Clinical relevance of Helicobacter pylori CagA-positive strains: gastroduodenal peptic lesions marker.

OBJECTIVES: peptic ulcer is characterized by its recurrent nature, which necessitates maintenance treatment in most patients. But this natural history can be changed in patients with peptic ulcer associated to Helicobacter pylori, as shown by the low rates of recurrence and decreased hemorrhagic recidivism associated with this infection. Whether CagA or VacA strains are associated with a greater risk of peptic ulcer is controversial. This study was designed to examine endoscopic findings and their relation with H. pylori phenotype (CagA or VacA). METHODS: 106 selected dyspeptic patients underwent upper gastrointestinal tract endoscopic examination between September 1996 and May 1997 [69 with H. pylori (Hp) and 37 without this infection]. Endoscopic findings were classified as gastric ulcer (GU), duodenal ulcer (DU), gastric erosions (GE), duodenitis (Du), chronic gastritis (CG) and normal mucosa (NM). Hp phenotype was analyzed with a western blot test. RESULTS: 75% of H. pylori strains were CagA-positive and 54.2% were VacA-positive. 82.4% of the cases of DU were associated with a CagA+ phenotype, but the association was not statistically significant. Otherwise 100% of gastric ulcers were associated with CagA+ strains (p < 0.005). VacA phenotype was not associated with any particular endoscopic finding. Peptic ulcer (DU or GU) was also associated with the CagA+ phenotype (p < 0.05). CONCLUSIONS: the CagA+ H. pylori phenotype seems to be a peptic lesion marker, but was more frequently related with GU than with DU in our sample of Spanish patients.     

Prevalence of peptic ulcer in Helicobacter pylori positive blood donors.

This study aimed to determine the importance of raised antibodies to Helicobacter pylori in an asymptomatic population. A total of 128 asymptomatic blood donors who were seropositive for H pylori and consented to endoscopy were investigated. These subjects were from a population of 1010 blood donors screened for antibodies to H pylori. A questionnaire was completed to determine if any subjects had complained of symptoms, and they subsequently had endoscopy. Altogether 121 of 128 were positive for H pylori by histology and urease test and/or culture and all 121 had chronic active gastritis on histology. Twenty five of these subjects had peptic ulcer (20 duodenal, five gastric), a further 21 had erosive duodenitis, and two were found to have gastric cancer. H pylori associated peptic ulcer disease and duodenitis occur more frequently than previously recognised and this suggests that H pylori infection, even if asymptomatic, is of far greater clinical relevance than originally thought.     

Helicobacter pylori and Duodenal Ulcer Recurrence

Preliminary evidence suggests that eradication of Helicobacter pylori (H. pylori) may lead to prolonged remission of duodenal ulcer (DU). The aim of this study was to assess the long-term effect of eradication of H. pylori on the natural history of DU. Fifty-one patients with endoscopically proven duodenal ulcers, who were found to have H. pylori infection on histology and culture, and who were successfully eradicated of H. pylori with combination treatment of colloidal bismuth subcitrate and antibiotics, were studied. All patients were endoscoped at entry, 4 wk after cessation of treatment and again at 1 yr or sooner, if symptoms recurred. At each endoscopy, two antral biopsies were taken and assessed histologically and microbiologically for evidence of H. pylori infection. Recurrence of H. pylori infection occurred in 18/51 patients (35.3%) and, of these, 12 patients had evidence of recurrent peptic disease (five DU, seven duodenitis). In contrast, of the 33 who remained negative for H. pylori at 1 yr, none developed evidence of recurrent DU. Overall, DU recurrence occurred in 5/51 patients (11.7%), and occurred only in patients reinfected with H. pylori. This relapse rate compares favorably with patients on maintenance H2-receptor antagonist treatment. These results lend further support to the hypothesis that antral reinfection with H. pylori is associated with relapse of DU.     

14C]-urea breath test to confirm eradication of Helicobacter pylori

BACKGROUND: Treatment for Helicobacter pylori reduces ulcer recurrence. Eradication rates of the organism vary with different drug regimens from 30% to 90%. There is a need to identify patients who have failed treatment. [14C]-Urea breath test (UBT) is non-invasive, sensitive, safe and highly reliable test for diagnosis of H. pylori infection. As there is a paucity of reports on the utility of [14C]-UBT in confirming H. pylori eradication, this study was undertaken. METHODS: Thirty-eight patients (age 34 +/- 17 years, range 16-84 years, 27 men) with upper gastrointestinal symptoms underwent upper gastrointestinal endoscopy. Baseline H. pylori infection was diagnosed by identification of the organism on antral biopsies and positive rapid urease test (RUT). After 1 month of completion of treatment, repeat RUT and histological examination of antral endoscopic biopsies were performed. Eradication of H. pylori was defined as absence of the organism on histology, and negative RUT. The [14C]-UBT was performed using 185 kBq [14C]-urea dissolved in 300 mL water. Breath samples were collected once before ingestion of [14C]-urea, and subsequently at 5 and 15 min. Results were expressed as 14CO2/mmol CO2 exhaled as per cent of administered urea. RESULTS: Endoscopy revealed antral gastritis (n = 14), duodenal ulcer (n = 8), duodenitis (n = 2), oesophagitis (n = 1), antral gastritis and duodenal ulcer (n = 3), antral gastritis and duodenitis (n = 7) and normal upper gastrointestinal endoscopy (n = 3). All the 20 patients who were negative for H. pylori on RUT and histology, tested negative for H. pylori on [14C]-UBT. However, of 18 patients shown to have H. pylori infection on RUT and histology, 16 were positive for H. pylori on [14C]-UBT. The sensitivity, specificity, positive predictive value, negative predictive value and accuracy of [14C]-UBT were 100, 89, 91, 100 and 95% respectively. CONCLUSIONS: The [14C]-UBT is a reliable indicator of H. pylori eradication after treatment. It can obviate the need for antral biopsies to confirm eradication of H. pylori after completion of treatment.     

十二指肠球部多发隆起病变与幽门螺杆菌和胃上皮化生的关系

目的探讨内镜下十二指肠球部多发隆起病变与幽门螺杆菌（Hp）感染和胃上皮化生等组织学异常关系.方法连续调查86例经胃镜检查证实十二指肠球部多发隆起病变患者,并以40例球部基本正常患者作为对照.病变组Hp阳性患者接受三联根除治疗（奥美拉唑20mg、克拉霉素250mg、甲硝唑400mg,每天2次）,疗程7 d,停药后随访6个月后复查胃镜;病变组Hp阴性者接受奥美拉唑20 mg,每天1次治疗,疗程4～6个月,停药后2周复查胃镜.比较2次胃镜检查结果,包括胃镜下隆起病变程度及球部黏膜胃上皮化生等组织学异常,分析Hp感染与上述胃镜下表现及组织学异常关系.结果对照组患者组织学仅部分发现轻度慢性炎症,未发现球部Hp感染.病变组患者Hp检出率为58.1%,胃上皮化生检出率为57.0%.Hp阳性与Hp阴性患者胃镜下隆起病变程度差异无统计学意义（P＞0.05）,但胃上皮化生检出率更高,程度更严重（P＜0.05）.76例患者复查胃镜,根除Hp或奥美拉唑治疗对Hp阳性或阴性患者球部多发隆起病变无明显作用,但根除Hp后6个月,53.6%（15/28）患者胃上皮化生消失,61.0%（25/41）患者绒毛萎缩恢复正常,所有患者淋巴滤泡完全消失（26/26）,杯状细胞减少完全恢复（25/25）,同时炎症和活动性显著减轻（P值均＜0.01）.奥美拉唑疗效不显著.结论十二指肠球部多发隆起病变患者半数以上有Hp感染.Hp感染与隆起病变伴随组织学炎症密切相关,而与其内镜下表现及严重程度无关.根除Hp可使炎症显著减轻,胃上皮化生范围缩小或消退.     

Diagnosis of Helicobacter pylori infection in patients with bleeding ulcer disease: rapid urease test and histology.

INTRODUCTION: The endoscopic diagnosis of Helicobacter pylori infection in patients with bleeding peptic ulcer is limited by a decreased sensitivity in standard invasive tests, rapid urease test and histology. There is controversy about the convenience of using one, neither, or both diagnostic tests. AIMS: To evaluate the results of simultaneously performed rapid urease test and histology in the diagnosis of Helicobacter pylori infection (H. pylori) in patients with bleeding peptic ulcer. PATIENTS AND METHODS: We included 173 patients, 98 male and 75 female, with an average age of 62 years (18-88), with upper gastrointestinal bleeding secondary to duodenal ulcer (115) or gastric ulcer (58), diagnosed within 24 hours after hospital admission. None of the patients had received treatment for H. pylori, proton pump inhibitors or antibiotics in the two weeks prior to the upper gastrointestinal bleeding episode. H. pylori infection was investigated in all patients by two antral biopsy samples for histological study (hematoxilin-eosin) and one or two antral biopsies for rapid urease test (Jatrox-H.p.-test). In cases with a negative urease test and histology, a 13C urea breath test was performed. Infection was considered present when at least one invasive test or the breath test was positive, whereas both invasive tests and the breath test had to be negative to establish an absent infection. RESULTS: 152 patients (88%) showed H. pylori infection, 104 patients (90%) with duodenal ulcer and 48 patients (83%) with gastric ulcer. In all 119 cases (78%) were diagnosed by the urease test and 112 cases (74%) by histology. Both methods were used to diagnose 134 of 152 cases (88%) (p < 0.05), these being positive in 97 cases and negative in 39 cases. In 18 of these 39 cases, the breath test was positive. CONCLUSIONS: Histology and urease test have similar diagnostic values for the identification of H. pylori in patients with bleeding peptic ulcer. Due to its rapid results, the urease test should be the method of choice. However, additional biopsies should be performed, and, when negative, a histological study should be carried out, since a combination of both methods allows a more precise diagnosis.     

Low sensitivity of invasive tests for the detection of Helicobacter pylori infection in patients with bleeding ulcer

BACKGROUND: A high false negative rate for antral infection with Helicobacter pylori when assessed by rapid urease test has recently been reported in patients with bleeding ulcer. This result could partly explain the differing prevalence of H. pylori infection in bleeding and non-bleeding ulcers. AIMS: To evaluate the accuracy of a rapid urease test (UT), histology and culture for detection of H. pylori in antral biopsies from acute bleeding peptic ulcer patients using a serological test as reference. PATIENTS AND METHODS: All consecutive patients with active bleeding gastric or duodenal ulcer at endoscopic examination admitted in six university hospitals in France were considered for inclusion. Five antral biopsies were taken during the diagnostic endoscopy for UT, culture and histology. A blood sample was taken for H. pylori serology. RESULTS: One hundred and eighty one patients were included and 129 (71%) had a positive serology. The sensitivity of UT, histology and culture for detection of H. pylori infection were 41%, 33% and 34%, respectively. The sensitivity and specificity of the combination of the three invasive tests were 48.8% (95% CI: 40.2-57.4) and 90.6% (95% CI: 82. 6-99) respectively. In the 52 serologically negative patients, only 5 had at least one invasive positive test. The sensitivity of the invasive tests decreased significantly with age but was not influenced by NSAIDs intake. Of 80 patients with a positive serological test and negative histological evaluation for H. pylori, chronic antral inflammation was found in 70 patients (87%). In 46 patients with both negative serological test and H. pylori negative test according to histology, only 13 (28%) had chronic antral inflammation. CONCLUSIONS: The sensitivity of invasive tests for detection of H. pylori is low during acute ulcer bleeding, and they should be used with caution in this condition. A serological test is recommended to identify patients with H. pylori infection in spite of negative invasive tests.     

Serologic detection of CagA positive Helicobacter pylori strains predicts the presence of peptic ulcer in young dyspeptic patients.

BACKGROUND: Helicobacter Pylori infection has been strongly associated with upper gastrointestinal (GI) disease, especially duodenal ulcer. Endoscopy or contrast radiography is needed to diagnose and appropriately manage peptic ulcer disease. These diagnostic procedures, however, are time consuming and expensive; endoscopy is invasive and contrast radiography cannot help in the diagnosis of H pylori infection. Our aim was to examine in a prospective study the relation between serologic detection of cytotoxic associated gene (CagA) H pylori strains and endoscopic findings among young dyspeptic patients to determine whether this noninvasive test can help differentiate patients with from those without ulcers. METHODS: One hundred patients younger than 45 years with dyspepsia referred for upper GI endoscopy were included in the study. During endoscopy antral biopsy specimens were obtained for the rapid urease test and histologic examination. At histologic examination gastritis was graded from 0 (normal histologic features) to 3 (severe gastritis). After endoscopy blood was obtained for serologic determination of CagA status. RESULTS: Among the 100 patients 56 were H pylori positive and 44 were H pylori negative. In the group of 56 H pylori-positive patients 36 (64.3%) had peptic ulcers and 20 (35.7%) did not. Among patients with peptic ulcer 34 of 36 (94.4%) were CagA positive and 2 (5.6%) were CagA negative. The respective values for the group of patients without ulcers were 9 of 20 (45%) and 11 of 20 (55%). The difference in the proportion of CagA-positive subjects between the group with and that without peptic ulcer was highly significant (p < 0.0001). CONCLUSIONS: Among young patients with dyspepsia, CagA seropositivity is highly associated with duodenal ulcer at endoscopy.     

Campylobacter pylori in peptic ulcer disease. II. Endoscopic findings and cultivation of C. pylori

Specimens from 153 consecutive patients were cultivated for C. pylori, and findings were correlated to the endoscopic findings. C. pylori was cultivated more frequently from males than from females. Culture-positive males had a high frequency of prepyloric abnormalities. No correlation between age or pH in gastric juice and cultivation of C. pylori was found. C. pylori was found significantly more often in patients with peptic ulcer and/or duodenitis than in patients with normal endoscopic findings. No differences could be detected between patients with gastritis or esophagitis and patients with normal endoscopic findings. C. pylori was found most frequently in the antral part of the stomach. It was cultivated significantly more often from patients with duodenal abnormalities than from patients with normal endoscopic findings. In less than half of the culture-positive patients with duodenal abnormalities we cultivated C. pylori from duodenal specimens. This study also showed C. pylori in esophageal specimens, which has not been previously described. Our results suggest that cultivation of C. pylori from duodenal specimens or gastric fluid samples gives no additional information beyond that obtained from the cultivation of antral biopsy specimens. It is our opinion that C. pylori, at least in some cases, may be a secondary infection.     

A comparative study on Helicobacter pylori infection in peptic ulcer disease patients with or without previous eradication therapy

BACKGROUND/AIMS: Although H. pyloric eradication therapy is indicated for peptic ulcer patients, the prevalence of H. pylori infection may be different between patients with active or chronic (scarred) peptic ulcers. This study aimed to compare the prevalence of H. pylori infection in active and chronic peptic ulcer patients with or without previous H. pyloric eradication therapy. METHODOLOGY: Both non-invasive (13C or 14C urea breath test) and invasive methods (rapid urease test and histology) were used to detect H. pylori. From Dec. 2002 to Jan. 2003, 153 patients with 63% male were enrolled in this study. Fifty-six patients who previously received H. pyloric eradication therapy were enrolled as treated patients, and 97 patients who did not receive therapy were enrolled as untreated patients. RESULTS: H. pylori infection rate was still high in untreated patients even when duodenal ulcer had been scarred (96% in active duodenal ulcer and 63% in scarred duodenal ulcer). In treated patients, H. pyloric infected rates were very low when peptic ulcers were scarred (0% in scarred gastric ulcer, 4% in scarred duodenal ulcer and 0% in both scarred ulcers). CONCLUSIONS: H. pyloric eradication therapy is indicated for untreated patients even when endoscopic examination revealed chronic scarred duodenal ulcer.     

Influence of sex and Helicobacter pylori on development and healing of gastroduodenal lesions in non-steroidal anti-inflammatory drug users

BACKGROUND AND AIMS: Factors predisposing to endoscopic ulcer formation or healing with non-steroidal anti-inflammatory drugs (NSAIDs) have not been well defined. METHODS: We used multivariate analysis of data from three large similar trials to identify factors associated with endoscopic lesions and healing. We compared the effectiveness of omeprazole 20 mg and 40 mg daily, misoprostol 200 micro g four times daily, and ranitidine 150 mg twice daily in healing ulcers and erosions at different sites and in patients who were Helicobacter pylori positive and negative. RESULTS: Older age, past ulcer history, rheumatoid arthritis, and H pylori infection were significantly associated with ulcers. Duodenal ulcer was significantly more likely than gastric ulcer with a past ulcer history (odds ratio 1.59, 1.16-2.17), H pylori infection (1.4, 1.04-1.92), and male sex (2.35, 1.75-3.16) while female sex, older age (> or = 60 years: 1.39, 1.03-1.88), and higher NSAID dose (>1 defined daily dose: 1.57, 1.16-2.14) were associated with gastric ulceration. Sex differences were seen in both H pylori positive and negative patients. Gastric and duodenal ulcer healing was significantly faster with omeprazole 20 mg than with misoprostol 200 micro g four times daily or ranitidine 150 mg twice daily although misoprostol was more effective at healing erosions. Gastric ulcer healing was slower with large ulcers (0.37, 0.25-0.54 for >10 mm v 5-10 mm) or a past ulcer history (0.51, 0.34-0.76), and faster with H pylori infection (1.55, 1.06-2.29), especially with acid suppression (72% v 37% at four weeks with ranitidine). CONCLUSIONS: Among NSAID users, H pylori and male sex independently increase the likelihood of duodenal ulceration. H pylori infection does not affect duodenal ulcer healing and enhances gastric ulcer healing by ranitidine and possibly other acid suppressing treatments.     

Duodenal erosions after eradication of Helicobacter pylori infection

BACKGROUND: There is interest in the development of GERD after Helicobacter pylori eradication. In contrast, the development of duodenal erosions after therapy has received scant attention. Patients were examined after eradication of H pylori infection to determine the frequency of post-therapy duodenal erosions (primary outcome) and whether there was a relation between development of duodenal and esophageal erosions. Additionally, factors were searched for that would identify patients at increased risk for duodenal erosions. METHODS: A single-center, endoscopist-blinded, observational study was conducted of 196 patients in whom H pylori was eradicated. The presence of esophageal or duodenal erosions was evaluated 4 weeks and 6 months after eradication. Serum gastrin and pepsinogen I (PG I) and II (PG II) levels were also determined for 83 patients entering the study during its final year. RESULTS: Multiple small duodenal erosions developed in 8.6% of patients after H pylori eradication and were more common in patients with pre-eradication duodenal ulcer (27.8%) compared with those with gastric ulcer (6.7%) or atrophic gastritis (1.4%) (p < 0.05). Duodenal erosions were associated with high levels of PG I before and after eradication. The frequency of duodenal erosions decreased over time (3.1% by 6 months). CONCLUSION: Duodenal erosions occur after H pylori eradication and appear to be related to duodenal ulcer and increased PG I levels, both of which are associated with increased acid secretion. Measurement of PG I may help to identify patients who have duodenal erosions develop after H pylori therapy for studies of the pathogenesis of these lesions.     

Helicobacter pylori status and endoscopy follow-up of patients having a history of perforated duodenal ulcer.

BACKGROUND: The aim of this study was to determine whether the recurrence of symptoms or ulcer disease in patients with a history of perforated duodenal ulcer is related to Helicobacter pylori infection. METHODS: One hundred sixty-three consecutive patients with history of perforated duodenal ulcer unrelated to nonsteroidal anti-inflammatory drugs underwent upper endoscopy. Any recurrent symptoms or complications were documented. Regardless of the endoscopic findings, three antral biopsy specimens were taken for histologic examination and a rapid urease test. RESULTS: There was a preponderance of men (male/female = 5.3:1). The mean age was 55.9 years. Sixty-seven (41.1%) patients gave a history of recurrent epigastric pain, seven of whom also had a history of bleeding ulcer. Upper endoscopy was performed at a mean of 74.5 +/- 7.1 months after operation. Positive endoscopic findings were noted in 68 (41.7%) patients; H. pylori was found in the biopsy specimens from 77 (47.2%) patients. Recurrent duodenal ulcer was found in 29 (17.8%) patients and was significantly related to male gender, recurrent epigastric pain, bleeding ulcer, longer interval from previous operation, and positive H. pylori status. Positive H. pylori status and male gender were independent factors associated with recurrent duodenal ulcer. CONCLUSIONS: Recurrent ulcer disease in patients with a history of perforated duodenal ulcer is related to H. pylori infection.     

Ideology of Helicobacter pylori prevalence in peptic ulcer disease in an inner-city minority population

GOALS AND BACKGROUND: The prevalence of Helicobacter pylori infection among patients with peptic ulcer disease has been reported to range from 61 to 94%. Recent studies show a reduction in the prevalence of H. pylori infection in patients with peptic ulcer disease. This study was conducted to determine the prevalence of H. pylori infection in peptic ulcer disease in an inner-city hospital in Washington, DC. METHODS: Medical records of all patients who had undergone upper gastrointestinal endoscopy from July 1997 through June 1999 were reviewed. All patients who had gastric ulcer and/or duodenal ulcer on upper gastrointestinal endoscopy were studied. Demographic characteristics, history of nonsteroidal antiinflammatory drug ingestion, alcohol consumption, and associated diseases were studied. H. pylori was considered to be present if CLOtest and/or histopathology were positive for H. pylori. Patients with negative pathology for H. pylori or negative pathology and CLOtest were considered negative for H. pylori. RESULTS: One-hundred fifty-six patients were found to have gastric and/or duodenal ulcers. Fifty-one ulcer patients did not meet the inclusion criteria and were excluded. Among the 105 patients who were included in the study, gastric ulcers were found in 48 patients (45.7%), duodenal ulcers were found in 46 patients (43.8%), and both gastric and duodenal ulcers were found in 11 patients (10.5%). H. pylori was present in 66.7% of gastric ulcer patients and in 69.5% of duodenal ulcer patients. Antral histology and CLOtest were in agreement 96% of the time. CONCLUSIONS: At the District of Columbia General Hospital, an inner-city hospital serving predominantly an African-American community, the prevalence of H. pylori in ulcer patients compares similarly to other more recent studies that have found a decreased prevalence of this bacterial infection in ulcer patients. This suggests that the treatment of H. pylori in minority patients is reducing the proportion of ulcers due to this bacterium, as has been seen with the majority population.     

Helicobacter pylori Reinfection Rate, in Patients with Cured Duodenal Ulcer

Objective: To determine the reinfection rate of the gastric mucosa in patients previously cured of duodenal ulcers, following the eradication oi Helicobacter pylori . Only those remaining H. pylori-negative beyond 12 months of follow-up were studied, to minimize the potential inclusion of patients with H. pylori recrudescence. Methods: Patients with endoscopically proven duodenal ulcers who had heen treated with triple therapy, resulting in documented eradication of H. pylori and cure of the ulcer for at least 4 years, were recalled and had their H. pylori status determined by the ¹⁴C-urea breath test. Those found positive for H. pylori underwent endoscopic confirmation of the infection. Results: Of the 94 patients restudied, with a follow-up period range of 48–96 months or a total of 549.8 yr, only two (2.2%) were again H. pylori positive. This gives an effective reinfection rate of 0.36% per patient year. In the two H. Pylori -positive patients, one had normal mucosa endoscopically, whereas duodenitis without active ulceration was present in the other. The former was asymptomatic, whereas the latter patient was using ranitidine daily for symptom control. Conclusion: In the Australian setting, following cure of duodenal ulcer disease by eradication of H. pylori , subsequent reinfection is an unusual phenomenon. We conclude that efforts aimed at eradication of H. pylori in duodenal ulcer are justified and are worthwhile.     

Helicobacter pylori infection, gastric metaplasia in the duodenum and the relationship with ulcer recurrence

OBJECTIVE: To study the prevalence of Helicobacter pylori (H. pylori) infection and gastric metaplasia (GM) in the duodenum a large group of patients with duodenal ulcer was evaluated to determine whether these factors are related to the number of ulcer recurrences. METHODS: Three hundred and seven patients diagnosed by endoscopy as having active duodenal ulcers were studied. At endoscopy, all patients had gastric biopsies taken for histology, the rapid urease test and culture. Three duodenal biopsies were also taken and processed for histology (haematoxylin & eosin, Giemsa, Warthin-Starry, and PAS stain). RESULTS: GM and H. pylori in the duodenum was identified in 73% (68-78%) and 66% (60-71%) of the cases, respectively. All patients with H. pylori in the duodenum also had GM at this location, while areas with GM but without H. pylori were described. The kappa statistic for concordance between GM and H. pylori at the duodenum was 0.82. The prevalence of GM and H. pylori, depending on the number of ulcer recurrences, was: 1st episode, 34% and 27%, respectively; 2nd episode, 84% and 80%; and > or = 3rd episode, 90% and 79% (P < 0.001 when comparing 1st vs 2nd or > or = 3rd episode). In the multivariate analysis, age and number of ulcer recurrences correlated both with GM and with H. pylori in the duodenum. Chronic duodenitis was demonstrated in all duodenal biopsies, 87% being active chronic duodenitis. H. pylori in the duodenum was more frequent in patients with active duodenitis (73%) than in those with inactive duodenitis (13%) (P < 0.001). CONCLUSIONS: Patients with recurrent ulcer disease have a higher prevalence of both GM and H. pylori infection in the duodenum, suggesting that these two factors are related with the chronicity and recurrence of duodenal ulcer disease. H. pylori infection in the duodenum always appears in areas of GM, although GM is not necessarily colonized by the organism. H. pylori infection cannot be excluded based only on the results of duodenal biopsies, as false negative results at this area are frequent.     

Helicobacter pylori and gastritis in patients with peptic ulcer and non-ulcer dyspepsia: ethnic differences in Singapore.

Peptic ulcer occurs with different frequencies in the three main racial groups in Singapore. This study aimed firstly to determine the prevalence of Helicobacter pylori in peptic ulcer and non-ulcer dyspepsia patients of the different races and secondly, to assess the relation between H pylori, histological gastritis, patient diagnosis, and race. Gastric antral biopsy specimens from 1502 patients undergoing gastroduodenoscopy were studied and 892 (59%) were positive for H pylori. H pylori was strongly associated with gastritis: 873 of 1197 (73%) patients with gastritis were positive compared with 19 of 305 (6%) without gastritis (p less than 0.0001). The prevalences of H pylori and gastritis were similar in peptic ulcer patients of different races. Malay patients with non-ulcer dyspepsia, however, were less likely to be positive for H pylori (10 of 46 (22%] or to have antral gastritis (17 of 46 (37%] than Chinese (292 of 605 (48%) were positive for H pylori and 421 of 605 (70%) had gastritis) and Indians (35 of 61 (57%) were H pylori positive and 42 of 61 (69%) had gastritis). Patients with duodenal ulcer were more likely to be positive for H pylori than those with non-ulcer dyspepsia, even when subjects with gastritis were considered separately. While our results do not help to explain the observed racial differences in peptic ulcer frequency it may be that the pathophysiology of non-ulcer dyspepsia is different in the different races in Singapore.     

Detection of Helicobacter pylori cagA gene by polymerase chain reaction in faecal samples.

OBJECTIVE: The polymerase chain reaction (PCR) has been extensively and successfully used to detect Helicobacter pylori in gastric juice and gastric biopsies. In contrast, the results obtained using faeces as biological samples for PCR are rather conflicting. This may be due to the presence of faecal inhibitory compounds (polysaccharides) which can inhibit the amplification reaction. The aim of this study was to characterize the H. pylori genotype in faecal samples by using specific primers for the cagA gene. To overcome the problem of contamination by polysaccharides, we used a filter-based extraction technique already applied in a previous study. METHODS: Antral and body biopsies were obtained from 30 symptomatic patients undergoing upper endoscopy. PCR was used to detect the presence of H. pylori organisms in faecal samples by using primers selected for the urease gene A. In addition, H. pylori organisms were characterized both in faecal samples and paraffin-embedded biopsies by PCR with specific primers for the cagA gene. RESULTS: All patients showed a positive CLO test (rapid urease test) and evidence of H. pylori by Warthin-Starry stain. PCR detected the urease A gene in the faecal samples of all patients. The cagA gene was detected in the faecal and biopsy samples of 18 subjects (60%). Duodenal ulcer and/or antral erosions were observed in 15 of the 18 cagA-positive patients (83.3%) and in five of the 12 cagA-negative patients (41.7%). Endoscopic features of normal mucosa or gastritis were observed in three cagA-positive patients (16.7%) and in seven cagA-negative patients (56.3%). cagA-positive status was found to be significantly related to the endoscopic features of duodenal ulceration and/or antral erosions. CONCLUSIONS: Our findings prove that faeces are suitable samples for the detection of cagA status. Moreover, they confirm the existence of a significant relationship between cagA-positive status and duodenal ulcer and/or antral erosions.     

The Helicobacter pylori breath test: a surrogate marker for peptic ulcer disease in dyspeptic patients.

BACKGROUND: There is interest in noninvasive H pylori testing as a means of predicting diagnosis and determining management in dyspeptic patients. AIMS: To assess the value of the 14C urea breath test as a predictor of peptic ulcer disease in patients presenting with dyspepsia. PATIENTS AND METHODS: 327 consecutive patients referred for investigation of dyspepsia had a 14C urea breath test performed before endoscopy. Patients were not included if they had previously confirmed ulcer disease, previous gastric surgery, or were taking non-steroidal anti-inflammatory drugs. RESULTS: Of the 182 patients with a positive 14C urea breath test, duodenal and/or gastric ulcers were present in 45% and erosive duodenitis in a further 2%. Oesophagitis was present in 12% of the breath test positive patients with two thirds of the oesophagitis patients having co-existent ulcer disease. The prevalence of ulcer disease in the H pylori positive dyspeptic patients was independently related to smoking and previous investigation status. If previously uninvestigated, the prevalence of ulcers was 67% in smokers and 46% in non-smokers. If previous upper gastrointestinal investigations were negative, the prevalence of ulcers was 53% in smokers and 28% in non-smokers. Of the 136 patients with a negative breath test, only 5% had peptic ulcers. The most frequent endoscopic finding in these H pylori negative subjects was oesophagitis, being present in 17%. CONCLUSIONS: This study demonstrates that a positive H pylori test is a powerful predictor of the presence of underlying ulcer disease in dyspeptic patients, especially if smokers, and that a negative H pylori test is a powerful predictor of the absence of ulcer disease. It also indicates that a negative upper gastrointestinal investigation does not preclude subsequent presentation with ulcer disease.     

Role of apoptosis induced by Helicobacter pylori infection in the development of duodenal ulcer

BACKGROUND: Helicobacter pylori affects gastric epithelium integrity by acceleration of apoptosis. However, it remains unclear what product of the bacteria causes apoptosis, or whether or not the apoptosis is involved in the development of ulcers. AIMS: To elucidate the factor from H pylori that causes acceleration of apoptosis and the role of apoptosis in the development of duodenal ulcer in H pylori infection. PATIENTS: Five H pylori negative healthy volunteers, 47 H pylori positive patients with duodenal ulcer, and 35 H pylori positive patients with gastric ulcer. METHODS: An endoscopic examination was carried out to diagnose ulcers and determine their clinical stage. To analyse apoptosis, a cell cycle analysis was performed using biopsy specimens. RESULTS: There was a significant correlation between the urease activity of the H pylori strain and the level of apoptosis induced by this bacterial strain. Moreover, in duodenal ulcer patients infected with H pylori, the patients with an active ulcer exhibited a significantly higher level of apoptosis than those with ulcers at both the healing and scarring stages. CONCLUSION: These findings suggest that acceleration of apoptosis in the antral mucosa caused by the urease of H pylori plays a crucial role in the development of ulcers in the duodenum.