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Introduction: There is no consensus on the benefit of performing a systematic complementary technique for the diagnosis of Helicobacter pylori infection. In our laboratory, a cresyl violet was carried out systematically until July 2014; since that date, a cresyl violet or immunohistochemistry is only made on request. We evaluated the value of cresyl violet staining of gastric biopsies to diagnose H. pylori infection by comparing a period of systematic staining to a time when it was made on demand., Material and Methods: We retrospectively studied the gastric biopsy of 786 consecutive patients from April to November 2014, taken in the absence of focal endoscopic lesion. During the first period, hematoxylin-eosin and cresyl violet were performed on all biopsies. During the second period, hematoxylin-eosin was performed and then, if necessary, cresyl violet or immunohistochemistry. All hematoxylin-eosin stained slides were revised to identify H. pylori. We performed immunohistochemistry in cases of active chronic gastritis without H. pylori identified on hematoxylin-eosin or cresyl violet., Results: We have shown that gastric biopsy performed in the absence of focal mucosal lesion are normal in 55% of cases. The percentage of H. pylori infection was similar in both groups. In cases of active chronic gastritis, H. pylori infection is visible, in most cases, on hematoxylin-eosin (94%). Immunohistochemistry should be prescribed only in case of chronic active gastritis without H. pylori identified on standard staining, with bacteria rare or atypically located., Conclusion: In our experiment, H. pylori is present only in case of active gastritis (33% of the biopsies in our series) and being almost always identifiable on the standard staining with H-E (in 94% of the cases), it is not It is not necessary to systematically perform, on all gastric biopsies, a complementary histo- or immunohistochemical technique., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

Purposes: Helicobacter pylori (H. pylori) infection is a chronic gastric Gram-negative infection that increases with age. Acquired in childhood, H. pylori infection may induce a whole cascade of events leading to gastric pathologies such as peptic ulcer diseases, gastric precancerous lesions, and gastric lymphomas (MALT). The characteristics of the diagnosis and the treatment of this infection in geriatrics are thus particularly important to take into account., Main Points: 1) The incidence of gastric and duodenal ulcers and their bleeding complications is increasing in old-aged populations. Clinical signs such as anorexia and malnutrition are proven to be excellent indications for endoscopic explorations in the elderly. NSAID-use and H. pylori infection were shown to be independent and unrelated risk factors for peptic ulcer and gastroduodenal bleeding in elderly subjects; 2) H. pylori infection diagnosis is difficult to realize in the very old population, and the urea breath test is the test which obtain the best performances in this population., Perspectives: Recent work showed the part played by H. pylori chronic infection in gastric aging and in appetite regulation in the elderly. Research tasks should be continued in this field in order to better understand the part played by this chronic infection in gastric aging and in other pathologies (i.e. neurological or cardiovascular diseases) in this population.

Unlabelled: Helicobacter pylori (H. pylori) is a Gram negative microaerophilic bacteria whose only known niche is the human gastric mucosa. The presence of H. pylori is associated with various pathologies ranging from peptic ulcer disease to gastric carcinoma. H. pylori virulence is dependent on its exceptional ability to resist to the stomach acidity by hydrolyzing urea into ammonia. Survival of H. pylori to acidity in the presence of urea relies on the activity of a membrane protein, UreI., Aims: We decided to better characterize the role of UreI (i) in vitro in ammonia production through the action of urease, and (ii) in vivo in the colonization of the gastric mucosa., Methods: Ammonia production by a wild type strain of H. pylori or by a UreI-deficient strain was measured as a function of extracellular pH. In addition, the kinetics of elimination of a UreI-deficient mutant in vivo were realized in the mouse model for colonization., Results: UreI was associated with an increase of ammonia production in acidic conditions in vitro and was necessary for the initial steps of the mouse stomach colonization., Conclusion: UreI thus behaves as a sensor of extracellular pH. This protein activates urease at acidic pH; thereby, it probably allows H. pylori to resist to acidity in vivo during the first steps of infection.

Direct or indirect methods are available to diagnose Helicobacter pylori infection. Direct assessment with histopathology, culture, rapide urease test, amplification of gene sequences requires the collection of biopsy samples via an endoscope. Culture is the gold standard, but histopathology is commonly used in clinical practice. Serology, 13C-urea breath test and detection of antigens in stools are indirect methods. In clinical practice, direct assessment is required for the initial diagnosis as only patients with endoscopic lesions need H. pylori eradication. Among indirect methods, serology should be used only in epidemiologic studies. Urea breath test and detection of antigens in stools are the most appropriate methods to assess eradication.

Helicobacter pylori is a risk factor for gastric carcinoma and an established carcinogenic bacterium. The relative risk to induce a gastric cancer is estimated to be 3 to 6 compared to that of individuals without H. pylori. Gastric atrophy and intestinal metaplasia in gastric mucosa are 2 well recognized precancerous lesions. Their occurrence and evolution are multifactorial depending on age at first infection, duration of infection and host's genetic characteristics. Prevention using H. pylori eradication is recommended only in individuals with high risk of cancer. Gastric lymphoma, although less frequent, may be due to H. pylori infection. Only in low grade lymphoma H. pylori eradication and periodic surveillance are recommended.

Helicobacter pylori is the prototype of bacteria belonging to a new genus, the Helicobacter genus. It is a gram-negative, highly motile and microaerophilic bacterium, with a spiral shape, that colonizes the human gastric mucosa and causes several gastroduodenal diseases. Pathogenicity of H. pylori relies upon its capacity to adapt to a hostile environment and to escape the host response. Resistance to acidity, motility, adhesion, molecular mimicry, resistance to phagocytosis, synthesis of a cytotoxin, induction of an inflammatory response are the major strategies developed by H. pylori to colonize persistently and damage gastric tissue.

One quarter of Meckel's diverticula are covered by ectopic gastric mucosa and many may present histological inflammatory changes. Helicobacter pylori grows preferentially on an acid ground but has been found in different parts of the gastrointestinal tract. A prior hypothesis of a pathogenic role for this bacterium in some of Meckel's diverticula with ectopic mucosa is not confirmed by this study covering 21 cases.

Helicobacter pylori is a Gram-negative bacterium with man as the unique reservoir and where the niche is the stomach. Transmission between individuals could be by fecal and oral route. In the stomach, the bacterium is mainly located at the mucus level and adhere to antral cells which are the privileged target. Within the colonized mucosa, H. pylori generates or secretes different deleterious compounds against the epithelial cells: urease, hydrolyzing urea into ammonia, a cytotoxic agent: monochloramine also cytotoxic, various enzymes and a vacuolyzing cytotoxin; all of these also contribute to the pathogenic potential. In addition the associated inflammatory reaction probably plays a part in the lesion process. One important consequence is peptic ulcer disease and particularly duodenal ulcer which can further degenerate into a precancer lesion and to a lesser extent some dyspeptic syndromes. Bacterial eradication can be obtained by the combination of an antisecretory drug with an antibiotic. Macrolides have a good activity against this bacterium. The azithromycin MIC50 is 0.12 mg/l. A bactericidal activity is observed at concentrations equal or higher than 0.10 mg/l. After a single dose of 500 mg, azithromycin concentrations are 0.48 micrograms/g in the mucus and 4 micrograms/g in the gastric tissue. Concentrations persist for a long time, due to long half life (3 days). In pilot clinical trials, with a tritherapy combining azithromycin with metronidazole and omeprazole, 80% of bacterial eradication was obtained. These promising need to be validated by larger clinical trials.

Objective: Four commercially available enzyme-linked immunosorbent assays (ELISA) were evaluated for serological diagnosis of Helicobacter pylori (H. pylori) infection in 79 untreated patients., Methods: Infection has been diagnosed in 40 patients, in whom culture and/or urease test and histopathology from antral biopsies, were positive for H. pylori., Results: Sensitivity (Se) and specificity (Sp) of these tests, calculated with indeterminate serological results (9 patients) classified as positive (ind +) or negative (ind -), were not statistically different: GAP-test (Bio-Rad), Se = 95% (ind +), 90% (ind -), Sp = 84.6% (ind +), 89.7% (ind -); Pylori-Stat (Biowhittaker), Se = 97.5% (ind + or -), Sp = 71.8% (ind +), 71.9% (ind -); Premier H. pylori (Biomedical Diagnostics), Se = 92.5% (ind +), 90% (ind -), Sp = 84.6% (ind +), 81.2% (ind -); Cobas-Core (Roche), Se = 92.5% (ind + or -), Sp = 76.9% (ind +), 79.5% (ind -). There was a strong correlation between mucosal inflammation and H. pylori status. Discrepancies between infectious status and at least one serology result were observed in 16 patients (11 H. pylori negative and 5 H. pylori positive patients)., Conclusion: These 4 tests are of equivalent diagnostic value. Thus, the selection of one of them should take into account cost and practicability.

The authors report the results of the detection of Helicobacter Pylori (HP) in gastric mucosa by the urease test, in 244 patients between January 1989 and August 1991. The overall prevalence of HP was 38.1%. It was 19.5% in patients with normal upper gastrointestinal endoscopy (UE), 61% in duodenal ulcer (p < 0.001) and 68.7% in congestive antritis (p < 0.001), significantly higher than in controls. There was no significant difference between controls and patients with erosive antritis or healed duodenal ulcers. The prevalence of HP rises with age in all patients and in those with lesions at UE but not in those with normal UE. A rise of this prevalence seems to exist in the months of June and December. The authors conclude by pointing out the rise of the overall prevalence of HP in congestive antritis compared with erosive antritis, the similarity of prevalence in normal subjects and those with healed ulcer and the lack of influence of age on this prevalence in subjects with normal UE. These conclusions are in need of confirmation by further studies on much more longer series.

A population of non ulcer dyspepsia outpatients with a normal gastroscopy was assessed. Clinical complaints, the type of the gastritis, its activity and bacterial density were evaluated. Helicobacter pylori (HP) was sought by histology, urease test and culture, on 3 distinct locations. HP was found in 62 p. cent of the patients, always in association with gastritis. Urease test and histology had the same sensitivity in the detection of HP. A randomized double blind study with amoxicillin vs placebo was carried out in 23 patients. At the end of 4 week treatment, a gastroscopy with biopsies was performed. The amoxicillin treated patients were significantly cured or improved. HP was undetectable or the bacterial density was decreased in this group. After amoxicillin, urease test was more sensitive than histology. HP might be involved in the pathophysiology of non ulcer dyspepsia in patients where HP was found.

The aim of this study was to determine whether there was any relationship between alcohol consumption, cirrhosis and Helicobacter pylori associated antral gastritis. One hundred and forty-four patients undergoing upper gastrointestinal endoscopy were prospectively included and classified in four groups. The first group of 23 patients had cirrhosis and an alcohol consumption below 80 g per day. The second group of 31 patients had cirrhosis and an alcohol consumption over 80 g per day. The third group of 34 patients had an alcohol consumption over 80 g per day without cirrhosis. The fourth group of 56 patients had an alcohol consumption below 80 g per day without any preexisting liver disease and underwent upper gastrointestinal endoscopy for non specific digestive symptoms. The diagnosis of Helicobacter pylori was made at histological examination using the hematoxylin and eosin stain and the Whartin-Starry stain in each case. Histopathological results were confirmed by a bacteriological study in 15 cases. One hundred and twelve of 144 patients (78 percent) had gastritis. Gastritis was more frequent (p less than 0.01) when Helicobacter pylori was present than when it was not (90 percent vs 68 percent). Gastritis was more frequent when alcohol consumption was high (86 percent vs 72 percent). Helicobacter pylori was found in 26 percent of the first group, 48 percent of the second group, 65 percent of the third group and 45 percent of the fourth group. These differences were significantly different (p less than 0.05). A statistically significant relationship between high alcohol consumption and the presence of Helicobacter pylori was noted, even in the presence of cirrhosis (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The presence of Campylobacter pylori on gastric mucosa was evaluated by touch cytology of gastric biopsies in a series of 100 patients. Results were compared to biopsy cultures. Of 43 culture-positive patients, cytology was positive in 37 (86 p. 100). Cytology was positive in 16 of 57 culture-negative patients, who had peptic ulcer and/or gastritis on biopsy, conditions widely associated with the presence of Campylobacter pylori. Cytologic examination, yielding quick results, is thus a sensitive diagnostic method for Campylobacter pylori. In addition, retrospective studies of previous specimens are possible: among 11 patients with a follow up of more than one year, three of the four Campylobacter pylori carriers subsequently developed an ulcer.

The presence of Campylobacter pylori in gastric mucosa is a proof of active gastritis. Diagnostic methods are based on endoscopy: culture--histology--cytology--urease test, or on noninvasive tests: C14 urea breath test and serology. The principles, results (sensitivity--specificity), advantages and problems of each test are discussed as well as the choice of a diagnostic method. In practice, we recommend the use of two methods, a morphological one (histology or cytology) and another based on bacterial activity (urease test or culture).

The aims of this study were to: a) evaluate the prevalence of Campylobacter pylori (CP) in patients referred to a gastroenterology unit for upper digestive tract endoscopy, b) compare the results of histologic (Warthin-Starry method) and bacteriologic (direct and culture) examinations, c) correlate the presence and abundance of CP with the "activity" of chronic gastritis as assessed by antral and fundic specimens, and d) report the preliminary results of an epidemiological survey in the area of Nantes, France. CP was observed in 30 of the 64 patients studied (46 p. 100 of cases), and was significantly associated with chronic gastritis of either the superficial or interstitial (87 vs. 12 p. 100 of patients positive and negative, respectively for CP studies, p less than 10(-9], and preatrophic and/or atrophic types (40 vs. 12 p. 100 of patients positive and negative, respectively, for CP studies, p less than 0.01). CP was also present in 7 of 10 patients with duodenal ulcers and in 4 to 6 with gastric ulcers. Histologic and bacteriologic studies gave concordant results in 94 p. 100 of cases, and had the same sensitivity for diagnosis. Patients positive for CP studies had a statistically significant increased incidence of epigastric burns, and, at endoscopic examination, their fundic area appeared congestive more frequently. CP were dictated in both the antrum and fundus, but lesions of chronic gastritis were more prominent in the former. There was a statistically significant correlation between the degree of inflammation observed in the lamina propria and the number of CP present in the same area (antrum and fundus).(ABSTRACT TRUNCATED AT 250 WORDS)

The authors report the results of systematic research on Campylobacter pylori during high endoscopy. Of the 60 patients examined, 12 were found to have the germ in their antral, gastric mucosa. All these patients had a history of chronic gastritis. They recall the role of this germ in creating chronic gastritis, and evoke the hypothesis that the mucosa becomes fragile facilitating the appearance of an ulcer.