Helicobacter pylori eradication may induce de novo, but transient and mild, reflux esophagitis: Prospective endoscopic evaluation

Backgrounds and Aim:  The effect on reflux esophagitis of eradicating Helicobacter pylori is variable and not fully defined. We previously reported that in patients who have reflux esophagitis associated with duodenal ulcer, a significant improvement in the pre-existing reflux esophagitis occurred after H. pylori was eradicated. In the present study, we asked whether H. pylori eradication leads to de novo development of reflux esophagitis in peptic ulcer patients.
Methods:  Prospective post-eradication evaluations were conducted in 1195 H. pylori -positive patients with peptic ulcer diseases who were confirmed not to have reflux esophagitis by endoscopic examination before eradication therapy. After eradication therapy, endoscopy and a urea breath test were performed yearly.
Results:  A total of 1187 patients were followed for up to 10.0 years (a mean of 3.6 years). Reflux esophagitis developed in 279 of 1000 patients cured of infection and in 26 of 187 patients who had persistent infection ( P  < 0.0001, Fisher's exact test). The esophagitis was mild (Los Angeles grade A) in most patients, transient in approximately one-half, and rarely necessitated long-term medication for the condition. Cure of infection, alcohol consumption, younger age, and high body mass index were identified as significant factors for the risk of developing non-transient reflux esophagitis.
Conclusions:  Cure of H. pylori infection may increase the risk of developing reflux esophagitis in patients with peptic ulcer, but the esophagitis is mostly mild and transient, and long-term medication is rarely required. Thus, H. pylori eradication therapy need not be withheld for fear of provoking reflux esophagitis.     

Helicobacter pylori eradication improves pre-existing reflux esophagitis in patients with duodenal ulcer disease.

BACKGROUND & AIMS: There has been significant controversy over the relationship between Helicobacter pylori infection and reflux esophagitis. We investigated the effects of eradicating H. pylori on the reflux esophagitis found in patients with peptic ulcers. METHODS: Prospective posteradication evaluations were conducted yearly in 162 H. pylori-positive patients who had reflux esophagitis together with peptic ulcer disease (4 women and 158 men, mean age = 49.1 yr). The Los Angeles classification of the patients' esophagitis was: grade A, 90; grade B, 63; and grade C, 9. The follow-up evaluations began 1 to 2 months after completion of the eradication treatment (mean time of follow-up = 22 mo), and consisted of endoscopy and an interview focusing on heartburn. RESULTS: Six patients were withdrawn from the study because of adverse drug reactions or a failure to regularly keep their appointments. After eradication therapy, we observed endoscopically that reflux esophagitis had improved in 87 (55.8%) of the 156 patients. The improvement rate was significantly higher in patients cured of infection (60.8%) than in those with persistent H. pylori infection (38.9%) (P = 0.04). Body mass index (odds ratio = 0.86, 95% confidence interval [CI] = 0.76-0.97), cure of infection (3.68, 95% CI = 1.56-8.69), the absence of a hiatal hernia (3.90, 95% CI = 1.83-8.28), and an ulcer located in the duodenum (2.75, 95% CI = 1.33-5.70) were identified as significant independent factors for the improvement of reflux esophagitis. CONCLUSIONS: In patients with reflux esophagitis associated with duodenal ulcer, a significant improvement in pre-existing reflux esophagitis was noted after H. pylori eradication.     

Barrett's Esophagus and the Presence of Helicobacter pylori

Objective: Although the role of Helicobacter pylori in the pathogenesis of peptic ulcer disease and antral gastritis has been well documented, the role of H. pylori in esophageal disease has not been clearly defined. To clarify this issue, we analyzed 141 patients with histologically confirmed esophageal disease.
Methods: The study group consisted of 82 patients with Barrett's esophagus, 19 with adenocarcinoma of the esophagus arising in columnar epithelium and 40 patients with reflux esophagitis without columnar metaplasia of the esophagus. In each of these cases the presence or absence of H. pylori was assessed histologically.
Results: H. pylori was present in 19 of 82 patients (23%) with Barrett's esophagus, but was absent in all patients with adenocarcinoma of the esophagus and in patients with reflux esophagitis without Barrett's metaplasia. H. pylori was found only in areas of gastric type metaplasia in the patients with Barrett's esophagus. All of the 19 Barrett's esophagus group with H. pylori had chronic inflammation, and in 16 the inflammation was severe. H. pylori was significantly associated with severity of inflammation in patients with Barrett's esophagus (   p < 0.001  ). Members of the Barrett's group with evidence of moderate to severe dysplasia were negative for H. pylori .
Conclusion: These data confirm that the presence of gastric type mucosa within the esophagus is a prerequisite for H. pylori colonization, and that H. pylori may contribute to the severity of inflammation in Barrett's epithelium.     

Prevalence of esophagitis in H. pylori-positive peptic ulcer disease and the impact of eradication therapy

BACKGROUND/AIMS: There have been recent reports of reflux esophagitis apparently occurring de novo after cure of H. pylori in peptic ulcer disease. The possibility that this phenomenon might be explained, at least in part, by unmasking of coexistent disease has not been assessed. The aim of this study was to assess the prevalence of esophagitis in H. pylori-positive peptic ulcer disease and examine the short-term impact of H. pylori therapy on the esophagus. METHODOLOGY: Esophagitis was systematically graded and the presence of hiatal hernia was noted in 244 peptic ulcer patients (duodenal 223; gastric 21) before and at least four weeks after triple therapy. H. pylori status was assessed using CLO test and histology, and esophagitis grade was assigned without knowledge of H. pylori status. RESULTS: Of the 244 patients, 49 (20%) had esophagitis which was grade 2 or more in over two-thirds. The prevalence of esophagitis was similar in duodenal and gastric ulcer patients. The presence of hiatal hernia was strongly associated with the finding of esophagitis (P < 0.001). Of 241 patients evaluable after therapy, 215 (89%) were H. pylori-negative and 26 remained H. pylori-positive. Esophagitis tended to improve or remain stable after H. pylori therapy and worsened in only 2 of the 49 patients (4%). Of 192 patients with a normal esophagus at baseline endoscopy, 14 (7%) showed evidence of esophagitis after therapy. The presence of hiatal hernia, but not cure of H. pylori, was significantly associated with the development of esophagitis. CONCLUSIONS: Our results indicate that esophagitis can coexist with peptic ulcer disease and persists after cure of H. pylori. Development of de novo esophagitis seems uncommon in the short-term after H. pylori therapy. Esophagitis in peptic ulcer disease is strongly associated with the presence of hiatal hernia.     

Prevalence of gastroesophageal reflux disease in immigrants living in the Zaanstreek region in the Netherlands

Racial differences in the incidence of reflux disease are reported but data on differences in ethnicity are rare. A study was undertaken to assess the prevalence of reflux disease, defined as the presence of reflux esophagitis, in immigrants and correlate the results with native inhabitants living in the same region. Consecutive patients with hiatus hernia and defective lower esophageal sphincter closure as well as reflux esophagitis were included. A large population of people of Turkish descent and a small contingent of people from northern Africa and the Middle East were studied separately. Reflux disease was diagnosed in 4165 patients. One hundred and sixty-seven (4%) were of Turkish descent, and 26 (0.6%) originated from Africa and the Middle East. Reflux disease occurred significantly less often in immigrants, 24% versus 55.5% (P < 0.0001). There was no difference relating to gender in the presence of reflux disease in native Dutch patients, while the number of men in the immigrant group with the condition was significantly higher than women; 51% versus 72%, respectively (P < 0.0001). The majority of immigrants only suffered from mild reflux esophagitis (P < 0.001). Immigrants with reflux disease are significantly younger than native Dutch patients, mean age 42 years versus 57 years, respectively (P < 0.0001). Reflux disease is less prevalent in immigrants, mostly people of Turkish descent. If the condition is present in this population, the majority of patients is male and belongs to the younger age cohorts.     

The occurrence of a duodenal or gastric ulcer in two different populations living in the same region: a cross-sectional endoscopical study in consecutive patients.

BACKGROUND: Marked differences in prevalence of Helicobacter pylori have been noted between population subgroups living in the same country. A cross-sectional endoscopical study in consecutive patients presenting with active ulcer disease was done, in order to study the H. pylori prevalence in relation to ethnicity in ulcer patients. METHODS: Consecutive patients with an active duodenal or gastric ulcer were eligible for inclusion. Biopsy specimens from the gastric antrum were taken for detection of H. pylori. People originating from Turkey were studied separately. RESULTS: In an 8-year period, 375 patients with active duodenal ulcer were seen. Three hundred one patients were ethnic Dutch. Seventy-four of the patients were of Turkish origin. These were statistically significant younger than ethnic Dutchmen, 35.9 vs. 61.2 years (P<0.0001). The number of men was significantly higher, 82.4% vs. 53.8% (P<0.001). H. pylori prevalence was significantly higher in Turkish patients with duodenal ulcer, 91 vs. 74% (P<0.0001). Gastric ulcer was seen in 218 patients. Only five patients were of Turkish descent. The number of Turkish patients was too small to permit statistical analysis, but the percentage of men is higher and the mean age is lower compared with ethnic Dutchmen. CONCLUSIONS: It is concluded that if ulcer disease and H. pylori prevalence is studied in a given population, ethnicity of the population understudy has to be taken into account.     

A low prevalence of H pylori and endoscopic findings in HIV-positive Chinese patients with gastrointestinal symptoms

AIM： To compare the prevalence of H pylori infection, peptic ulcer, cytomegalovirus （CNV） infection and Candida esophagitis in human immunodeficiency virus （HIV）- positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections.
METHODS： A total of 151 patients （122 HIV-positive and 29 HIV-negative） with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of Hpylori infection, CMV, candida esophagitis and histologic chronic gastritis.
RESULTS： The prevalence of Hpylori was less common in HIV-positive patients （22.1%） than in HIV-negative controls （44.8%; P 〈 0.05）, and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer （20.7% vs 4.1%; P 〈 0.01）, but a higher prevalence of chronic atrophy gastritis （6.9% vs 24.6%; P 〈 0.05）, Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis （P 〈 0.05）. In HIV-positive patients, chronic active gastritis was not significantly different between those with Hpylori infection and those without.
CONCLUSION： The lower prevalence of H pylori infection and peptic ulcer in HIV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer. The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to Hpylori infection.     

Impact of Helicobacter pylori eradication on the anti-secretory efficacy of lansoprazole in gastroesophageal reflux disease patients

BACKGROUND: Helicobacter pylori eradication was recommended for the prevention of atrophic gastritis in gastroesophageal reflux disease (GERD) patients on long-term omeprazole treatment. It has been also shown that the treatment with proton pump inhibitors produces lower intragastric pH after H. pylori eradication in subjects with peptic ulcer and healthy individuals. The aim of the present study was to test the hypothesis of whether the efficacy of lansoprazole is reduced after the eradication of H. pylori in GERD patients with peptic esophagitis. METHODS: Eight-hour intragastric pH recordings were performed before and after an 8-day course of lansoprazole (30 mg once daily) in 10 H. pylori-positive male patients with reflux esophagitis and were repeated after the H. pylori eradication. Intragastric acidity was measured by using an antimony electrode placed 10 cm below the cardia. RESULTS: Baseline median preprandial, post-prandial, total intragastric pH and the percentage of time with pH < 3 were not different before and after H. pylori eradication without lansoprazole treatment. During lansoprazole treatment, median post-prandial intragastric pH was lower (4 vs 2.7; P < 0.05) and the percentage of time with pH < 3 was longer (3.4%vs 41.8%; P < 0.05) after H. pylori eradication. Median total intragastric pH tended to be lower after eradication but no difference was found in preprandial median pH. CONCLUSIONS: In patients with reflux esophagitis treated with lansoprazole, intragastric pH increased significantly when H. pylori was present, especially in the post-prandial period, whereas baseline pH remained unchanged after H. pylori eradication.     

Empirical treatment based on "typical" reflux symptoms is inappropriate in a population with a high prevalence of Helicobacter pylori infection

BACKGROUND: Empirical therapy or early endoscopy have been recommended as acceptable management options for GERD. The objective of this study was to determine whether diagnosis and empirical treatment based on reflux symptoms alone are appropriate as initial management for patients with gastroesophageal reflux. METHOD: Consecutive patients presenting with weekly reflux symptoms were evaluated with a structured questionnaire followed by endoscopy. Patients with dyspepsia as the predominant symptom, "alarm" symptoms (weight loss, dysphagia, or bleeding), history of peptic ulcer or gastric surgery, or recent nonsteroidal anti-inflammatory drugs intake were excluded. RESULTS: Four hundred sixty patients were studied: 82 (18%) were found to have peptic ulcer disease and 78 (95%) were infected with Helicobacter pylori. Concomitant erosive esophagitis was found in 26 (32%) of these patients with peptic ulcer disease. In the remaining 378 patients, 218 (58%) had erosive esophagitis and 1 had esophageal cancer. Among the 159 patients with no endoscopic lesion, 148 (93%) had relief of symptoms when treated with a proton pump inhibitor. Multivariate analysis showed that male gender (OR: 1.8, p = 0.03), age greater than 60 years (OR: 2.2, p = 0.01) and H pylori infection (OR: 3.6, p = 0.008) were significantly associated with a diagnosis of peptic ulcer disease. Coexisting dyspeptic symptom was not a predictor (p = 0.13) for peptic ulcer disease. CONCLUSIONS: In populations with a high prevalence of H pylori infection, a significant proportion of patients with GERD have concomitant peptic ulcer disease. Empirical treatment based on "typical" GERD symptoms alone may not be appropriate.     

Effectiveness of acid suppression in preventing gastroesophageal reflux disease (GERD) after successful treatment of Helicobacter pylori infection

There is evidence that Helicobacter pylori eradication might predispose to gastroesophageal reflux disease (GERD). The aim of this prospective study was to examine the effectiveness of antisecretory treatment, after successful H. pylori eradication, in preventing GERD, since no data exist so far. Eighty initially H. pylori(+) patients, without GERD at the time of H. pylori eradication [50 peptic ulcer (PU) and 30 nonulcer (NU), 55 men, 25 women, median age 38 years, range 19–57], after successful H. pylori eradication were randomized to recieve either omeprazole 20 mg daily (group A) or no treatment (group B) for one year. All patients underwent upper gastrointestinal endoscopy at 0, 6, and 12 months or when GERD symptoms occurred. There were 40 patients in each group, and there were no statistically significant differences between the two groups in terms of sex, age, body weight, ulcer/no ulcer ratio, and other demographic data. Seven patients from group A and five patients from group B were lost to follow-up, and therefore there were 33 and 35 patients in groups A and B, respectively, who completed the study. One of 33 patients in group A (3%) and 10/35 (28.5%) in group B developed GERD symptoms during follow-up (P = 0.0022). The respective values for esophagitis were 0/33(0%) and 6/35(17.1%) (P = 0.0083). In conclusion, antisecretory treatment in H. pylori(+) patients, after successful eradication, is effective in preventing GERD.     

A low prevalence of H pylori and endoscopic findings in HTV-positive Chinese patients with gastrointestinal symptoms

AIM: To compare the prevalence of H pylori infection,peptic ulcer, cytomegalovirus (CMV) infection and Candida esophagitis in human immunodeficiency virus (HIV)-positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections.METHODS: A total of 151 patients (122 HIV-positive and 29 HIV-negative) with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of H pylori infection,CMV, candida esophagitis and histologic chronic gastritis.RESULTS: The prevalence of H pylori was less common in HIV-positive patients (22.1%) than in HIV-negative controls (44.8%; P ＜ 0.05), and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer (20.7% vs 4.1%; P ＜ 0.01), but a higher prevalence of chronic atrophy gastritis (6.9% vs 24.6%; P ＜ 0.05), Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis (P＜0.05). In HIV-positive patients, chronic active gastritis was not significantly different between those with H pylori infection and those without.CONCLUSION: The lower prevalence of H pylori infection and peptic ulcer in HTV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer.The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to H pylori infection.     

The impact of Helicobacter pylori eradication on peptic ulcer healing

Objective: Current literature was reviewed analyzing the outcome of peptic ulcer healing in relation to the results of the posttherapeutic Helicobacter pylori (HP) status.
Methods: Literature was reviewed along with an analysis of 60 studies, comprising a total of 4329 patients.
Results: Successful Helicobacter pylori eradication was found to induce a better response in peptic ulcer healing, regardless of diagnosis: gastric ulcer 88% vs 73% (odds ratio [OR] 2.7,   p < 0.01  ), duodenal ulcer 95% vs 76% (OR 5.6,   p < 0.0001  ), and peptic ulcer 95% vs 76% (OR 6.6,   p < 0.0001  ), for patients having their HP infection successfully cured versus those remaining HP-positive, respectively (Fisher's exact test). For all evaluated time points (≤ 6, 7–8, and 10–12 wk after beginning treatment), HP-negative patients had higher healing rates than HP-positive patients (95% vs 82%, 94% vs 69%, and 96% vs 78% with corresponding OR of 4.2, 6.5, and 7.4, all   p < 0.0001  , Fisher's exact test). The use of concomitant acid suppression therapy during initial HP eradication provided a benefit on peptic ulcer healing only for patients with persistent HP infection (improved healing rates of 78% vs 67%; otherwise rates were 94–96%). Likewise, prolonged acid inhibition in HP treatment failures after the initial HP treatment phase resulted in 7–20% improved healing rates, whereas patients becoming HP-negative did not profit.
Conclusion: Successful HP eradication therapy accelerates peptic ulcer healing even without concomitant acid suppression.     

A low prevalence of H pylori and endoscopic findings in HIV-positive Chinese patients with gastrointestinal symptoms

AIM: To compare the prevalence of H pylori infection,peptic ulcer,cytomegalovirus (CMV) infection and Candida esophagitis in human immunodeficiency virus (HIV)-positive and HIV-negative patients,and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections. METHODS: A total of 151 patients (122 HIV-positive and 29 HIV-negative) with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of H pylori infection,CMV,candida esophagitis and histologic chronic gastritis. RESULTS: The prevalence of H pylori was less common in HIV-positive patients (22.1%) than in HIV-negative controls (44.8%; P < 0.05),and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group,HIV-positive patients had a lower incidence of peptic ulcer (20.7% vs 4.1%; P < 0.01),but a higher prevalence of chronic atrophy gastritis (6.9% vs 24.6%; P < 0.05),Candida esophagitis and CMV infection. Unlike HIV-negative group,H pylori infection had a close relationship to chronic active gastritis (P < 0.05). In HIV-positive patients,chronic active gastritis was not significantly different between those with H pylori infection and those without. CONCLUSION: The lower prevalence of H pylori infection and peptic ulcer in HIV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer. The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to H pylori infection.     

Eradication of helicobacter pylori reduces the rate of duodenal ulcer rebleeding: a long-term follow-up study

Objectives: The long-term efficacy of Helicobacter pylori eradication to reduce the rate of recurrence of peptic ulcer bleeding is still uncertain. We evaluated the rate of duodenal ulcer rebleeding for 48 months after H. pylori eradication.
Methods: Thirty-two male patients with H. pylori infection and duodenal ulcer bleeding were treated with omeprazole (40 mg/day for 4 wk), colloidal bismuth (480 mg/day for 2 wk), amoxicillin (2 g/day for 1 wk), and metronidazole (750 mg/day for 1 wk), and followed up for 48 months. Endoscopy and tests for H. pylori infection were repeated every year.
Results: Ulcer healed in all patients, but H. pylori infection persisted or recurred in 11 patients. Within 48 months, rebleeding occurred in nine (81.8%) of these patients, whereas the 21 patients who were persistently negative for H. pylori infection remained asymptomatic without rebleeding (0/21 = 0%,   p < 0.002  ) during the whole follow-up.
Conclusions: Eradication of H. pylori can reduce the rate of duodenal ulcer rebleeding for at least 4 yr, thus potentially modifying the natural history of the disease.     

H. pylori and Reflux Esophagitis in Turkish Patients Living in the Zaanstreek Region in The Netherlands

There are data on the prevalence is of reflux esophagitis in a population with a high prevalence of H. pylori infection. A cross-sectional study was done in a Turkish population in The Netherlands. A total of 1640 consecutive patients with reflux esophagitis were included. Sixty-one patients were of Turkish descent. Reflux esophagitis occurred significantly more often in ethnically Dutchpeople (overall 33% vs. 9.7%, P < 0.001). H. pylori was present in 60.6% of Turkish patients and in 18.5% of Dutch patients. All Turkish patients only suffered from mild esophagitis. It is concluded that the occurrence of reflux esophagitis is low in a population of Turkish patients with a high prevalence of H. pylori.     

Reflux esophagitis and hiatal hernia as concomitant abnormality in patients presenting with active duodenal or gastric ulcer: cross-sectional endoscopic study in consecutive patients

BACKGROUND: Follow-up studies have shown that patients with ulcer disease are at risk of developing reflux esophagitis (RE) after successful eradication of Heliobacter pylori. It is still not clear whether this is induced by eradication of H. pylori or whether RE is already present at the time the ulcer is diagnosed. A cross-sectional study was done in consecutive patients suffering from active ulcer disease in order to assess coincidental RE. METHODS: Patients with an active duodenal or gastric ulcer were included in the study. Concomitant RE and the presence of hiatal hernia (HH) were scored. Biopsy specimens were taken for detection of H. pylori. RESULTS: In 375 patients (77%), an active duodenal ulcer was the only abnormality. In 43 patients (8.8%), duodenal ulcer and concomitant RE were present and 69 patients (14.2%) had a duodenal ulcer with concomitant HH. Patients with a duodenal ulcer were significantly younger than patients with concomitant RE or HH. From 374 patients (76.8%) with a duodenal ulcer, biopsy specimens were available for the detection of H. pylori. The majority of duodenal ulcer patients were H. pylori-positive. H. pylori was significantly more often present in patients with an active duodenal ulcer than it was in duodenal ulcer patients suffering from concomitant RE (P=0.04). In 218 patients (76%), a gastric ulcer was the only abnormality. Fifteen patients (5.2%) also had RE and 54 patients (18.8%) had a concomitant HH. There was no difference in H. pylori status in these three groups of patients. CONCLUSIONS: Given the low prevalence of concomitant RE, it is concluded that this condition is likely to occur in a large percentage of patients suffering from H. pylori-positive ulcer disease after successful eradication therapy.     

Ulcer recurrence after gastric surgery: is helicobacter pylori the culprit?

Objectives: Helicobacter pylori is the most important cause of recurrent peptic ulcer disease. However, its role in ulcer recurrence after peptic ulcer surgery is unclear. We aimed at studying the prevalence and distribution of H. pylori in patients who had undergone peptic ulcer surgery, and any association between H. pylori infection and ulcer recurrence in these patients.
Methods: Patients with previous vagotomy or partial gastrectomy presenting with dyspepsia or ulcer bleeding were recruited. Ulcer recurrence was documented by endoscopy. Biopsy specimens were taken from the gastric remnant and gastroenteric anastomosis in patients with previous partial gastrectomy, or from the antrum and corpus in vagotomized patients. H. pylori infection was detected by either a positive rapid urease test or the presence of the bacteria on histology.
Results: Ninety-three patients were studied; 73 patients (78%) had partial gastrectomy and 20 (22%) had vagotomy with drainage. H. pylori infection was documented in 36 patients (49%) in the gastrectomy group and in 13 (65%) in the vagotomy group. Thirty-six patients in the gastrectomy group had recurrent ulcers and 15 (42%) of them had H. pylori infection. Twelve patients in the vagotomy group had recurrent ulcers and eight (67%) of them were H. pylori positive. The prevalence of H. pylori infection did not differ between patients with or without ulcer recurrence.
Conclusion: H. pylori infection cannot account for ulcer recurrence after peptic ulcer surgery.     

Phenotypic and genotypic characterization of Helicobacter pylori from patients with and without peptic ulcer disease

BACKGROUND: Helicobacter pylori plays an important role in peptic ulcer disease, although not all H. pylori-infected persons will develop a peptic ulcer. Currently, H. pylori strains cannot be divided into commensals and pathogens. METHODS: Fifty H. pylori strains were cultured from patients divided into five groups on the basis of upper endoscopic findings: gastric ulcer, duodenal ulcer, gastritis, esophagitis, or normal. The ultrastructural adherence pattern in vivo, autoagglutination, hemagglutination, adhesion to human gastric adenocarcinoma (AGS) cells, and the lipopolysaccharide (LPS) profile of H. pylori strains were recorded; randomly amplified polymorphic DNA (RAPD) and urease gene typing were performed and correlated with diagnostic groups. RESULTS: Electron micrographs showed that H. pylori strains from patients with gastric ulcers adhered more frequently through filamentous strands and were less frequently found free in mucus than any other diagnostic group (P < 0.0001). Neither median hemagglutination titer nor median adhesion capacity to a human gastric adenocarcinoma cell line was related to endoscopic findings. Nevertheless, H. pylori strains from patients with gastric ulcers were more prone to autoagglutinate than were strains from the other diagnostic groups (P = 0.03). H. pylori strains from gastric ulcer patients were found to be more homogeneous, as determined by RAPD and urease gene typing, than strains from the other diagnostic groups (P < 0.01). In addition, a positive correlation was found between a patient's age and the adhesion to AGS cells of the patient's H. pylori strain (P = 0.006). CONCLUSION: A combination of an H. pylori autoagglutination test, RAPD, and urease gene typing may be useful in separating gastric ulcer-related strains from duodenal ulcer-related and non-ulcer dyspepsia-related strains.     

Reflux esophagitis in patients with partial gastrectomy and Billroth I or II reconstruction

BACKGROUND: Data on the occurrence of reflux esophagitis and Barrett's esophagus in patients with Billroth I or II resection is sparse. For this reason a cross-sectional study was done in order to assess reflux disease in Billroth resection. METHODS: Consecutive patients were included in the study. Coincidental pathology (hiatus hernia, ulcer, esophagitis, and cancer) was noted. RESULTS: Over a period of 12 years, 370 consecutive patients with a partial gastrectomy were seen (268 Billroth II, 102 Billroth I) and three groups of patients were identified. Group 1 included 64 patients (17%) with a hiatus hernia; group 2, 16 patients (4%) with reflux esophagitis; and group 3, 290 patients (78%) with only a Billroth resection. Reflux disease occurred significantly more often in men than in women (7.5% vs. 2%, p<0.05). There was no difference in type of resection or in the presence of reflux esophagitis. Four patients had an esophageal cancer (only one adenocarcinoma). CONCLUSION: Only a minority of patients with partial gastrectomy has signs of esophagitis in the long term.     

Prevalence of Helicobacter pylori in a representative Anglo-Celtic population of urban Melbourne

The aims of this study were to assess the prevalence of Helicobacter pylori and its relationship with different epidemiological factors in an Anglo-Celtic Australian population in the Melbourne urban area. Two hundred and seventy-three (120 men and 153 women with a mean age of 55.6 and range of 20 to 80 years) of 396 eligible subjects randomly sampled from the telephone directory were studied. An ELISA technique was used to detect H. pylori immunoglobulin (Ig)G antibody and self-administered questionnaires were completed. The overall seroprevalence of H. pylori was 38% and increased with age from 18% (20–30 years old) to 53% (over 70 years; P < 0.0001). The acquisition of H. pylori infection was 1% per year. The prevalence of H. pylori was 48% in men and 30% in women ( P < 0.01). The frequency of H. pylori was also associated with low-income levels and current smoking, but was not associated with peptic ulcer disease history. The prevalence of H. pylori infection in a representative Australian population was found to be similar to other developed countries. The risk factors for H. pylori infection include age, male sex, low household income and a smoking habit. No correlation between H. pylori status and dyspepsia symptoms were observed.