in von Meyenburg complexes; the liver was not cirrhotic. Patients with an association of genetic haemochromatosis and von Meyenburg complexes might have a predisposition to cholangiocarcinoma, even before cirrhosis occurs. Patients with this association should undergo regular and early hepatic surveillance of hemochromatosis.

[Treatment of Helicobacter pylori infection]. / Traitement de l'infection à Helicobacter pylori.

The eradication rate of H. pylori after an initial course of antibiotic treatment is only 70%. It is therefore essential to inform patients from the onset that a follow-up verification of eradication will be needed 4 to 6 weeks after the first course of treatment and a second or even a third course may be required. After two treatment failures, antibiotic treatment should be adapted to the specific bacterial sensitivity, which necessitates endoscopy with biopsy and culture. The recent increase in bacterial resistance to clarithromycin will probably lead to modifications in the French guidelines within the next 2 years. Recognition of the carcinogenic role of H. pylori has increased the indications for bacterial eradication.

Frequent and rapid progression of atrophy and intestinal metaplasia in gastric mucosa of patients with MALT lymphoma.

OBJECTIVES: Association of gastric mucosa-associated lymphoid tissue (MALT) low-grade lymphoma and adenocarcinoma has repeatedly been reported. The aim of this study was to evaluate the frequency and the spreading of atrophy and intestinal metaplasia in gastric mucosa of patients with gastric MALT lymphoma followed after conservative treatment. METHODS: Forty-five patients (mean age 45 +/- 2.1 yr) with gastric MALT lymphoma, treated by Helicobacter pylori eradication, chemotherapy with per os single alkylating agents, or both treatments have been followed by gastroscopy with biopsies in antrum and corpus at least once a year. Univariate and multivariate analysis evaluated the association between the appearance of atrophy and intestinal metaplasia in antrum or corpus and different factors related to patients, H. pylori status, lymphoma features, and treatment. In addition, histological aspects of gastric biopsies at the diagnosis period and at the end of follow-up were compared with those of two control groups of age-matched patients with H. pylori gastritis. RESULTS: At the diagnosis time, only intestinal metaplasia in corpus was more frequent in patients with gastric MALT lymphoma than in patients with nonulcer dyspepsia. Within median follow-up of 54.4 months (range 9-196), the percentage of patients with gastric atrophy and intestinal metaplasia increased significantly and became significantly higher than in age-matched nonulcer dyspepsia patients. Multivariate analysis showed significant association between corpus intestinal metaplasia and corpus atrophy, intestinal metaplasia in antrum, and duration of the follow-up. CONCLUSIONS: Conservative management of gastric MALT lymphoma including H. pylori eradication is associated with progression of gastric atrophy and intestinal metaplasia with frequent involvement of the corpus which is known to be a precancerous condition. These findings show that long-term endoscopic monitoring should be recommended in such patients.