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.     

The impact of peptic ulcer disease and infection with Helicobacter pylori on life expectancy

OBJECTIVE: Knowledge about the influence of H. pylori-related disease on life expectancy might affect physician behavior in dealing with such disease. The aim of this study was to assess how life expectancy is influenced by H. pylori infection and peptic ulcer disease. METHODS: The declining exponential approximation of life expectancy was used to model the effects of H. pylori and various peptic ulcer disease conditions on life expectancy. Deaths from peptic ulcer and gastric cancer were determined from the Vital Statistics of the United States. H. pylori prevalence rates were derived from the existing literature. RESULTS: Cure of active peptic ulcer increases life expectancy by 2.3 yr in persons aged 40-44 yr and 121 days in persons aged 70-74 yr. More substantial impact occurs in complicated ulcer, with increases in life expectancy ranging between 26.1 and 6.3 yr. Primary prevention of H. pylori could increase life expectancy by 190 days in those aged 40-44 yr and 26 days in 70-74-yr-old subjects. CONCLUSION: The benefit of ulcer cure or H. pylori prevention diminishes as age advances. Cure of ulcers in young patients or in those who have sustained complications results in an appreciable increase in life expectancy. Successful primary prevention of H. pylori in selected populations could substantially increase life expectancy.     

Risk for gastric lymphoma in persons with CagA+ and CagA- Helicobacter pylori infection

Infection with Helicobacter pylori increases the risk for gastric non-Hodgkin's lymphoma (GNHL). Strains that express CagA protein are thought to be particularly virulent. It was determined whether CagA+ H. pylori infection increased the risk for GNHL more than CagA infection. Thirty-two cases and 130 controls previously tested for H. pylori antibodies were tested for CagA antibodies by ELISA. The risk for GNHL was compared among CagA+, CagA-, and uninfected persons by use of conditional logistic regression. CagA+ subjects had 8.2 times the risk for GNHL than uninfected persons (95% confidence interval [CI], 2.5-26.7). CagA- subjects had 4.4 times the risk for GNHL than uninfected persons (95% CI, 1.2-16.5). Among infected subjects only, CagA+ infection was not associated with significantly increased risk for GNHL when compared with CagA- infection (odds ratio, 2.1; 95% CI, 0.8-5.4). This study does not support a major role for CagA in lymphomagenesis.     

Prognostic factors and scoring systems in myelodysplastic syndromes

The treatment of peptic ulcers has been revolutionized by the discovery that Helicobacter pylori (H. pylori) bacteria is a causative agent for ulcer formation. However, when patients present with dyspepsia or epigastric discomfort, more than 80% of patients will not have ulcer disease and empiric treatment of H. pylori is not recommended for these patients. Eradication of H. pylori has not been demonstrated to improve the symptoms of non-ulcer dyspepsia compared with non-ulcer dyspepsia patients treated with placebo. Therefore, we recommend that patients should first be evaluated for peptic ulcers with endoscopy or upper gastrointestinal series before the diagnosis and treatment of H. pylori. Generally, the treatment of H. pylori should be limited to patients with peptic ulcers, mucosal-associated lymphoid tissue lymphomas, and gastric cancers. Most diagnostic tests for H. pylori, including quantitative IgG antibody, urea breath tests, rapid urease tests (CLO), tests of gastric mucosal biopsies, and staining of gastric mucosal biopsies, have equivalent diagnostic characteristics. Therefore, the choice of diagnostic test for H. pylori should be based on cost, ease of use, and lack of complications. Multiple antibiotic regimens are available for the treatment of H. pylori. Triple antibiotic therapy is the least expensive but has the highest rate of side effects and the least compliance. Combining a proton pump inhibitor with clarithromycin and another antibiotic will eradicate H. pylori with fewer side effects and better compliance but this is the most expensive antibiotic regimen.     

cagA positive and negative Helicobacter pylori strains are simultaneously present in the stomach of most patients with non-ulcer dyspepsia: relevance to histological damage

BACKGROUND/AIMS: Infection with Helicobacter pylori strains harbouring the cagA gene (cagA+) is associated with an increased risk of developing peptic ulcer and gastric cancer. The aim of this study was to assess whether H pylori isolates with different cagA status were present in patients with non-ulcer dyspepsia, and whether a variable cagA status is relevant to histological gastric mucosal damage and glandular cell proliferation. METHODS: Well separated H pylori colonies (between 2 and 25) from primary plates, per gastric area, for each of 19 patients with non-ulcer dyspepsia were examined for cagA by hybridisation. Western blotting was used to examine both representative colonies for CagA expression and the patients' sera for antibody response to CagA. Glandular gastric cell proliferation was assessed immunohistochemically. RESULTS: Of the 747 colonies examined, 45.3% were cagA+. All colonies from four patients were cagA+, and all colonies from two patients were cagA-. In 13 patients (68%) both cagA+ and cagA- colonies were found. CagA expression of isolates corresponded to their cagA status. H pylori strains with different CagA molecular masses were present in three patients. Results based on all 19 patients studied showed that the prevalence of cagA+ colonies in areas with mucosal atrophy associated or not with intestinal metaplasia (67.9%) was significantly higher than in normal mucosa (44.7%) and mucosa from patients with chronic gastritis (44.0%) (p < 0.001). High levels of cell proliferation were associated with histological atrophy with or without intestinal metaplasia, but not with the possession of cagA by organisms colonising the same mucosal sites. CONCLUSIONS: Most patients with nonulcer dyspepsia are infected by both cagA+ and cagA- H pylori colonies. The cagA status of infecting organisms may play a role in the development of atrophy and intestinal metaplasia.     

A three-day octreotide-containing helicobacter pylori eradication therapy for cure of peptic ulcers

BACKGROUND/AIMS: Octreotide is used to arrest peptic ulcer hemorrhage. Since it has anti-secretory properties, it could also be used in Helicobacter pylori eradication therapy, to cure peptic ulcer before discharging patients from hospital. The aim of this pilot study was to determine safety and efficacy of an ultra short quadruple octreotide containing H. pylori eradication therapy in patients with peptic ulcer. METHODOLOGY: Twenty-six consecutive symptomatic H. pylori-positive patients with duodenal (n = 20) or gastric ulcer (n = 6), were treated with a three-day course of octreotide 0.3 mg/day subcutaneously, amoxicillin plus metronidazole 2 g/day orally and colloid bismuth subcitrate 480 mg/day. CLO-test, culture and crush tissue smears were performed on admission to the study, at 4 and 8 weeks post treatment. The effect of octreotide on intragastric pH (n = 10) was also investigated. RESULTS: Octreotide significantly increased the mean 24-hour intragastric pH > 3 over 68.9% of the time (37.1%-99.5%). There were no treatment side effects. Ulcer pain was abolished at between 2-12 days. By intention-to-treat 24/26(92.3%, 95% CI 82%-100%) ulcers had healed at 4 weeks. H. pylori eradication rate at 8 weeks was 88.5% (23/26) (95% CI 76%-100%). CONCLUSIONS: Our ultra-short octreotide containing quadruple therapy is a safe and effective regime in eradicating H. pylori and healing peptic ulcers. It may be a suitable therapy for hospitalized patients with peptic ulcer hemorrhage.     

Randomised trial of eradication of Helicobacter pylori before non-steroidal anti-inflammatory drug therapy to prevent peptic ulcers

BACKGROUND: Helicobacter pylori infection is common in patients with peptic ulcers caused by the use of non-steroidal anti-inflammatory drugs (NSAIDs). But the pathogenic role of H pylori in this disease is controversial. We studied the efficacy of eradication of H pylori in the prevention of NSAID-induced peptic ulcers. METHODS: We recruited patients with musculoskeletal pain who required NSAID treatment. None of the patients had previous exposure to NSAID therapy. Patients who had H pylori infection but no pre-existing ulcers on endoscopy were randomly allocated naproxen alone (750 mg daily) for 8 weeks or a 1-week course of triple therapy (bismuth subcitrate 120 mg, tetracycline 500 mg, metronidazole 400 mg, each given orally four times daily) before administration of naproxen (750 mg daily). Endoscopy was repeated after 8 weeks of naproxen treatment or when naproxen treatment was stopped early because of bleeding or intractable dyspepsia. All endoscopic examinations were done by one endoscopist who was unaware of treatment assignment. The primary endpoint was the cumulative rate of gastric and duodenal ulcers. FINDINGS: 202 patients underwent endoscopic screening for enrolment in the trial, and 100 eligible patients were randomly assigned treatment. 92 patients completed the trial (47 in the naproxen group, 45 in the triple-therapy group). At 8 weeks, H pylori had been eradicated from no patients in the naproxen group and 40 (89%) in the triple-therapy group (p < 0.001). 12 (26%) naproxen-group patients developed ulcers: five had ulcer pain and one developed ulcer bleeding. Only three (7%) patients on triple therapy had ulcers, and two of these patients had failure of H pylori eradication (p = 0.01). Thus, 12 (26%) patients with persistent H pylori infection but only one (3%) with successful H pylori eradication developed ulcers with naproxen (p = 0.002). INTERPRETATION: Eradication of H pylori before NSAID therapy reduces the occurrence of NSAID-induced peptic ulcers.     

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.     

Current aspects of using ketamine in childhood]

In this audit we tried to assess the effect of the detection of Helicobacter pylori on the change of outcome and symptoms of peptic ulcer disease outside well defined prospective studies, and its influence on treatment praxis by general practitioners. The study was carried out in the canton of Uri, a geographically closed area of Switzerland. The records of all patients with peptic ulcer disease diagnosed from 1991 to 1994 were evaluated retrospectively. In addition, the patients were followed by contact through their family doctors who were asked to fill out questionnaires on the immediate and long-term treatment of acute peptic ulcer, H. pylori therapy, recurrence of ulcers in light of symptoms or endoscopy, and on any surgery performed for ulcer disease. We found 453 patients with peptic ulcer disease proven by endoscopy, 134 patients presented with signs of ulcer bleeding, 45% of these had used nonsteroidal anti-inflammatory drugs previously. Only 9 of 453 patients required surgery. In 430 patients follow-up was possible (median of 18 months). H. pylori eradication was the primary treatment in 24% of the patients in 1991 and in 79% in 1994. Long-term prophylaxis with histamine H2 antagonists had been selected in 22%. Recurrence of the ulcer disease was seen in 157 patients during the follow-up period. The recurrence rate was 8% (3/39) in patients with documented H. pylori eradication, 43% (62/145) in patients with H. pylori eradication therapy without documentation of the result, 57% (31/54) in H. pylori positive and 50% (14/28) in H. pylori negative patients on long-term treatment with histamine H2 antagonists. 33% of the patients still had substantial abdominal pain despite using long-term histamine H2 antagonists as prophylaxis against recurrence, but this was the case in only 5% (2/39) after successful H. pylori eradication. The rate of successful antibiotic treatment improved substantially during this audit. This follow-up study demonstrates that patients with successfully eradicated H. pylori remain largely free of symptoms and of ulcer recurrence. Control of the eradication result seems to be necessary outside controlled studies. In contrast, symptoms and ulcer recurrence are frequent despite long-term treatment with histamine H2 antagonists. Few patients need surgery for ulcer disease today. Audits like this are a valuable method to improve acceptance and success of a new treatment modality.     

Diversity of Helicobacter pylori vacA and cagA genes and relationship to VacA and CagA protein expression, cytotoxin production, and associated diseases

The vacuolating cytotoxin and the cytotoxin-associated protein, encoded by vacA and cagA, respectively, are important virulence determinants of Helicobacter pylori. Sixty-five H. pylori strains were isolated from dyspeptic patients (19 with peptic ulcer disease, 43 with chronic gastritis, and 3 with gastric cancer) and studied for differences in the vacA and cagA genes and their relationship to VacA and CagA expression, cytotoxin activity, and the clinical outcome of infection. By PCR, fifty-four (83.1%) of 65 strains had the vacA signal sequence genotype s1 and only 10 (15.4%) had the type s2. After primer modification, the vacA middle-region types m1 and m2 were detected in 24 (36.9%) and 41 (63.1%) strains, respectively. The combinations s1-m2 (31 [47.7%]) and s1-m1 (23 [35.4%]) occurred more frequently than s2-m2 (10 [15.4%]) (P = 0.01). No strain with the combination s2-m1 was found. All 19 patients with peptic ulcers harbored type s1 strains, in contrast to 32 (74.4%) of 43 patients with gastritis (P = 0.02). The vacA genotype s1 was associated with the presence of cagA (P < 0.0001), VacA expression (P < 0.0001), and cytotoxin activity (P = 0.003). The cagA gene was detectable in 48 (73.8%) of 65 isolates and present in 16 (84.2%) of 19 ulcer patients and 29 (67.4%) of 43 patients with gastritis (P = 0.17). The vacA genotypes of German H. pylori isolates are identical to those previously reported. H. pylori strains of vacA type s1 are associated with the occurrence of peptic ulceration and the presence of cagA, cytotoxin activity, and VacA expression.     

Peptic ulcer in Greenland Inuit: evidence for a low prevalence of duodenal ulcer

In an eight years period new peptic ulcer was diagnosed in 127 Inuit patients at the Central Hospital, Dronning Ingrids Hospital, Nuuk/Godth?b. The ratios: duodenal ulcers (DU): prepyloric ulcers (PPU): gastric ulcers (GU) were 17:22:88. The male:female ratio was 2:1. 46 of the patients were living permanently in Nuuk, 81 in The Districts. There were no significant differences in the type of ulcers among the two groups. The incidence of GU among the Nuuk population was comparable to the incidence in the Danish population (0.63/1000 inhabitants per year), whereas the mean age at the time of diagnosis was only 45 years, thus the patients were approximately 15 years younger than the Danish counterparts. The incidence of DU among the Inuits was 0.15/1000 inhabitants per year, significantly less than in the Danish population. The frequency of Helicobacter (H.) pylori infection among 56 Inuits with dyspeptic symptoms was: 0.61. Only 6/12 patients suffering from DU had a positive test for H. pylori infection. Conclusions: The incidence of duodenal ulcers in the Inuit population was only 10% of the incidence in a Danish population, whereas the incidence of gastric ulcers among the Inuits was comparable to the incidence among Danes. Only 50% of Inuit patients with proven DU had a positive test for H. pylori infection, whereas the frequency of H.pylori infection in a population with dyspeptic symptoms corresponded very well to the frequency reported from other populations.     

Serum antibodies against Helicobacter pylori proteins VacA and CagA are associated with increased risk for gastric adenocarcinoma

Infection with Helicobacter pylori is associated with the development of gastric cancer. To study whether the infection with H. pylori strains expressing the vacuolating cytotoxin (VacA) and/or the cytotoxin-associated protein (CagA) is associated with an increased risk of developing gastric adenocarcinoma, sera of 90 patients with gastric cancer and 90 matched controls with cardiovascular diseases were investigated for the presence of antibodies to VacA and CagA by immunoblot. Although no significant difference in the overall H. pylori seropositivity was found between cancer patients and controls, antibodies against VacA or CagA were significantly more frequent in cancer patients than in control subjects. Seventy-five (97.4%) of 77 H. pylori-positive patients in the cancer group, but only 60 (84.5%) of 71 H pylori-positive control patients had antibodies against either VacA or CagA (chi 2 = 6.63; relative risk, 2.00; 95% confidence interval, 1.18-3.39; P = 0.01). The presence of antibodies against VacA or CagA alone was also associated with an increased cancer risk (92.2% vs 80.3%; chi 2 = 5.30; relative risk, 1.74; 95% confidence interval, 1.08-2.78; P = 0.021, for VacA; and 87.0% vs 74.6%; chi 2 = 4.90; relative risk, 1.61; 95% confidence interval, 1.06-2.45; P = 0.037, for CagA). The relative risk for gastric cancer was mainly elevated in patients under 65 years, but not in patients at or over 65 years. There is evidence that infection with VacA- or CagA-producing H. pylori strains increases the risk of developing gastric cancer, especially in younger patients.     

Relationship between local immune response to Helicobacter pylori and the diversity of disease: investigation of H. pylori-specific IgA in gastric juice

In order to evaluate the relationship between local immune response to Helicobacter pylori and the diversity of disease, 77 asymptomatic subjects who underwent a health examination were studied. Helicobacter pylori-specific IgG in serum and H. pylori-specific IgA in gastric juice were measured by ELISA, and the measured IgA titre was classified into two grades, low or high. Histological classification of gastritis was performed according to the Sydney system. Cytokines in gastric juice were also measured, and the cytotoxin-associated gene A (cagA) status of H. pylori was tested by PCR. Of the 65 subjects who were positive for H. pylori-specific IgG in serum, 38 (58.5%) were classified as H. pylori-specific IgA low titre in gastric juice and 27 (41.5%) had high titres. In the IgG-positive, IgA-low group, the rate of peptic ulcers (especially duodenal ulcers) in endoscopic findings was higher (P < 0.05); the score of activity and the density of H. pylori were higher (P < 0.001 and P < 0.05, respectively); the score of metaplasia was lower (P < 0.05); and the level of interleukin-1 beta was lower (P < 0.05) than in the IgG-positive, IgA-high group. The positive rate of the cagA gene was 84.4% and there was no significant difference between the two groups. There were differences in endoscopic and histological findings between the IgG-positive, IgA-low and the IgG-positive, IgA-high groups. It is suggested that persons infected with H. pylori can be divided into two different states of disease according to local immune response.     

Effectiveness of an ambulatory care clinical pharmacist: a controlled trial

Medical therapy for duodenal or gastric ulcer disease has traditionally involved gastric acid antisecretory therapy for 4 to 8 weeks to promote initial healing and indefinitely to prevent recurrences of ulcer. The discovery of Helicobacter pylori in most patients with peptic ulcer disease has led to a change in this approach. Therapy designed to eradicate H pylori may facilitate ulcer healing with acid antisecretory agents and, more important, may greatly reduce the incidence of ulcer recurrence, obviating the need for maintenance antisecretory therapy. Regimens designed to eradicate H pylori are difficult to comply with, however, and are associated with adverse effects in some patients. In this article we review the diagnosis and treatment of H pylori infection in patients with peptic ulcer disease and make recommendations regarding the use of conventional ulcer therapies and therapies designed to eradicate H pylori.     

Ether extract of fetal calf serum protects cultured rat cortical neurons against glutamate cytotoxicity

OBJECTIVE: To elucidate the role of Helicobacter pylori in relapsing disease after partial gastrectomy for peptic ulcer. DESIGN: Retrospective study of gastroscopies between January 1985 and February 1988. SETTING: Department of Surgery, Helsinki University Central Hospital, Finland. PARTICIPANTS: One hundred and fifty-five patients, who had undergone partial gastrectomy for peptic ulcer disease. MAIN OUTCOME MEASURES: Correlation between clinical and laboratory data, macroscopic findings at gastroscopy and histopathology. RESULTS: At gastroscopy 41 patients showed an ulcer at the site of anastomosis or in the gastric stump and two patients had a history of a previous ulcer recurrence. The median time interval between operation and relapse was 4 years. There was no correlation between ulcer recurrence, sex, age, ABO blood group or other diseases. Smokers and patients using non-steroidal anti-inflammatory drugs (NSAIDs) or alcohol had more relapses, but the difference was not significant. The recurrence rate was higher after Billroth II (BII; 34%) than after Roux-en-Y (14%; P = 0.03) or Billroth I (BI) reconstruction (24%). Giemsa staining demonstrated H. pylori in the gastric stump of 37% of the patients. H. pylori expression was related to age but unrelated to sex, ABO blood group, NSAID use, smoking or alcohol consumption. H. pylori positivity was more common (52%) after BI than after BII (28%; P = 0.04) or Roux-en-Y resection (40%). Recurrent ulcer was more often found in gastric remnants with normal mucosa (36%) than in those with H. pylori-positive gastritis (18%; P = 0.03) or H. pylori-negative gastritis (26%). CONCLUSION: It seems that H. pylori infection plays a minor role in the pathogenesis of ulcer recurrence after partial gastrectomy for peptic ulcer disease. Eradication of H. pylori of the remnant stomach is therefore presumably not effective in preventing ulcer recurrence.     

Rapid recurrence of Helicobacter pylori infection in Peruvian patients after successful eradication. Gastrointestinal Physiology Working Group of the Universidad Peruana Cayetano Heredia and The Johns Hopkins University

Helicobacter pylori is associated with gastritis, peptic ulcer disease, and gastric cancer. Since gastric cancer is common in Peru, eradication of H. pylori may help to reduce the occurrence of gastric cancer. This study involved three randomized trials to determine the efficacy of four different triple-drug therapy regimens. The most successful regimen was furazolidone combined with bismuth subsalicylate and amoxicillin, which eradicated infection in 82% of patients. Patients successfully treated were followed every 2-3 months to determine the recurrence rate of H. pylori infection. Of 105 patients with H. pylori eradication documented by pathology and culture, 52% (55) returned for follow-up endoscopy, and in 73% (40) of these 55 the infection recurred during the 8-month follow-up period. Thirty-five patients from whom H. pylori was eradicated and who were tested for antibodies to H. pylori remained consistently seropositive. Rapid recurrence of H. pylori infection after successful eradication suggests that measures other than antimicrobial therapy are needed to fight H. pylori in developing countries.     

Neutrophils, Helicobacter pylori, and nonsteroidal anti-inflammatory drug ulcers

BACKGROUND & AIMS: Gastric injury by nonsteroidal anti-inflammatory drugs (NSAIDs) is minimal in neutropenic animals. This study examined peptic ulcer development in the presence or absence of gastric neutrophils in patients requiring long-term use of NSAIDs. METHODS: Gastric histology, neutrophils, and Helicobacter pylori were assessed in 120 patients randomized to receive placebo or 20 or 40 mg famotidine twice daily as prophylaxis against NSAID-related ulcers and who underwent endoscopy at 0, 4, 12, and 24 weeks. RESULTS: In 43 patients without gastric neutrophils, ulcers developed in 1 of 14 (7.7%) taking placebo, 2 of 16 (12.5%) taking 20 mg famotidine, and none of 13 taking 40 mg famotidine. However, in 77 patients with neutrophils, ulcers developed in 13 of 28 (47. 4%) taking placebo (P < 0.001), 3 of 26 (12.6%) taking 20 mg famotidine, and 3 of 23 (13%) taking 40 mg famotidine. Eight of 46 patients (17%) without H. pylori had neutrophils compared with 69 of 74 (93%) with both H. pylori and neutrophils (P < 0.001). CONCLUSIONS: Gastric neutrophils increase the incidence of ulceration in long-term NSAID users. Because neutrophils exist with H. pylori, eradicating this infection might prevent NSAID-related peptic ulcers.     

One-week antibiotics versus maintenance acid suppression therapy for Helicobacter pylori-associated peptic ulcer bleeding

Bleeding peptic ulcer is the most important cause of upper gastrointestinal bleeding. Our aim was to compare the effect of anti-Helicobacter therapy with maintenance treatment of H2-receptor antagonist in the prevention of relapses of ulcer and bleeding. Patients with bleeding duodenal or gastric ulcers and H. pylori infection were randomized to receive either a one-week course of triple therapy with bismuth subcitrate, metronidazole, and tetracycline plus ranitidine or a six-week course of ranitidine 300 mg/day. After the ulcers healed, the antibiotic-treated patients were not given any medication, whereas the ranitidine-treated patients continued to receive a maintenance dose of 150 mg/day. One hundred twenty-six patients were randomized to receive anti-Helicobacter therapy and 124 patients to receive long-term ranitidine. H. pylori eradication was achieved in 98.2% in those who received triple therapy and 6.1% in those who received ranitidine (P < 0.0001). At the six-week follow-up, ulcer healing was documented in 88.2% in those who received triple therapy and 86.1% in those who received ranitidine (P = 0.639). Recurrent ulcer developed in nine of the ranitidine-treated patients and three of them presented with recurrent upper gastrointestinal bleeding. One patient in the antibiotic group developed recurrent ulcer without rebleeding (P = 0.01). It is concluded that eradication of H. pylori is sufficient for the prevention of recurrent bleeding ulcers.     

Helicobacter pylori infection and peptic ulcer disease in cirrhosis

An increased frequency of peptic ulcer disease is noted in patients with cirrhosis, but the role of H. pylori in this disorder remains to be determined. The diagnosis of cirrhosis was confirmed by a combination of clinical, biochemical, radiological, and histological methods. The severity of cirrhosis was assessed by Pugh's modification of Child's criteria. Upper gastrointestinal endoscopy was performed consecutively to evaluate the presence of varices and gastroduodenal mucosa. H. pylori status was assessed by histology, urease test, and serology. In all, 130 patients with cirrhosis were recruited into the study; there were 86 males and 44 females with a mean (SD) age of 54.4 (12.7) years. The H. pylori prevalence was 76.2%. There was no difference in age between the H. pylori-positive and -negative cirrhotics (P = 0.29). The H. pylori prevalence revealed no difference among cirrhotics with Child A (77.8%), Child B (72.9%), and Child C (78.6%) (P = 0.8), and neither was there a difference in H. pylori prevalence in cirrhotics with and without congestive gastropathy (77% vs 73.7%, P = 0.84). The prevalence of H. pylori in cirrhotics with and without varices did not show a statistical difference (75% vs 81.8%, P = 0.68). There also was no difference in the H. pylori prevalence between cirrhotic patients with and without peptic ulcers (84.4% vs 69.7%, P = 0.09). In conclusion, the prevalence of H. pylori or peptic ulcer is independent of the severity of cirrhotic liver disease. The association between H. pylori infection and peptic ulcer disease is weak in cirrhosis.     

Quantitative noninvasive testing for Helicobacter pylori does not predict gastroduodenal ulcer disease

BACKGROUND: Helicobacter pylori is strongly associated with gastric and duodenal ulcer disease. However, the diagnosis of gastroduodenal ulcers requires an endoscopic or radiographic examination. In this study, we attempted to establish a relationship between the magnitude of [13C]urea breath test results or serum H. pylori IgG levels and endoscopic findings in H. pylori-infected individuals. METHODS: Patients who had undergone endoscopy and had a positive [13C]urea breath test and/or positive H. pylori IgG serology were identified. Endoscopic diagnoses included duodenal ulcer, gastric ulcer, nonulcer dyspepsia, and others. Results of 6% or greater on the [13C]urea breath test was defined as positive for H. pylori infection. H. pylori IgG serology was determined by an enzyme linked immunosorbent assay with values of greater than or equal to 1.0 being seropositive. RESULTS: One hundred seventy-five patients were seropositive (mean = 3.01 +/- 1.58). One hundred sixty-eight patients had a positive [13C]urea breath test (mean = 25.43 +/- 16.90). One hundred fifty-five patients were common to both the groups. Statistical analysis did not reveal any relationship between quantitative [13C]urea breath test results or H. pylori IgG values and endoscopic diagnoses. CONCLUSION: The magnitude of [13C]urea breath test or H. pylori IgG serology cannot be used to predict the presence or absence of gastroduodenal ulcer disease.