Helicobacter pylori and gastroduodenal lesions in 547 symptomatic young adults

OBJECTIVES: Helicobacter pylori (H. pylori) is involved in the pathogenesis of gastric inflammatory disorders. Both antral chronic gastritis and H. pylori infection prevalence increase with age. The aim of the study was to assess the prevalence of H. pylori infection in young adults and to study the relationship between endoscopical and histological features and H. pylori infection. METHODS: The study concerned 547 young patients (age: 18-25 years), undergoing endoscopy for upper gastrointestinal symptoms. The severity and the activity of chronic gastritis was graded by histological examination of antral biopsies. The diagnosis of H. pylori infection was based on histology and culture or urease test. RESULTS: Fifty-three percent of the patients had a normal endoscopy; 44 ulcers were found: 34 duodenal ulcers and 10 gastric ulcers. H. pylori infection was detected in 34% of cases. The prevalence of H. pylori infection was 29.8% in non-ulcer patients, 50% in gastric ulcers and 91% in duodenal ulcers (P < 0.01). Duodenal ulcer, aspect of antral mosaic mucosa and nodular gastritis, were closely related to the presence of H. pylori. There was a significant relationship between H. pylori infection and both the severity (P < 0.01) and the activity (P < 0.01) of the antral chronic gastritis. The prevalence of follicular gastritis was 22% : it was present in 60% of H. pylori positive patients and 2.4% of H. pylori negative patients. H. pylori infection was more frequent in patients from Africa than in Europeans (P < 0.01). There was no significant association between H. pylori infection and different types of diets, settlements (rural vs urban) or symptoms. CONCLUSION: These results show that in the young population studied, duodenal ulcer, nodular gastritis, antral mosaic mucosa, active chronic gastric and follicular gastritis are closely related to H. pylori infection. They suggest that in the subgroup of non ulcer symptomatic patients, H. pylori prevalence is higher than in the general population.     

Consistent improvement in sphincterotome orientation with manual grooming

AIMS: To determine the prevalence of lymphoid follicles in Helicobacter pylori positive and negative gastritis in antral and body type gastric mucosa in patients with non-ulcer dyspepsia (NUD), duodenal ulcer, or gastric ulcer; to correlate follicle presence with patient age; to evaluate the correlation between the prevalence of lymphoid follicles and active and inactive gastritis and its severity; and to assess the positive predictive value of lymphoid follicle prevalence with respect to H pylori infection. METHODS: Gastric biopsy specimens, graded according to the Sydney system, from 337 patients were studied. RESULTS: Lymphoid follicles occurred more often in antral mucosa (78%) than in body type mucosa (41%) and were observed in 85% of patients with H pylori positive gastritis. There was no significant difference between NUD and gastric and duodenal ulcer disease with regard to the presence of lymphoid follicles. The positive predictive value of the presence of lymphoid follicles in H pylori infection was 96%. Lymphoid follicles were more commonly observed in patients aged between 10 and 29 years. Lymphoid follicles were more frequently found in pangastritis of all subtypes than in antral gastritis and also in active gastritis than in inactive gastritis. The presence of lymphoid follicles correlated strongly with the degree and severity of gastritis. CONCLUSION: Lymphoid follicles are a constant morphological feature of H pylori associated gastritis.     

Isolation identification and quantitative culture of Helicobacter pylori from gastric mucosa

The biopsy specimens were homogenized and diluted ten-fold serially in Hank's solution. Each dilution samples were streaked on Skirrow's selective medium. The plates were incubated at 37 degrees C 5 to 7 days under micro-aerobic condition and counting the viable cell of H. pylori. The positive rate of specimens with H. pylori in active gastric ulcer tissue (62.0%) was higher than that in scarred tissue (51.9%). Number of H. pylori viable cells in active ulcer tissue was significantly larger than in scarred tissue. The positive correlation between Raw's gastritis score of specimens from patients with erosive gastritis and number of H. pylori viable cells was clearly noticed.     

Hazards from surgical gloves

We describe the case of a child with Sch?nlein-Henoch purpura (SHP), bleeding duodenal ulcer and Helicobacter pylori (H. pylori) associated gastritis. 5-year-old girl was hospitalized with typical symptoms of SHP. On the third day, the child has several episodes of hematemesis with bright red blood, accompanied by increased pain of the epigastric region. Gastroduodenal endoscopy revealed signs of atrophic gastritis in the antrum, duodenitis with diffuse petechiae, small erosions and bleeding ulcer. The gastric biopsy showed a moderately severe chronic gastritis with activity and H. pylori was detected. The therapy with ranitidine, metronidazole and amoxycillin was introduced for a period of 30 days. At follow-up 2 months later, clinical examination and routine laboratory tests were normal. A repeated endoscopy revealed no evidence of lesions and H. pylori negative gastric biopsy. In our case, the associated chronic antral gastritis and H. pylori infection may well have aggravated the gastrointestinal symptoms of SHP. We feel it would be useful to check for H. pylori in patients with gastrointestinal manifestations of SHP, such as bleeding and important epigastric pain.     

Gastroesophageal reflux disease versus Helicobacter pylori infection as the cause of gastric carditis

To explore the potential contributions of gastroesophageal reflux disease, as opposed to Helicobacter pylori infection, to the development of gastric carditis, we evaluated gastric carditis (using the criteria of the updated Sydney system for the classification of gastritis), clinical and morphologic features of esophagitis, and H. pylori infection (evaluation of Steiner stains) in biopsy specimens from the gastroesophageal squamocolumnar junction. We correlated clinical, endoscopic, and histologic features in an unselected group of 116 patients. Some degree of carditis was found in 107 (92%) of the patients. The mean age of the patients increased with increasing severity of carditis (P < .05). The various groups of patients with different degrees of carditis did not differ significantly in sex ratio, ethnic background, presence of obesity, percentage having symptoms of gastroesophageal reflux disease (such as heartburn, regurgitation, dysphagia, or odynophagia), endoscopic evidence of esophagitis and columnar epithelium in the distal esophagus, or histologic evidence of active esophagitis. The presence, however, of active gastritis and H. pylori infection in the distal stomach and/or in the cardia was significantly associated with carditis. In patients without carditis, H. pylori was not detected in any cardiac or distal gastric biopsy specimen. In contrast, H. pylori was demonstrated in gastric tissue samples (either from the cardia or distally) of patients with carditis, with the prevalence rate increasing with greater degrees of cardiac inflammation. The H. pylori prevalence rate was 12% in the group with mild carditis, 40% in those with moderate carditis, and 57% in patients with marked carditis (P = .0001). In summary, carditis is commonly found in patients with symptoms related to upper gastrointestinal diseases. From analysis of our study cohort, we concluded that carditis was significantly associated with H. pylori infection and active gastritis but not with symptoms or signs of gastroesophageal reflux disease. These findings suggest that carditis with histologic features similar to those of gastritis in the distal stomach was a sequel of H. pylori infection and represented a part of an H. pylori--associated gastric inflammation.     

Proposed recommendations for research on biochemical markers for problematic drinking

Successful eradication of Helicobacter pylori infection in children has required long treatment regimens that may result in noncompliance with failure to eradicate this organism. Despite full compliance with shorter therapeutic regimens, such as amoxycillin and omeprazole for 2 wk, the H. pylori eradication rate is poor in children. OBJECTIVES: The aim of this study was to evaluate the efficacy of, and compliance with, a 2-wk treatment with metronidazole, omeprazole, and clarithromycin in eradicating H. pylori disease in children. METHODS: Over a 15-month period, children diagnosed to be H. pylori positive by Steiner's stain of gastric antral biopsy specimens were treated with metronidazole, omeprazole, and clarithromycin. Follow-up upper GI endoscopy was performed 6-8 wk after completion of therapy. RESULTS: Of 15 patients with H. pylori-positive antral gastritis, 11 had duodenal ulcer disease; three patients with severe abdominal pain and one with vomiting had H. pylori gastritis only. H. pylori eradication was seen in 11 of 11 (100%) patients with duodenal ulcer disease and in three of four (75%) with gastritis only; the overall success rate was 93%. Duodenal ulcer disease healed when H. pylori was eradicated in all but one patient, who at presentation had a penetrating ulcer with a duodenobiliary fistula. Fourteen of 15 patients (93%) were fully compliant, and no adverse reactions were reported. CONCLUSIONS: Two weeks of therapy with metronidazole, omeprazole, and clarithromycin is effective H. pylori therapy in children. It is well tolerated, and full compliance can be achieved.     

Beta1B subunit of voltage-dependent Ca2+ channels is predominant isoform expressed in human neuroblastoma cell line IMR32

BACKGROUND: In adults, Helicobacter pylori infection is always associated with gastritis or ulcer. However, very active gastritis and ulcers are rarely seen in children. The aim of the present work was to study the relationships between H. pylori and gastric mucosa in children. METHODS: Eighty infected children and adolescents including 48 (60%) neurologically impaired institutionalized patients, aged 2 months-22 years (mean 11.7 +/- 5.2 years) were studied retrospectively. All the patients underwent gastroscopy, and three antral and two fundic biopsy specimens were taken for histology and bacteriology. RESULTS: A normal gastric mucosa was found in 22 of 80 patients (27.5%), whereas the others had gastritis (n = 58, 72.5%). There were no statistical differences between patients with normal histology and those presenting with gastritis for age, sex, ethnic background, symptoms, and the degree of bacterial colonization. The macroscopic aspect of gastritis was less frequently found in children with a normal histology compared with those with histological gastritis (p < 0.001). CONCLUSIONS: These data show that H. pylori infection can be associated with a normal gastric histology in children.     

Helicobacter pylori may cause "reflux" gastritis after gastrectomy

Patients with "reflux" gastritis after gastrectomy suffer from a variety of symptoms, and this type of gastritis may sometimes compromise the quality of life of these patients. Since Helicobacter pylori is considered to be one of the most important pathogenetic factors in gastritis, the association between H. pylori and reflux gastritis was investigated in this study. A total of 145 patients with gastrectomy were entered into the study. Five biopsy specimens from the gastric remnant were taken at upper gastrointestinal endoscopy. One specimen was examined pathohistologically, and the remaining four were examined for H. pylori infection. Fifty-two patients (36%) demonstrated H. pylori infection. The prevalence of H. pylori was significantly higher in patients who had a partial gastrectomy, and it was significantly lower in patients who had undergone gastrectomy more than 4 years previously. The histologic gastritis score in patients with H. pylori infection was significantly higher. Furthermore, H. pylori was eradicated in patients with some symptoms of gastritis and no bile reflux to the residual stomach at endoscopy; in these patients the symptoms were relieved and the histologic gastritis score decreased significantly. In conclusion, possible involvement of H. pylori is suspected in the pathogenesis of "nonreflux" gastritis after gastrectomy.     

Prevalence and pattern of Helicobacter pylori gastritis in the gastric cardia

OBJECTIVES: Helicobacter pylori has a predilection for antral colonization. Local acid production is the major determinant of colonization. Because production is low in the antrum and cardia, H. pylori should also colonize the cardia. We therefore investigated the histologic pattern of gastritis and the prevalence of H. pylori in the cardia compared with the antrum and corpus. METHODS: From 135 H. pylori-infected patients with gastritis, ulcer disease, or reflux esophagitis, biopsies were obtained from the antrum, corpus, and cardia. The prevalence, topography, and histologic parameters of gastritis were examined. RESULTS: All 135 patients had active antral H. pylori gastritis: in the cardia, 132 of these patients (97.7%) showed active gastritis, and 124 patients (91.9%) had H. pylori visible on staining. Gastritis of the cardia in most patients resembled antral gastritis, but the density of bacteria and the inflammatory responses were less marked. The most striking finding in the cardia of patients with gastroesophageal reflux was a lower density of bacteria compared with antrum and corpus. Intestinal metaplasia was found in 32 patients in antral mucosa (23.7%) versus 28 patients in the cardia (20.7%), versus 11 patients in the corpus (8.1%), and was multifocal in 17 patients (12.6%). CONCLUSIONS: H. pylori gastritis commonly involves the cardia. The histologic density of the bacteria and inflammatory responses are lower than in the antrum. Intestinal metaplasia in the cardia is a common finding in H. pylori gastritis. The cause of the lower bacterial density in the cardia of patients with reflux esophagitis needs further investigation.     

Diagnosis of otitis media with effusion by acoustic reflectometry

Colonization of human gastric mucosa with Helicobacter pylori leads to chronic active gastritis and induces the occurrence of an acquired mucosa-associated lymphoid tissue (MALT) in the stomach. This remodelling of the gastric mucosa together with chronic antigen persistence may induce autoimmune reactions. The aim of this study was to investigate humoral autoimmune reactions to human gastric mucosa in H. pylori gastritis and their clinical relevance. Sera from patients with dyspeptic symptoms were tested for presence of IgG immunoglobulins against H. pylori. Gastric infection with H. pylori and alterations of gastric mucosa were demonstrated by histological examination of gastric biopsy specimens. All sera were tested for reactivity against human gastric mucosa by immunohistochemistry. Two different in-situ binding sites of antigastric autoantibodies were observed. Binding to canalicular structures within parietal cells was significantly correlated with antibodies to H. pylori, elevated basal gastrin levels and atrophy of gastric corpus glands. Our data indicate that autoimmune reactions to antigens in the human gastric mucosa occur in H. pylori gastritis and that they may play a role in the pathogenesis of the disease.     

In vitro cytotoxic effects of vacuolating cytotoxin produced by clinical isolates of Helicobacter pylori

The vacuolating cytotoxin produced by Helicobacter pylori is considered to be one virulence factor causing peptic ulceration. In this study, we examined the activity of vacuolating cytotoxin in induction of intracellular vacuolation of rabbit gastric epithelial cells (RGECs). We used culture supernatants of H. pylori as a source of vacuolating cytotoxin and quantitated cytotoxic activity by the MTT method. Intracellular vacuolation of RGECs was observed in the presence of 36 of 57 (63%) clinically isolated H. pylori strains. However, there were no differences in the incidence of H. pylori strains with positive vacuolating cytotoxin (Tox+) among patients with gastritis, gastric ulcers or duodenal ulcers. The MTT assay showed that the cytotoxic activity of H. pylori supernatants obtained from patients with gastric ulcers was significantly higher than in patients with gastritis (p < 0.01), but was not different to duodenal ulcer patient supernatants. Similar results were also observed in Tox+ isolates, however, there were no significant differences between patients with regard to the incidence of vacuolating cytotoxin-negative isolates. Although our data may not indicate a clear correlation between prevalence of vacuolating cytotoxin and clinical manifestations, they suggest that H. pylori harboring vacuolating cytotoxin may particularly induce damage to the gastric epithelium in patients with gastric ulcers.     

Free and total bupivacaine plasma concentrations after continuous epidural anaesthesia in infants and children

OBJECTIVES: The aim of this study was to elucidate the prevalence of Helicobacter pylori and its distribution in order to clarify the frequency of H. pylori infection and the most appropriate site of endoscopic biopsy for studies of H. pylori infection associated with different gastric diseases. DESIGNS AND METHODS: Swiss role mucosal strips from 275 resected stomachs, which included the greater curvature, anterior wall and lesser curvature of the antrum, incisura and corpus, were stained with haematoxylin-eosin and H. pylori antibody. RESULTS: The prevalence of H. pylori infection was 97% in duodenal ulcers, 98% in gastric ulcers, 98% in intestinal-type carcinomas and 99% in diffuse-type carcinomas. H. pylori was present at a rate of 100% in any site in cases of duodenal ulcer, but was diffusely distributed in the antrum and patchily distributed in the corpus. The detection rate of H. pylori was 50-100% in gastric ulcers, 30-100% in intestinal-type adenocarcinomas and 63-100% in diffuse-type adenocarcinomas depending on the site of the stomach examined. CONCLUSIONS: The prevalence of H. pylori infection was very high in peptic ulcers of the duodenum and stomach and gastric carcinomas of Japanese patients. Biopsy specimens for evaluation of H. pylori infection should be taken routinely from both the greater curvature of the antrum and corpus. Immunohistochemical staining should be used to assay for H. pylori when few organisms are present or eradication therapy has been used.     

Prevalence of Helicobacter pylori infection and gastric mucosal abnormalities in chronic pancreatitis

OBJECTIVE: Chronic pancreatitis is often associated with abnormal gastric acid secretion. However, previous studies have taken into consideration neither the potential role of Helicobacter pylori (H. pylori) infection nor histological features of the gastric mucosa in this context. The aim of this study was to analyze the prevalence of H. pylori infection as well as the pattern of gastritis in patients with chronic pancreatitis. METHODS: Forty patients with chronic alcoholic pancreatitis were included in the study: 40 patients with alcoholic liver cirrhosis and normal exocrine pancreatic function and 40 asymptomatic nonalcoholic subjects matched for age and sex used as control subjects. Endoscopy was performed in all patients, and five biopsy specimens from the antrum (three from the gastric body and two from the cardia) were taken for histological grading of gastritis and H. pylori assessment. RESULTS: Prevalence of H. pylori infection was similar in subjects with chronic pancreatitis (38%), asymptomatic subjects (28%) and liver cirrhosis (30%). Topography and expression of H. pylori-associated chronic gastritis was also not different among the three groups of subjects. In H. pylori-negative subjects, the presence of moderate to severe chronic antral gastritis was significantly more common in patients with chronic pancreatitis (40%) than in subjects with liver cirrhosis (18%) and in asymptomatic subjects (14%) (p < 0.05). No difference was found among the three groups of patients with regard to gastritis activity, atrophy, and intestinal metaplasia in the various gastric regions. The chronicity grade of gastritis did not correlate with the severity of pancreatic insufficiency. CONCLUSION: Prevalence of H. pylori infection is not different in patients with chronic pancreatitis as compared with subjects alcoholic liver cirrhosis and asymptomatic subjects. A severe H. pylori-negative chronic gastritis is more common in patients with chronic pancreatitis. This chronic inflammation of the gastric mucosa could contribute to determining the changes in gastric physiology described in patients with chronic pancreatitis.     

Helicobacter pylori infection and duodenal ulcer in children and adolescents

To investigate the relationship between H. pylori infection and duodenal ulcer in children and adolescents, the markers of H. pylori infection were studied in 22 children and adolescents who had duodenal ulcers and were followed prospectively (Group A). Another 36 patients with gastrointestinal symptoms, but without ulcer, were also studied for comparison (Group B). Antral and duodenal tissues were biopsied and analyzed for the presence of H. pylori using three standard methods: urease test, culture and histology. The specific IgG antibody against H. pylori positivity using the ELISA method were also analysed. By these three methods, H. pylori positivity in the antral tissues, chronic active antral gastritis, and seroprevalence rate were found to be much higher in Group A than Group B. However, a similar trend was not found in the duodenal tissues. H. pylori was found in four of five patients during postoperative follow-up for duodenal ulcer. Among the four patients, no duodenal ulcer but chronic active gastritis was detected endoscopically in three who received vagotomy. Only the one who received simple closure of the perforated duodenal ulcer had a recurrent duodenal ulcer. It was concluded that a close relationship among duodenal ulcer, chronic active gastritis and H. pylori is present in children and adolescents.     

The effect of H. pylori in perforation of duodenal ulcer

BACKGROUND/AIMS: H. pylori has been described as an opportunistic pathogen attracted by changes in the gastric mucosa caused by inflammation and ulceration. However, the role of H. pylori infection in the perforation of duodenal ulcers has not yet been clearly determined. The aim of this study was to assess the prevalence of H. pylori infection in patients undergoing laparotomy for repair of a perforated duodenal ulcer. METHODOLOGY: Patients who underwent surgery for a perforated duodenal ulcer in our Surgical Unit between January 1994 and July 1996 were included in this study. The study population consisted of eighteen patients with a mean age of 32.7 (21-48) years. All of the patients were male. Patients with chronic duodenal ulcer perforation and with no contraindications for definitive surgery, such as peritonitis, shock (blood pressure <90 mm Hg), age >60 years, or more than a 12-hour elapse from the time of perforation, were treated by bilateral truncal vagotomy and Weinberg pyloroplasty. The ulcer was excised with the pyloric ring. The cut was then extented by about 2 cm on both the gastric and duodenal sides. Two biopsies were taken from the antral mucosa by endoscopic biopsy forceps. The defect was closed transversely. The ulcer specimen and the antral biopsies were fixed separately in 10% formalin solution and sent to the department of Histopathology. The specimens were stained with Hematoxylin-Eosin and examined for H. pylori . Sections of the ulcer specimen were especially investigated for the presence of H. pylori through all layers of the ulcer. RESULTS: H. pylori was found in the antral biopsies of 16 patients (88.8%). In seven of the ulcer specimens (38.8%), H. pylori was present in the mucosa and also extended through the wall of the ulcer. H. pylori was positive in the antral biopsies of all patients with H. pylori present in the ulcer wall. CONCLUSIONS: In our study, H. pylori was present at a high ratio in the antral biopsies of patients with duodenal ulcer perforation. The presence of H. pylori throughout the ulcer wall to a considerable extent emphasizes the fact that eradication of H. pylori is important in the treatment of perforated duodenal ulcer.     

Symptomatic Helicobacter pylori infection in a neurorehabilitation population

Helicobacter pylori infection has been associated with acute and chronic gastritis, peptic ulcer disease, hypertension, and possibly gastric carcinoma and coronary artery disease. The prevalence of H pylori infection is more than 50% in people older than 60 years; however, the prevalence is not known in patients with traumatic brain injury (TBI) or cerebrovascular accidents who are treated in inpatient rehabilitation services. This report describes 10 symptomatic patients with TBI and strokes who were diagnosed with and treated for H pylori infection after transfer to a neurorehabilitation unit during a 12-month period. Physicians who treat patients with TBI and stroke need to be aware of the possible high prevalence of H pylori infection in their patients. The authors recommend H pylori screening for symptomatic patients in neurorehabilitation units and providing definitive treatment to prevent recurrent gastrointestinal bleeding, peptic ulcer disease, and gastritis.     

Skull base aspergillosis granuloma originating from the sphenoid sinus: a case report

To clarify the prevalence of Helicobacter pylori infection in enlarged fold gastritis, serum immunoglobulin (Ig) G antibody to H pylori was determined in 19 patients with severely enlarged gastric body folds (the widest fold greater than 10 mm on the radiograph), 55 patients with moderately enlarged folds (6 to 10 mm) and 44 control subjects (5 mm or less). The prevalence of serum IgG antibody to H pylori in the severe (100%) and moderate groups (100%) was significantly higher than that in controls (34.1%) (P < 0.01). There were significant differences among the three groups in serum gastrin, pepsinogen I and pepsinogen II levels (severe had the highest levels, followed by moderate and then controls, P < 0.001). H pylori colonization in the gastric mucosa was confirmed by culture, urease test or both, and inflammation by hematoxylin and eosin stain in the 25 H pylori seropositive patients who underwent endoscopy and biopsy. Results suggest that H pylori infection is highly prevalent in enlarged fold gastritis. Further studies on enlarged fold gastritis and H pylori infection are needed.     

Helicobacter pylori CagA antigen antibodies

BACKGROUND: CagA antigen of Helicobacter pylori is highly immunogenic in humans. There is an increasing evidence that infection with CagA-positive strains is related to the development of peptic ulcer disease, atrophic gastritis, or gastric cancer. The aim of our study was to assess seropositivity to CagA in a group of 95 clinically symptomatic adults who underwent gastroduodenoscopy and to correlate results to their disease characteristics. METHODS AND RESULTS: Serum immunoglobulin G antibodies to CagA detected by ELISA kit (Helicobacter p120, Viva Diagnostika, Germany) were compared to standard IgG specific antibodies against a pool of H. pylori antigens Synelisa Pin plate, ELIAS, Germany). Immunoglobulin G antibodies to CagA were present in 5/31 (16%) serum samples from H. pylori negative persons and 10/28 (36%) serum samples from H. pylori positive patients without peptic ulcer disease compared with 8/11 (73%) H. pylori positive patients with peptic ulcer disease in the past, 11/13 (85%) H. pylori positive patients with duodenal ulcers or duodenitis and 4/5 (80%) H. pylori positive (1/7, 14% H. pylori negative) serum samples from patients with gastric resection for peptic ulcers in the past. Serum levels of antibodies to CagA in the groups of patients with peptic ulcer disease in the past, with present duodenal ulcers of duodenitis and in H. pylori infected patients with gastric resection were significantly higher then those of H. pylori infected patients without peptic ulcer disease (P < 0.05). On the other hand, there was no significant difference in the presence of the specific antibodies against at pool of H. pylori antigens between these four groups. CONCLUSIONS: These data suggest that serologic response to the CagA antigen is more prevalent in H. pylori positive persons with present or past peptic ulceration than among infected persons without peptic ulcer disease. The presence of antibodies to CagA in H. pylori positive persons may be useful for the identification of patients with higher risk or more severe disease.     

Helicobacter pylori in 1997

In this review Helicobacter pylori (H. pylori) infection and its relation to different diseases is presented. H. pylori doesn't cause inconvenience to most infected people, though all infected persons have chronic active gastritis. The 10 year risk of peptic ulcer for people infected with H. pylori is about 10%. Randomized double-blinded trials have shown that eradication of H. pylori can cure most patients with peptic ulcer disease. Some people infected with H. pylori develop atrophic gastritis which is a risk factor for development of gastric cancer. It is not known if H. pylori screening and eradication would have a prophylactic effect against gastric cancer. It is also unknown if persons with non-organic dyspepsia and persons in long-term treatment with proton-pump-inhibitors would benefit from H. pylori eradication.     

Recommendations for the molecular diagnosis of familial adenomatous polyposis

OBJECTIVES: We investigated the relationships between gastric metaplasia occurring during the healing and scarring stages of duodenal ulcers and Helicobacter pylori by examining the course of gastric metaplasia in H. pylori-eradicated and non-eradicated patients. METHODS: One hundred and six H. pylori-positive patients with active duodenal ulcers were assigned to either a non-eradication group or an eradication group. The non-eradication group received lansoprazole for 6 wk, followed by an H2-receptor antagonist. The eradication group also received amoxicillin and metronidazole for 1 wk, in addition to lansoprazole, after initial endoscopic examination. In both groups, biopsy specimens were obtained from the ulcer margin in the active stage and from the center of the scar in the scarring stage. Specimens were examined microscopically as well as by rapid urease test to assess the extent of gastric metaplasia and to detect the presence of H. pylori. RESULTS: The extent of gastric metaplasia increased as the ulcers healed. The extent of gastric metaplasia was of a lesser degree in the non-eradication group than in the eradication group at the time of healing, and this tendency became increasingly apparent in the course of follow-up, resulting in reduced defense mechanisms against acidity to promote the recurrence of ulcers. In the eradication group, among those in whom eradication was successful, gastric metaplasia presented a well-developed appearance with abundant intracellular mucus and remained in this condition for a prolonged period, resulting in adequate defense mechanisms against acidity to prevent the recurrence of ulcers. CONCLUSION: By the eradication of H. pylori, gastric metaplasia becomes well-developed and remains so for a prolonged period. Thus, the eradication of H. pylori appears to play a role in the prevention of ulcer recurrences by developing adequate defenses against acidity.