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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).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 habit4 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.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: age50 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 diarrhea12 months (OR=2.0, 95% CI=1.1-3.5), recent introduction of new drugs (OR=3.7, 95% CI=2.1-6.6; P0.0001), and the presence of a known autoimmune disorder (OR=5.5, 95% CI=2.5-12).Age50 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.

Background & Aims Little is known about the magnitude of the risk of anal and rectal cancer in patients with anal and/or perineal Crohn's disease. We aimed to assess the risk of anal and rectal cancer in patients with Crohn's perianal disease followed up in the Cancers Et Surrisque Associe aux Maladies Inflammatoires Intestinales En France (CESAME) cohort. Methods We collected data from 19,486 patients with inflammatory bowel disease (IBD) enrolled in the observational CESAME study in France, from May 2004 through June 2005; 14.9% of participants had past or current anal and/or perianal Crohn's disease. Subjects were followed up for a median time of 35 months (interquartile range, 29–40 mo). To identify risk factors for anal cancer in the total CESAME population, we performed a case-control study in which participants were matched for age and sex. Results Among the total IBD population, 8 patients developed anal cancer and 14 patients developed rectal cancer. In the subgroup of 2911 patients with past or current anal and/or perianal Crohn's lesions at cohort entry, 2 developed anal squamous-cell carcinoma, 3 developed perianal fistula–related adenocarcinoma, and 6 developed rectal cancer. The corresponding incidence rates were 0.26 per 1000 patient-years for anal squamous-cell carcinoma, 0.38 per 1000 patient-years for perianal fistula–related adenocarcinoma, and 0.77 per 1000 patient-years for rectal cancer. Among the 16,575 patients with ulcerative colitis or Crohn's disease without anal or perianal lesions, the incidence rate of anal cancer was 0.08 per 1000 patient-years and of rectal cancer was 0.21 per 1000 patient-years. Among factors tested by univariate conditional regression (IBD subtype, disease duration, exposure to immune-suppressive therapy, presence of past or current anal and/or perianal lesions), the presence of past or current anal and/or perianal lesions at cohort entry was the only factor significantly associated with development of anal cancer (odds ratio, 11.2; 95% CI, 1.18-551.51; P = .03). Conclusions In an analysis of data from the CESAME cohort in France, patients with anal and/or perianal Crohn's disease have a high risk of anal cancer, including perianal fistula–related cancer, and a high risk of rectal cancer.

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.

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.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.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.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.

Points essentiels Le traitement recommande pour l’eradication de Helicobacter pylori est une tritherapie de 7 jours associant un inhibiteur de pompe a protons (IPP) a double dose et 2 antibiotiques. Le risque d’echec eleve, de l’ordre de 30 %, justifie de proposer systematiquement un controle d’eradication apres ce premier traitement. Le controle d’eradication est fait par test respiratoire a l’uree 13C ou plus rarement par endoscopie lorsqu’un controle endoscopique ou histologique gastrique est necessaire. En cas d’echec d’eradication, une tritherapie plus prolongee et avec d’autres antibiotiques est proposee. Le taux d’echec apres une deuxieme ligne de traitement est de 9 a 10 %. Si une troisieme ligne de traitement est necessaire, la culture de la bacterie est recommandee pour adapter le choix des antibiotiques aux resultats de l’antibiogramme.

Summary Aim : To compare the efficacy of different regimens in patients in whom previous Helicobacter pylori eradication therapy has failed. Methods : In this study named StratHegy patients (n = 287) were randomized to receive one of three empirical triple therapy regimens or a strategy based on antibiotic susceptibility. The empirical regimens were omeprazole, 20 mg b.d., plus amoxicillin, 1000 mg b.d., and clarithromycin, 500 mg b.d., for 7 days (OAC7), clarithromycin, 500 mg b.d., for 14 days (OAC14) or metronidazole, 500 mg b.d., for 14 days (OAM14). In the susceptibility-based strategy, patients with clarithromycin-susceptible strains received OAC14, whilst the others received OAM14. The 13C-urea breath test was performed before randomization and 4–5 weeks after eradication therapy. Results : In the intention-to-treat analysis, the eradication rates for empirical therapies were as follows: OAC7, 47.4% (27/57); OAC14, 34.5% (20/58); OAM14, 63.2% (36/57); it was 74.3% (84/113) for the susceptibility-based treatment (P

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.

Summary Background The proportion (and even the reality) of peptic ulcer disease (PUD) not related to H. pylori or NSAID/aspirin is debated. Aim To analyse the current epidemiological and clinical characteristics of peptic ulcer disease in French general hospitals. Methods Prospective multicentre study of patients with peptic ulcer disease in 32 French general hospitals over 1 year. H. pylori status was assessed by histology, and/or serology and/or C13-urea breath test. NSAID/aspirin intake (obtained by direct interview) and data about concomitant diseases were collected on the day of endoscopy. Results Nine hundred and thirty-three patients were selected during the year 2009. After exclusion of 118 patients with only erosive duodenitis, 24 with major missing data, 13 with other causes of ulcer and 65 negative for H. pylori by only one test, 713 patients were classified into four groups: 285 (40.0%) had only H. pylori infection; 133 (18.7%) only gastrotoxic drugs; 141 (19.8%) had both and 154 (21.6%) neither H. pylori infection nor gastrotoxic drug intake (‘idiopathic ulcers’). Patients with idiopathic ulcers differed in many ways both from H. pylori and NSAID/aspirin groups. However, multivariate analysis identified only three independent predictors: age, French metropolitan origin and the presence of comorbidities. Conclusion In a general hospital-based population in France, peptic ulcer disease appears idiopathic in a fifth of cases.

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

Background elicobacter 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 cag PAI 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 vacA s2m2 allele and lacks the genes encoding the major virulence factors (absence of cag PAI, bab B, bab C, sab B, and hom B). 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.

Fasting gastrinemia, fundic argyrophil cell density, mast cell number, basal fundic histamine content and histidine decarboxylase activity were determined in 20 antrectomized patients and 20 control subjects. Fasting gastrinemia and fundic argyrophil cell density were significantly lower in antrectomized patients than in controls, whereas fundic mast cell number, basal histamine content, and histidine decarboxylase activity did not differ significantly between the two groups. In antrectomized patients the basal fundic histamine content appears related to the fundic mast cell number, as a consequence of the reduced effect of gastrin on argyrophil cells.

Resume Les septicemies a Pasteurella sont rares. Nous rapportons 6 cas observes pendant une periode de 8 ans. Durant cette periode, 26 souches de P. multocida ont ete isolees dans notre centre hospitalier. La contamination qui se fait habituellement par griffure ou morsure de chat n'a ete retrouvee que dans 1 cas sur 2. Tous nos patients presentaient une pathologie sous-jacente dont 2 fois une cirrhose hepatique (33 %). Il existait une predominance feminine inhabituelle (5/6) qui n'a pas ete expliquee. Malgre la sensibilite habituelle de P. multocida aux antibiotiques, notamment a l'ampicilline, la letalite de ces infections reste elevee (66 % dans nos cas), en rapport avec le terrain sur lequel elles surviennent.

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.

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.

To compare the efficacy of different regimens in patients in whom previous Helicobacter pylori eradication therapy has failed.In this study named StratHegy patients (n=287) were randomized to receive one of three empirical triple therapy regimens or a strategy based on antibiotic susceptibility. The empirical regimens were omeprazole, 20 mg b.d., plus amoxicillin, 1000 mg b.d., and clarithromycin, 500 mg b.d., for 7 days (OAC7), clarithromycin, 500 mg b.d., for 14 days (OAC14) or metronidazole, 500 mg b.d., for 14 days (OAM14). In the susceptibility-based strategy, patients with clarithromycin-susceptible strains received OAC14, whilst the others received OAM14. The 13C-urea breath test was performed before randomization and 4-5 weeks after eradication therapy.In the intention-to-treat analysis, the eradication rates for empirical therapies were as follows: OAC7, 47.4% (27/57); OAC14, 34.5% (20/58); OAM14, 63.2% (36/57); it was 74.3% (84/113) for the susceptibility-based treatment (P0.01 when compared with OAC7 and OAC14). In patients receiving clarithromycin, the eradication rates were 80% for clarithromycin-susceptible strains and 16% for clarithromycin-resistant strains; in patients receiving OAM14, the eradication rates were 81% for metronidazole-susceptible strains and 59% for metronidazole-resistant strains.Eradication rates of approximately 75% can be achieved with second-line triple therapy based on antibiotic susceptibility testing. If susceptibility testing is not available, OAM14 is an appropriate alternative.

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.

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.

A patient with previous left caudal pancreatectomy and splenectomy presented with Zollinger-Ellison syndrome. Abdominal CT and endoscopic ultrasonography revealed a mass in the splenic area. Somatostatin receptor scintigraphy showed a nodular increase of the uptake corresponding to the lesion detected with conventional imaging. A second laparotomy was performed and the mass was resected. Histological analysis showed that the nodular lesion was an accessory spleen. Since physiologic uptake of 111In-pentetreotide is seen in the spleen, an accessory spleen mimicking a tumor, specially after previous splenectomy, may result in false-positive somatostatin receptor scintigraphy.

We report the case of a duodenal varix rupture in a 37-year-old man revealing an alcoholic cirrhosis. Endoscopic diagnosis of this duodenal varix was difficult because of its atypical and changing appearance. Endoscopic sclerotherapy was completely successful and there was no recurrent bleeding. Although duodenal varix is rare, this case and the literature emphasize the importance of considering this diagnosis in all patients with duodenal tumoral lesions and suspected portal hypertension. In this context, duodenal biopsy can be dangerous and should be avoided. In case of duodenal varix rupture, endoscopic sclerotherapy appears to be a safe and efficient first-choice therapy.

Background/Aims: In the gastric mucosa of Helicobacter pylori -infected subjects, we previously detected N α -methyl histamine ( N α -MeHA), a minor catabolite of histamine and a potent agonist of histamine H 3 receptors. The origin of N α -MeHA and its effects on gastric histamine and somatostatin in infected subjects were investigated. Methods: Ten noninfected patients and 13 patients with intense colonization were compared. N α -MeHA content and its synthetic enzyme activity, N α -histamine methyltransferase, binding of [ 3 H] N α -MeHA, histamine and somatostatin contents, and histidine decarboxylase activity were assayed in antral and fundic biopsy specimens and in cultured H. pylori strains. Results: Gastric histamine and somatostatin contents as well as histidine decarboxylase activity were decreased in infected patients and were restored to normal after antimicrobial treatment. Both N α -MeHA and N α -histamine methyltransferase activity were present in the mucosa of infected patients and in cultured strains and were very low in noninfected patients or after eradication of H. pylori . [ 3 H] N α -MeHA bound to gastric mucosa but not to cultured strains. The [ 3 H] N α -MeHA specific binding sites were characterized as H 3 receptors. The amount of bound [ 3 H] N α -MeHA seemed correlated positively with somatostatin content and histidine decarboxylase activity and negatively with N α -MeHA content and N α -histamine methyltransferase activity. Conclusions: H. pylori is the main source of gastric N α -MeHA that may lower histidine decarboxylase activity and somatostatin content through H 3 receptors.