Influence of Helicobacter pylori on gastric mucosal adaptation to naproxen in man

Our objective was to determine whether H. pylori influences gastric mucosal injury and adaptation caused by naproxen. Twenty-four healthy volunteers, 12 H. pylori-positive and 12 H. pylori-negative, were given a 28-day course of naproxen 500 mg twice a day. They were each gastroscoped to assess gastric mucosal damage and mucosal blood flow before and at 1, 7, and 28 days during treatment. Maximal gastric mucosal damage (median grade + IQR) occurred during the first 24 hr in both groups and was of similar magnitude (H. pylori-positive: 2.5, 2.0-3.0 P < 0.01; H. pylori-negative: 2.0, 1.0-3.0 P < 0.01). This damage was associated with a fall in antral but not corpus mucosal blood flow. With continued NSAID administration, gastric damage resolved confirming adaptation (H. pylori-positive 1.0, 0-2.0, H. pylori-negative: 1.0, 0-1.0) and antral mucosal blood flow returned to baseline in both groups by day 28. These observations suggest that initial gastric mucosal injury is not influenced by H. pylori colonization and adaptation occurs regardless of its presence.     

Transplantation of hepatocytes for prevention of intracranial hypertension in pigs with ischemic liver failure

BACKGROUND: How Helicobacter pylori infection affects gastric acid secretion is still unclear. METHODS: Gastric juice pH, ammonia concentration in gastric juice, serum gastrin level, and grade of gastritis in accordance with the Sydney System were determined for patients with gastric ulcer (GU) and duodenal ulcer (DU) before and after treatment with lansoprazole and amoxicillin, and results were compared with those of H. pylori-negative controls. RESULTS: Scores for H. pylori density, atrophy, metaplasia, and activity of gastritis in the corpus were higher in patients with GU, especially those with proximally located GU, than in those with DU. Gastric juice pH was significantly higher in GU patients than in DU patients and controls. After H. pylori eradication, gastric juice pH and serum gastrin levels in both GU and DU patients were significantly decreased to control levels. In patients without eradication, no significant changes in these factors were observed. CONCLUSIONS: These findings suggest that H. pylori infection and gastritis in the corpus suppress acid secretion and increase gastric juice pH, resulting in hypergastrinemia, and that eradication of H. pylori normalizes acid secretion and serum gastrin levels.     

Enhanced levels of C-X-C chemokine, human GROalpha, in Helicobacter pylori-associated gastric disease

C-X-C Chemokines play an important role for neutrophil extravasation through microvessels. Although the level of interleukin (IL)-8 is known to increase in the Helicobacter pylori-infected gastric mucosa, another C-X-C chemokine, GROalpha, has not been evaluated in the H. pylori-associated gastric mucosal injury. The present study was designed to investigate gastric contents of GROalpha in relation to those of IL-8 in the gastric mucosa of H. pylori-infected peptic ulcer patients. Thirty-eight patients with gastric ulcer and 41 with gastritis underwent endoscopy with informed consent and 49 were found to be H. pylori positive and 30 H. pylori negative. Biopsies from the gastric corpus were performed in each patient to examine the H. pylori colonization by bacterial culture, the rapid urease test and histological specimens as well as measurement of the contents of human GROalpha and IL-8. Helicobacter pylori infection was eradicated in 21 patients by triple therapy (lansoprazole 30 mg, amoxycillin 2.0 g, clarithromycin 600 mg; 2 weeks). The samples for GROalpha and IL-8 assay were homogenized in 0.02% aprotinin containing phosphate-buffered solution and the mucosal contents of GROalpha and IL-8 in the supernatants were quantified by sandwich enzyme immunoassay methods. The levels of GROalpha and IL-8 in H. pylori-positive gastric mucosa were significantly higher than those in the H. pylori-negative mucosa. There was a significant linear correlation between the levels of GROalpha and IL-8 (r = 0.798, P < 0.01). After the eradication of H. pylori by the triple therapy, the levels of GROalpha and IL-8 were significantly decreased. The GROalpha showed an increase in the H. pylori-positive gastric mucosa in a similar fashion as IL-8 contents, suggesting a pathogenetic role for GROalpha in H. pylori-associated gastric mucosal injury.     

Can the C-14 urea breath test replace follow-up endoscopic biopsies in patients treated for Helicobacter pylori infection?

BACKGROUND: The C-14 urea breath test (UBT) is the most specific noninvasive test to detect Helicobacter pylori, with reported sensitivity and specificity rates of 90% and 95%, respectively. This test has not been evaluated for eradication after a therapeutic trial. The goal of this study was to assess the accuracy of C-14 UBT in the diagnosis and eradication of H. pylori infection in patients with duodenal ulcer who were treated with a triple drug regimen. METHODS: Sixty patients with active duodenal ulcers who tested positive for the rapid urease test had a C-14 UBT at 0 weeks (at enrollment) and at 6 and 12 weeks using 5 microCi (185 KBq) of C-14 urea. A single breath sample was collected at 15 minutes for UBT. H. pylori was eradicated using lansoprazole and two antibiotics. RESULTS: Receiver operator characteristic curves showed that, using a value of 400 counts per minute (cpm), UBT had a sensitivity rate of 91%, specificity rate of 93%, positive predictive value of 77%, and a negative predictive value of 97% in the prediction of H. pylori eradication. The mean + 3 SD of H. pylori-negative patients was 380.1 cpm; at this cutoff value, the sensitivity and specificity rates were 91.3% and 92.8%, respectively. CONCLUSION: The C-14 UBT was an accurate, rapid, and easily administered test to diagnose initial H. pylori infection and to monitor its eradication, thereby obviating the need for repeated endoscopic biopsies.     

Erosive duodenitis: prevalence of Helicobacter pylori infection and response to eradication therapy with omeprazole plus two antibiotics

OBJECTIVES: To study the prevalence of Helicobacter pylori infection in patients with erosive duodenitis (ED), the associated gastric histological lesions and their response to eradication therapy with omeprazole plus two antibiotics. METHODS: A prospective study was made of 57 patients with ED (mean age 46 +/- 16 years, 72% males). At endoscopy, biopsies from gastric antrum and body were obtained for histological study (haematoxylin and eosin). A 13C-urea breath test was also performed. Omeprazole 20 mg twice daily plus two antibiotics (amoxycillin 1 g twice daily, clarithromycin 500 mg twice daily, metronidazole 500 mg twice daily) were administered for 1 week. Endoscopy and breath test were repeated 1 month after completing therapy, and the breath test was performed again at 6 months. RESULTS: All patients were H. pylori positive. Overall eradication was achieved in 86% (95% CI 75-93%). Duodenal erosion healing was obtained in 45 patients (79%). Healing was achieved in 86% (CI 73-93%) of cases with successful eradication therapy, but only in 3/8 (37%; CI 8.5-75%) patients with therapy failure (P < 0.01). In the multivariate analysis, H. pylori eradication was the only variable which correlated with erosion healing (odds ratio 10; CI 2-51; P < 0.01). Histological improvement, in both the gastric antrum and body, was demonstrated when eradication was achieved (P < 0.001). Six months after diagnosis H. pylori absence was confirmed in all patients with initial therapy success (all of them asymptomatic), and infection was confirmed in the eight patients who were H. pylori positive after therapy (six of them symptomatic). At 6-month follow-up, endoscopy was normal in 6/7 H. pylori-negative patients with previously persistent ED, while erosions were still present in 4/5 H. pylori-positive patients with previously persistent ED. CONCLUSION: A high prevalence (100%) of H. pylori infection in patients with ED was observed. A 1-week twice daily therapy with omeprazole plus two antibiotics (clarithromycin plus amoxycillin or metronidazole) was very effective in H. pylori eradication, duodenal erosion healing, symptomatic improvement, and in disappearance of associated histological gastritis. These observations suggest that ED should be considered a variant form of duodenal ulcer disease and treated accordingly; that is, with H. pylori eradication therapy.     

Eradication of Helicobacter pylori in patients with duodenal ulcer lowers basal and peak acid outputs to gastrin releasing peptide and pentagastrin

BACKGROUND: Patients with duodenal ulcer (DU) have high basal (BAO) and peak (PAO) acid outputs. The effect of Helicobacter pylori eradication on these variables is unclear. AIM: To discover if gastric acid hypersecretion in patients with DU is caused by H pylori. PATIENTS AND METHODS: BAO, gastrin releasing peptide (GRP), and pentagastrin stimulated PAO in 10 H pylori negative controls, and in 10 H pylori positive patients with DU was measured before and six months after H pylori eradication. H pylori status was determined by histology, culture, and by the 13C-urea breath test. After collecting a 30 minute basal aspirate, GRP 40 pmol/kg/h was infused for 45 minutes, and after a 30 minute washout, pentagastrin 6 micrograms/kg was injected intramuscularly. RESULTS: Basal and stimulated acid output (PAOGRP and PAOPg) were significantly higher in H pylori positive DU than in H pylori negative controls. Six months after H pylori eradication, basal and stimulated acid outputs were all significantly lower than before H pylori eradication. CONCLUSIONS: This study has shown that BAO, PAOGRP, and PAOPg are higher in H pylori positive DU than in H pylori negative controls. All decreased significantly six months after H pylori eradication, to fall within the range of controls. These results are compatible with a hypothesis that acid hypersecretion in duodenal ulcer disease is caused by H pylori infection.     

Helicobacter pylori eradication as a surrogate marker for the reduction of duodenal ulcer recurrence

OBJECTIVES: An abundance of data exists documenting the association of H. pylori eradication with the reduction in duodenal ulcer recurrence. AIM: To evaluate the validity of using H. pylori eradication as a surrogate marker for the reduction in duodenal ulcer recurrence using rigorously controlled studies. METHODS: Three controlled clinical trials were conducted in patients with uncomplicated, active duodenal ulcers. Patients were treated with various combinations of omeprazole and amoxycillin. Ulcer healing and H. pylori eradication were assessed. For patients whose duodenal ulcer healed, duodenal ulcer recurrence was determined over a 6-month period in patients with H. pylori eradication and those remaining positive for H. pylori at least 4 weeks after treatment. To support the data obtained from these clinical trials, a search of the medical literature was conducted to identify additional human clinical trials in which duodenal ulcer recurrence rates were measured and categorized by H. pylori status at least 1 month post-treatment. RESULTS: In 11 controlled trials, the overall 6-18-month duodenal ulcer recurrence rate was 54% among patients remaining positive for H. pylori at least 4 weeks after treatment compared to 6% among patients with H. pylori eradication following treatment. This finding was corroborated by the uncontrolled trials, in which the duodenal ulcer recurrence rate was 64% among patients found to be H. pylori-positive and 6% for patients found to be H. pylori-negative at least 4 weeks after treatment. A time course of duodenal ulcer recurrence rates using pooled data from both controlled and uncontrolled studies demonstrated that duodenal ulcer recurrence rates for H. pylori-negative patients persisted for up to 4 years following treatment. Duodenal ulcer recurrence rates for H. pylori-positive patients increased for the first year, then levelled off. A comparison of the duodenal ulcer recurrence rates for different treatment regimens revealed that eradication regimens based on omeprazole plus antibiotics and bismuth plus antibiotics exhibited similar duodenal ulcer recurrence rates for H. pylori-positive and -negative patients. CONCLUSION: Regardless of treatment regimens, H. pylori eradication produced a consistent and significant reduction in duodenal ulcer recurrence. Therefore H. pylori eradication, 4 weeks post-therapy, can be used as a surrogate marker for reduced duodenal ulcer recurrence in investigational clinical trials.     

CT in Fournier''s gangrene

BACKGROUND: Few outcome studies directly compare Helicobacter pylori eradication therapy with maintenance H2-antagonist therapy in duodenal ulcer disease. AIM: To examine prospectively the efficacy of H. pylori eradication therapy with ranitidine maintenance therapy over 1 year in patients with confirmed chronic duodenal ulcer. METHODS: One hundred and nineteen patients with active H. pylori infection were randomized to receive ranitidine, 150 mg/day initially (58 patients), or omeprazole, 40 mg/day, amoxycillin 2 g/day and metronidazole 1.2 g/day for 14 days, or omeprazole 40 mg/day and clarithromycin 1.5 g/day, for 14 days (if penicillin-allergic). Symptoms were assessed using the Gastrointestinal System Rating Scale (GSRS) and SF36 quality of life index. RESULTS: 13C urea breath testing confirmed overall treatment success in 100% of patients (58/58) per protocol and 95.1% (58/61) on an intention-to-treat basis. At 4 and 12 months there were no differences in any GSRS symptoms between treatment groups. SF36 analysis showed a perceived health improvement at 4 and 12 months in patients who received H. pylori eradication. However, despite successful H. pylori eradication, one-fifth of patients still required antisecretory therapy. CONCLUSION: Following successful H. pylori eradication, chronic duodenal ulcer patients were at least as well symptomatically as when taking maintenance ranitidine. They perceived that their health had improved, but a subgroup was still acid-suppression dependent.     

Duodenal bicarbonate secretion: eradication of Helicobacter pylori and duodenal structure and function in humans

BACKGROUND & AIMS: Eradication of Helicobacter pylori expedites duodenal ulcer healing and prevents recurrences. Most patients with duodenal ulcers have impaired proximal duodenal mucosal bicarbonate secretion (DMBS). In patients with inactive, healed duodenal ulcers and normal subjects, the effect of H. pylori infection on DMBS and proximal duodenal secretory function and structure were examined. METHODS: DMBS was quantitated before and after eradication of H. pylori. Mucosal structure (duodenal bulb histopathology) and function (DMBS at rest and stimulated, effect of active vs. healed ulcer and of age) were determined in patients with duodenal ulcers and normal subjects. RESULTS: In patients with duodenal ulcers, H. pylori eradication normalized proximal DMBS. Histological examination of duodenal biopsy samples was comparable in patients with duodenal ulcers and normal subjects without apparent relationship between inflammation and DMBS. Significantly impaired DMBS occurred in response to all agonists tested (luminal acid, prostaglandin E2, and cephalic-vagal stimulation) in patients with duodenal ulcers, suggesting a generalized secretory defect. Neither the presence of active (vs.inactive) ulcer nor age significantly affected bicarbonate secretion. CONCLUSIONS: In patients with duodenal ulcers, eradication of H. pylori normalized proximal DMBS and may thereby reduce ulcer recurrences. Altered DMBS in patients with duodenal ulcers was unrelated to histopathologic abnormalities. Impaired bicarbonate secretion in patients with duodenal ulcers could be caused by a cellular and/or physiological regulatory transport defect possibly related to H. pylori.     

Evaluation of the PyloriTek test for detection of Helicobacter pylori infection in cases with and without eradication therapy

OBJECTIVE: The accuracy of the PyloriTek test (a 1-h rapid urease test) used after eradication therapy of Helicobacter pylori (H. pylori) has not been well clarified. This study was done to evaluate the accuracy of the PyloriTek test results for cases with and without eradication therapy, using culture and histology as gold standard methods, and to establish the suitable timing of the PyloriTek test after eradication treatment. METHODS: One hundred sixty-three patients undergoing upper endoscopy were randomly selected; 100 patients had not received eradication therapy and 63 had. Three biopsy specimens each were obtained from the gastric antrum and the body for examination by PyloriTek, culture, and histology. The absence of H. pylori was established with negative results from both culture and histology. RESULTS: In cases without eradication therapy, PyloriTek, correctly identified 66 of 67 H. pylori-positive cases and 30 of 33 H. pylori-negative cases, yielding 98.5% sensitivity and 90.9% specificity. In cases with eradication therapy, PyloriTek gave correct diagnoses in 10 of 17 H. pylori-positive cases and in 45 of 46 H. pylori-negative cases, for 58.8% sensitivity and 97.8% specificity. However, when PyloriTek was used more than 4 months after the end of eradication therapy, both the sensitivity and the specificity increased to 100%. CONCLUSION: Considering time and cost, the use of PyloriTek alone may be satisfactory for detecting H. pylori infection in cases without eradication therapy. When patients are examined more than 4 months after intervention, the use of PyloriTek alone may be sufficient for correctly diagnosing H. pylori infections.     

Platelet-derived growth factor BB mediated regulation of 12-lipoxygenase in porcine aortic smooth muscle cells

BACKGROUND & AIMS: Recently, we postulated a new concept of duodenal ulcer pathogenesis suggesting that antral Helicobacter pylori infection blocks inhibitory pathways to the gastrin and parietal cells, resulting in an increased and prolonged postprandial acid secretion. the aim of this study was to examine duodenal acid load and duodenal bulb pH after a meal before and after eradication of H. pylori. METHODS: Using a marker-dilution method and a pH electrode in the duodenal bulb, gastric emptying, acid secretion, gastrin release, duodenal acid load, and duodenal bulb pH were studied during 2 hours after peptone meals of pH 7.0 and 2.0 in 8 H. pylori-negative controls and 8 H. pylori-infected subjects before and 6 months after eradication. RESULTS: The H. pylori-infected subjects had an increased gastric emptying, gastrin release, and acid secretion, higher duodenal acid load, and lower duodenal bulb pH after the meals. These responses were normalized after eradication. CONCLUSIONS: H. pylori-infected subjects have an increased and prolonged postprandial acid secretion, partly caused by an impaired low pH inhibition of acid secretion, gastrin release, and gastric emptying, resulting in an increased duodenal acid load and a prolongation of low pH in the duodenal bulb, as a general prerequisite for the development of duodenal ulcer disease.     

A comparison of the effect of ski sidecut on three-dimensional knee joint kinematics during a ski run

BACKGROUND: Knowledge of Helicobacter pylori infection has grown rapidly during the last decade and management of its associated pathology has changed concordantly. METHODS: We surveyed the management of H. pylori infection among members of the Dutch Society of Gastroenterology in 1995 via a postal questionnaire. RESULTS: Almost all 226 respondents (response rate 54%) treated patients for H. pylori infection and the responses suggested that at least 0.1% of Dutch citizens were treated for H. pylori infection in 1995 by this group of specialists. 98% of the respondents treated the H. pylori infection in patients with duodenal ulcer, 91% in cases of gastric ulcer, 56% in cases of gastric lymphoma, 33% in cases of premalignant changes in gastric mucosal histology, 32% in cases of non-ulcer dyspepsia, and 30% in cases of chronic use of proton pump inhibitors. The main diagnostic methods used were histology (93%), urease test (60%), and culture (46%). Triple therapy was most commonly used (54%), followed by quadruple therapy (26%) and double therapy (13%). Follow-up detection of H. pylori was routinely done by 42% of the respondents, while 48% did so only when confirmation of eradication was considered clinically relevant. Most specialists did follow-up detection after 8-12 weeks. CONCLUSIONS: In 1995 most Dutch specialists treated H. pylori in patients with associated ulcer disease. There was no consensus on its role in other diseases. Diagnostic methods and treatment regimens for eradication differed widely.     

Eradication of Helicobacter pylori in patients with end-stage renal disease undergoing dialysis treatment

The aim of the present study was to examine the efficacy and safety of combination therapy with amoxicillin (AMPC), lansoprazole, and plaunotol for the eradication of H. pylori in dialysis patients. The subjects consisted of 15 dialysis patients (10 men and 5 women, mean age of 56 +/- 2.4 years) in whom H. pylori was found in the stomach. H. pylori status was evaluated by histology, culture and rapid urease test with biopsy specimens of the gastric mucosa. The patients were treated with AMPC 500 mg once a day for 3 weeks, lansoprazole 30 mg once a day for 8 weeks and plaunotol 80 mg three times a day for 24 weeks. In addition, the concentrations of serum gastrin and gastric juice ammonia were measured. Fourteen patients completed the treatment schedule, while one discontinued treatment because of nausea and diarrhea. Among the 14 patients, H. pylori was eradicated in 11 without any side effects (eradication rate 78.6%). Concentrations of gastric juice ammonia and serum gastrin were reduced significantly in patients who became H. pylori-negative. The present study indicates that combination therapy with AMPC, lansoprazole and plaunotol is safe and efficient for the eradication of H. pylori in dialysis patients. The results also suggested that elevated concentrations of gastric juice ammonia and serum gastrin in dialysis patients can be attributed, at least in part, to H. pylori infection.     

New one-week, low-dose triple therapy for the treatment of duodenal ulcer with Helicobacter pylori infection

BACKGROUND: Antimicrobial therapy is the recommended treatment for duodenal ulcer associated with Helicobacter pylori infection. The eradication of bismuth-based triple therapy with bismuth subcitrate, metronidazole and amoxicillin is limited by low compliance, drug resistance and side-effects. Two-week proton pump inhibitor (PPI)-based triple therapy has a higher eradication rate but is costly. This study was designed to compare the efficacy, patient compliance and cost of short-term PPI-based triple therapy with those of bismuth-based triple therapy. METHODS: Ninety patients with active duodenal ulcer disease and H pylori infection, proven with the 13C-urea breath test and CLO test (Campylobacter-like organism test) were treated randomly in three therapeutic groups: Group A, DeNol 120 mg, amoxicillin 500 mg and metronidazole 250 mg four times a day orally for 14 days; Group B, omeprazole 20 mg plus clarithromycin 500 mg twice a day and amoxicillin 500 mg four times a day for 14 days; Group C, omeprazole 20 mg, clarithromycin 250 mg and metronidazole 500 mg twice a day for seven days. Nizatidine 150 mg twice a day was given continuously following the end of anti-H pylori therapy for each group. Two months later, endoscopy, the CLO test and 13C-urea breath test were repeated to assess the eradication rate of H pylori and the ulcer-healing rate. Drug tolerance was evaluated by patients themselves by daily recording of any side-effects. RESULTS: Eighty-four patients completed the entire course of therapy and evaluation for H pylori infection. The H pylori eradication rates in Groups A, B and C were 75% (21/28), 93% (26/28) and 89% (25/28), respectively (p = 0.466). The ulcer healing rate was 86% (24/28) in Group A and 89% (25/28) in Groups B and C (p = 0.764). A total of 74 patients (88%) were free from symptoms at the end of the triple therapy. Symptom relief was faster in patients with PPI-based triple therapy (Groups B and C) (days 3 and 4) than for patients with bismuth-based triple therapy (day 5). The cost of Group C therapy was lower than that for Groups A and B. There were no major side-effects in any of the patients. CONCLUSIONS: One-week triple therapy with omeprazole, clarithromycin and metronidazole is highly effected for the eradication of H pylori. A therapeutic regime of one week's duration with lower cost, good compliance and mild side-effects may offer a good choice for treatment of duodenal ulcer associated with H pylori infection in clinical practice.     

Gastric mucosal hepatocyte growth factor in Helicobacter pylori gastritis and peptic ulcer disease

OBJECTIVES: Hepatocyte growth factor (HGF) is increasingly recognized for its role in a variety of hepatic and systemic diseases. Its relationship to gastritis has not been studied. We aimed at measuring gastric mucosal HGF levels in the presence or absence of Helicobacter pylori gastritis, in peptic ulcers, and in response to H. pylori eradication. METHODS: Fifty one patients were studied. Patients were not entered if they had liver disease, malignancy, or any systemic illness. HGF was measured in gastric antral incubates using an enzyme-linked immunosorbent assay. Assessments were repeated 6 wk after a 2-wk course of anti-H. pylori triple therapy in 12 patients. Code numbers were used for blinding. RESULTS: The median gastric mucosal HGF level was 36 ng/gm/tissue in patients with H. pylori gastritis (n = 33) compared with 19 ng/gm in 18 negative controls (p = 0.0024), 18 ng/gm after the eradication of H. pylori (p = 0.021), 23 ng/gm in all patients with ulcers (n = 10), and 26 ng/gm/tissue in H. pylori-positive ulcers (n = 7). CONCLUSIONS: Gastric mucosal HGF levels were elevated in H. pylori gastritis and reduced by its eradication. These results are relevant to our understanding of the increased gastric cell proliferation in patients with H. pylori-related gastritis.     

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.     

Helicobacter pylori eradication and ulcer healing with daily lansoprazole, plus 1 or 2 weeks co-therapy with amoxycillin and clarithromycin

BACKGROUND: Proton pump inhibitor based combination therapy is one standard strategy for Helicobacter pylori eradication. AIM: To compare the eradication and duodenal ulcer healing efficacy of two 2-week, single dose, lansoprazole based combination therapies. METHODS: Healthy adult patients with endoscopically confirmed, H. pylori associated duodenal ulcer disease (3 mm > ulcer < 20 mm) were eligible for the study. All patients received a 14 day course of lansoprazole 30 mg o.m., and were randomized to receive either 7 or 14 days of amoxycillin 1 g b.d. and clarithromycin 500 mg b.d. Patients were endoscoped at entry and 14-17 days later. Symptomatic, unhealed patients received a further 14 days of therapy with lansoprazole 30 mg o.m. Eradication was confirmed a minimum of 28 days after cessation of all therapy by urease reaction and histological assessment of gastric body and antral biopsies (three biopsies each site). RESULTS: Sixty-two patients were randomized to a treatment arm, of which 58 could be included in an intention-to-treat and key-point-available analysis. H. pylori eradication rates were identical, at 93% (95% CI: 73-98% (1 week), 78-99% (2 week)). In the combined group, all but 13 ulcers were healed at 2 weeks; six required further therapy because of symptoms, while six of the seven asymptomatic patients went on to heal. CONCLUSION: An eradication regimen, based on a 2-week course of single dose lansoprazole with 1 week of antibiotic co-therapy, is effective in eradicating H. pylori, while the 2 weeks of acid suppression is usually effective in duodenal ulcer healing.     

Role of Helicobacter pylori in reflux esophagitis

It is now widely accepted that peptic ulcer disease (PUD) is a result of chronic infection of Helicobacter pylori (H. pylori). Thus, treatment of PUD should be aimed toward eradication of H. pylori with antibiotics. One the other hand, recent study from England suggested that eradication of H. pylori may provoke development of reflux esophagitis in duodenal ulcer patients. Despite duodenall ulcer patients with concomitant esophagitis is a specific type of esophagitis, it is important to recognize the development of reflux esophagitis after cure of H. pylori infection. Whether the development of reflux esophagitis is occurred in other H. pylori-related disease such as gastric ulcer remains to be studied.     

Factors influencing Helicobacter pylori eradication with 2 week combination therapy of lansoprazole and amoxycillin: intragastric distribution of colonization and gastric mucosal atrophy

In Japan, gastric ulcers are often accompanied by marked gastric mucosal atrophy. We evaluated the dual therapy of double-dose lansoprazole and amoxycillin for Helicobacter pylori eradication in Japanese ulcer patients and investigated the effects of intragastric distribution of H. pylori colonization and gastric mucosal atrophy on eradication with this combination therapy. Seventy-six H. pylori-positive ulcer patients received lansoprazole (30 mg) plus amoxycillin (500 mg) twice daily for 2 weeks (LA-60 group), lansoprazole (30 mg once daily) plus amoxycillin (500 mg twice daily) for 2 weeks (LA-30 group) or lansoprazole (30 mg once daily) for 6 or 8 weeks (LPZ group). Infection was evaluated by light microscopy, culture and biopsy urease tests. Helicobacter pylori colonization was classified as localized to the corpus (localized type) or involving the antrum and corpus (whole type). Fundic mucosal atrophy was graded according to endoscopic and histological features. Eradication was achieved in 67.6% in the LA-60 group, 31.6% in the LA-30 group, and 0% in the LPZ group, and moderate or severe histological gastritis was improved in the LA-60 group. Eradication was better in localized-type colonization (92%) than whole-type (56%), and better with fundic mucosal atrophy (84%) than without, but poor in both whole-type colonization and scanty mucosal atrophy (47%). The LA-60 therapy achieves better eradication in Japanese ulcer patients with localized H. pylori colonization and/or gastric mucosal atrophy, which are likely to be important predictors for the successful eradication with dual therapy.     

Prospective, randomized, investigator-blind trial of Helicobacter pylori infection treatment in patients with refractory duodenal ulcers. Healing and long-term relapse rates

In this study, 26 patients with duodenal ulcers refractory to treatment with H2-receptor antagonists for 8-12 weeks were randomly assigned to eight weeks of treatment with colloidal bismuth subcitrate (120 mg four times a day) alone (N = 12) or in combination with tetracycline hydrochloride (500 mg four times a day, days 0-14) and metronidazole (500 mg three times a day, days 15-28). Symptoms were scored and endoscopy, histology, and CLO tests were performed before, on completion of treatment, and 3, 6, 12, and 18 months after treatment. Treatment was considered successful when Helicobacter pylori was not detected by CLO tests and Warthin-Starry stains on gastric biopsies taken from antrum, body, and fundus. On triple therapy, ulcers healed in 12/14 patients (85.71%) and 10/14 (71.42%) patients became Helicobacter pylori-negative. On bismuth, only one patient became Helicobacter pylori-negative (8.33%, P < 0.0001), but ulcers healed in 8/12 patients (67%, P = NS). Six patients on bismuth, whose ulcers remained unhealed or relapsed early after healing, were offered triple therapy, which resulted in ulcer healing in three and Helicobacter pylori clearance in two patients. At 18 months, none of the Helicobacter pylori-negative patients had ulcer relapse. On the contrary, ulcers relapsed in all but one patient, who remained Helicobacter pylori-positive. Smoking and drinking did not influence the therapeutic outcome. The data confirm previous reports that many duodenal ulcers are infectious and therefore curable.