Trends in state laws and regulations affecting nurse-midwives: 1995-1997

Increased epithelial cell proliferation is associated with an increased risk of gastric carcinoma. Helicobacter pylori infection is an established risk factor for gastric cancer and the organism has recently been classified as a group I carcinogen by an IARC working group. In this study, we describe differences in gastric epithelial cell proliferation between a H. pylori eradicated group (n = 21) and a not eradicated group (n = 8) after anti-H. pylori eradication therapy to show that increased cell proliferation is associated with H. pylori infection. H. pylori infection was determined by rapid urease test and immunohistochemical method with anti-H. pylori polyclonal antibody. Gastric epithelial cell proliferation was assessed using immunohistochemical method using Ki-67 monoclonal antibody. Ki-67 positive cells in H. pylori associated chronic active gastritis were observed in the glandular neck and the upper portion of foveolar epithelium. Patients who cleared their H. pylori infections showed a significant decrease of Ki-67 labeling index after therapy (0.73 +/- 0.10 vs. 0.48 +/- 0.08, p < 0.01). By contrast, Ki-67 labeling index before and after treatment in patients who remained positive for H. pylori showed no significant difference (0.78 +/- 0.08 vs 0.74 +/- 0.10, p > 0.05). These results indicate that H. pylori infection increases the proliferation of gastric foveolar epithelium, which is reduced by the eradication therapy. We suggest that anti-H. pylori eradication therapy can prevent mucosal cell proliferation to be closely associated with gastric carcinogenesis.     

Salivary immunoglobulin G assay to diagnose Helicobacter pylori infection in children

An in-house enzyme-linked immunosorbent assay (ELISA) for measurement of Helicobacter pylori-specific immunoglobulin G (IgG) and IgA in saliva was evaluated by comparison with histopathologic (Giemsa staining) and biochemical (urease quick test) examination of gastric biopsy specimens obtained from 112 children referred for diagnostic gastroscopy. Serum H. pylori IgG was also measured in a subgroup of 50 children by the same ELISA. Salivary H. pylori IgG levels were significantly higher in H. pylori-positive (n = 57) than in H. pylori-negative (n = 55) children (P < 0.001). The sensitivity and specificity of the salivary IgG test were 93 and 82%, respectively; the positive and negative predictive values were 84 and 92%, respectively; and the accuracy was 87.5%. Salivary H. pylori IgA did not distinguish H. pylori-positive from H. pylori-negative children. The performance of serum H. pylori IgG was slightly (3 to 6%) better than that of salivary H. pylori IgG. The salivary IgG test can be considered a useful tool for the screening of H. pylori infection in children.     

Once-daily gentamicin therapy for experimental Escherichia coli meningitis

BACKGROUND: Eradication of Helicobacter pylori by antibiotics in combination with gastric acid inhibition can result in overgrowth of non-H. pylori bacterial flora. This may confound the histological detection of H. pylori at eradication control if non-specific staining methods are used. OBJECTIVE AND METHODS: In 18 patients treated with amoxycillin (2 weeks) and omeprazole (6 weeks), endoscopically obtained gastric juice was cultured and two biopsies of corpus, antrum and duodenum were taken before and after eradication therapy (with gastric acid inhibition still going on) for culture and for histology to assess the intragastric bacterial flora. By histology, modified Giemsa (MG) and an H. pylori-specific immunohistochemical stain (IMM) were evaluated. RESULTS: Median pH of gastric juice was 1.5 (n = 18) before and 7 (n = 17) after eradication therapy, when patients were still on omeprazole. After therapy, culture showed a significant decrease (P < 0.05) in mean amount of H. pylori in corpus, antral and duodenal biopsies and a significant increase of non-H. pylori flora (P < 0.05) in gastric juice, corpus, antral and duodenal mucosa. With culture as a standard, 16 and 4 biopsy specimens were scored falsely positive for H. pylori by MG and IMM, respectively, and H. pylori was not detected in 23 and 13 biopsy specimens when culture was H. pylori-positive. CONCLUSION: Because of the possible presence of non-H. pylori flora after eradication therapy, the use of IMM is recommended in this situation for the histological detection of H. pylori, especially in those patients with ongoing gastric acid inhibitory therapy.     

Proposed recommendations for research on biochemical markers for problematic drinking

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

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.     

Does smoking influence the eradication of Helicobacter pylori and duodenal ulcer healing with different regimens?

To determine the effect of smoking on Helicobacter pylori eradication and ulcer healing, we investigated 232 patients with H. pylori-positive duodenal ulcer. Patients were given one of seven different treatment protocols and divided into three groups according to smoking habits. Group 1 (n = 128) consisted of non-smokers, group 2 (n = 65) of mild smokers (5-20 cigarettes/day) and group 3 (n = 39) of heavy smokers (> 20/day). The eradication of H. pylori and ulcer healing rate was controlled eight weeks later after ceasing the therapy. The overall eradication rate was 66% in all patients and 68%, 66%, 59% in each group, respectively. The eradication rates showed no statistical difference between groups. Complete ulcer healing was achieved in 84% of all patients and ulcer healing rate between groups did not show any significance (85%, 83% and 82% respectively). These results suggest that smoking status does not influence the eradication of H. pylori and duodenal ulcer healing rates at eight weeks in patients on different treatment schedules.     

Accuracy of IgG serology and other tests in confirming Helicobacter pylori eradication

BACKGROUND: In this study we assessed the accuracy of IgG serology and other tests in confirming Helicobacter pylori eradication. METHODS: The outcome of anti-H. pylori therapy was established by at least two of the following tests: rapid urease test (RUT), culture, 14C urea breath test (non-capsule or capsule UBT), and IgG serology (Orion Diagnostica Pyloriset New EIA-G). RESULTS: Successful H. pylori eradication was confirmed in 698 of 794 patients (88%). The percentage decrease in IgG antibody titre was related to the patients' pre-treatment IgG titre and time interval after treatment. A decrease in IgG titres of 40% or more confirmed H. pylori eradication with 100% specificity, whereas the sensitivity was 82%, 90%, 98%, and 98% 3, 4, 5, and 6 months after therapy, respectively. The 40% cut-off confirmed eradication 3 to 6 months after therapy in 328 of 339 patients (97%) with pre-treatment IgG titres of >700, in 36 of 45 patients (80%) with pre-treatment titres of 300-700, and in 5 of 12 patients (42%) with pretreatment titres of <300. The sensitivity and specificity of the other tests 2 months after treatment were as follows: RUT, 84% and 100%; culture, 88% and 100%; non-capsule UBT, 100% and 89%; and capsule UBT, 100% and 97%. CONCLUSION: A decrease in IgG antibody titre of 40% or more 3 to 6 months after therapy and the capsule 14C UBT at the 2-month follow-up were both highly accurate in confirming H. pylori eradication.     

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.     

A comparison of 10 and 14 days of lansoprazole triple therapy for eradication of Helicobacter pylori

BACKGROUND: Data from large, multicenter, US studies determining the efficacy of triple therapy for the eradication of Helicobacter pylori are lacking, especially for a treatment duration of less than 14 days. METHODS: Patients with H pylori infection and active duodenal ulcer disease or a history of duodenal ulcer disease within the past year were randomized to receive 30 mg of lansoprazole, 1 g of amoxicillin, and 500 mg of clarithromycin twice daily for 10 or 14 days. The primary efficacy end point was the eradication of H pylori as confirmed by negative histological and culture results at 4 to 6 weeks after the completion of treatment. RESULTS: Of 284 patients enrolled in the study from 46 US sites, 236 met the entry criteria. At 4 to 6 weeks after the end of therapy, H pylori was eradicated in 85% (96/ 113) of the patients receiving 14-day triple therapy and in 84% (103/123) of those receiving 10-day triple therapy by per-protocol analysis (95% confidence interval for treatment group differences, -10.5 to 8.1; P>.05). There was also no significant difference between the 14- and 10-day treatment groups when analyzed by an intent-to-treat analysis of H pylori eradication. A similar proportion of patients in each treatment group reported an adverse event related to therapy (34% [46/136] vs 38% [56/148], respectively). CONCLUSIONS: In patients with an active or a recent history of duodenal ulcer, lansoprazole-based triple therapy for 10 or 14 days is highly effective in the eradication of H pylori. The duration of therapy may be reduced from 14 to 10 days without a significant effect on regimen efficacy.     

Significant improvement of atrophy after eradication therapy in atrophic body gastritis

Chronic atrophic body gastritis may be induced by H. pylori. Results on the effect of H. pylori eradication therapy have been conflicting. Here, we report on the effect of eradication therapy on both body atrophy and inflammation in 7 patients. They presented with severe or moderate atrophy of the oxyntic mucosa and positive H. pylori histology (Warthin-Starry) and/or serology. Eradication was performed with a standard double or triple therapy regimen. At least 6 weeks after successful eradication therapy, patients underwent rebiopsy and histopathological evaluation of the gastric body. In all 7 patients, the grade of body gastritis improved significantly. Among the patients with severe atrophy before H. pylori eradication, 2 had normal mucosa, 3 low-grade atrophy, and one moderate atrophy after treatment. The one case with moderate atrophy before treatment had normal mucosa after H. pylori eradication. In addition, inflammatory infiltration of the mucosa cleared up in 6 cases and improved from severe to mild in one case after treatment. From these results, we conclude that in patients with histologically demonstrated H. pylori and/or positive H. pylori serology atrophic body mucosa can recover after successful eradication therapy.     

Safety and efficacy of rabeprazole in combination with four antibiotic regimens for the eradication of Helicobacter pylori in patients with chronic gastritis with or without peptic ulceration

OBJECTIVES: Rabeprazole is a new fast acting proton pump inhibitor that has recently been proven to be effective in the treatment of peptic ulceration and reflux esophagitis. The aim of this study was to evaluate rabeprazole in combination with antibiotics for the eradication of Helicobacter pylori (H. pylori) in patients with chronic active gastritis with or without peptic ulcer disease. METHODS: Seventy-five H. pylori-infected patients were randomized in a double-blind fashion to receive a 7-day treatment regimen consisting of: RAC, RAM, RCM, or RC (R=rabeprazole 20 mg b.d., A=amoxycillin 1 g b.d., C=clarithromycin 500 mg b.d., M=metronidazole 400 mg b.d.). Randomized patients were H. pylori-positive by gastric biopsy urease test, histology and 13C urea breath test (13C-UBT). H. pylori eradication was assessed by 13C-UBT, 4 and 8 wk after finishing treatment. Endoscopy with histology and culture for antibiotic sensitivity testing was performed pretreatment and if treatment failed. RESULTS: On an intention-to-treat analysis, treatment success was: RCM 100%, RAC 95%, RAM 90%, and RC 63%. The most common side effects were loose stools, headache, and taste disturbance, but there were no serious adverse events related to the study medication. The two patients failing RAM treatment had metronidazole-resistant strains before and after treatment. None of the pretreatment H. pylori isolates from six patients failing RC were clarithromycin resistant, but three of five successfully cultured posttreatment had developed clarithromycin resistance. CONCLUSION: Rabeprazole-based triple therapy with two antibiotics for 1 wk is safe and effective in eradicating H. pylori. Dual therapy with clarithromycin is less successful, and the majority of treatment failures develop clarithromycin resistance.     

p53 expression is of independent predictive value in lymph node-negative breast carcinoma

OBJECTIVES: To compare the diagnostic accuracy of the most widely available tests for diagnosis of Helicobacter pylori infection after antibiotic treatment. METHODS: A total of 59 H. pylori-positive, duodenal ulcer patients (mean age, 40.7 +/- 11.7 yr; 40 male and 19 female) were treated for 2 wk with either amoxicillin-metronidazole (n = 36) or omeprazole-amoxicillin-tinidazole (n = 23), and after 4 wk, were tested for H. pylori infection by [14C]urea breath test (UBT), serum IgG antibody level, and multiple antral biopsies for rapid urease testing, histology, Warthin-Starry stain, and polymerase chain reaction to detect H. pylori DNA. Infection status was established by a concordance of test results. RESULTS: H. pylori was eradicated in 47 patients (80%). UBT and rapid urease testing had the best sensitivity and specificity, although not statistically different to Warthin-Starry stain and polymerase chain reaction. Serology and histology had little diagnostic value in this setting due to high proportion of false-positive results. CONCLUSIONS: Noninvasive UBT is as accurate in predicting H. pylori status after antibiotic treatment as rapid urease testing and Warthin-Starry stain. Especially for duodenal ulcer patients, UBT could be considered the gold standard to confirm eradication of H. pylori.     

Helicobacter pylori reinfection is virtually absent after successful eradication

This study examined whether reinfection or recrudescence accounts for the reappearance of Helicobacter pylori infection after apparent successful eradication. In a prospective study, 173 patients cured from H. pylori infection underwent follow-up endoscopies, with biopsies for culture and histopathology, every 3 months during the first year after treatment. Subsequently, elective half-yearly endoscopies were performed in 124 patients; the remaining 49 underwent follow-up endoscopy only in 1995. At reappearing infection, DNA profiles of pretreatment and recurrent strains were compared. After 3.5 years (range, 1.0-9.2), H. pylori infection recurred in 9 patients (5.2%). Reappearing infections were classified as endoscopically transmitted reinfection (n = 2), unclassified because of loss of pretreatment isolate (n = 1), or recrudescence (identical DNA patterns before and after treatment; n = 6). The reappearance rate of infection, discarding endoscopic transmission, was 1.2% (7/601 H. pylori-negative patient-years). There was virtually no reinfection with H. pylori after eradication in this adult Western population. These data do not rule out acquisition of H. pylori.     

Comparative effect of lansoprazole/amoxicillin with omeprazole/amoxicillin for the eradication of Helicobacter pylori in patients with duodenal ulcer

Lansoprazole, a potent antisecretory drug, possesses on an equimolar basis a 4-fold higher in vitro anti-Helicobacter pylori activity than omeprazole. In a prospective randomized study we compared lansoprazole 30 mg b.i.d. and amoxicillin 1 g b.i.d. with omeprazole 40 mg b.i.d. and amoxicillin 1 g b.i.d. for 14 days followed by lansoprazole 30 mg q.d. or omeprazole 20 mg q.d. for 14 additional days in 50 H. pylori positive duodenal ulcer patients (14f, 36m, age 27-83 [mean 43] years). H. pylori infection was diagnosed by histology (3 antral biopsies and 2 from gastric body, H & E- and Giemsa stain), rapid urease test (CLO) and culture in 39 patients, or by histology and rapid urease test in 11 patients. Control endoscopy was performed 4-6 weeks after the end of treatment. For eradication, a negative result in all 3 diagnostic modalities was required. The eradication rate was 43% (9/21 patients) in both treatment groups. 8 patients were lost to follow-up. The ulcer healing rate was 100% in both groups. Nonsmokers had a significantly higher (p = 0.026) eradication rate than smokers. No relevant adverse effects of the therapy occurred. 24 patients with persistent H. pylori infection were subsequently treated with lansoprazole 60 mg b.i.d. and amoxicillin 1 g b.i.d. for 14 days. Eradication was achieved in 5/22 (23%) patients (3/14 smokers, 2/8 nonsmokers), while 2 patients were lost to follow-up. 17 patients with persistent H. pylori infection after the second treatment received quadruple therapy consisting of metronidazole 500 mg t.i.d., tetracycline 500 mg q.i.d. bismuth-subcitrate 120 mg q.i.d. and lansoprazole 30 mg for 10 days. H. pylori eradication was achieved in 12/15 patients (80%). In conclusion, lansoprazole plus amoxicillin was equal to omeprazole plus amoxicillin in the treatment of H. pylori infected duodenal ulcer patients. Patients with eradication failure after dual therapy were successfully treated by quadruple therapy. In contrast, high dose lansoprazole and amoxicillin therapy was effective in only 23% of patients with persistent infection after standard dual therapy.     

A review of esthetic alternatives for the restoration of anterior teeth

Helicobacter pylori infection is an important cause of peptic ulcer disease and chronic gastritis. Infection with this bacterium stimulates the production of immunoglobulin (Ig) G antibody. Salivary IgG antibody tests to detect H pylori infection offer a convenient and noninvasive method of diagnosis. To evaluate an IgG salivary antibody kit, saliva was collected from 157 out-patients with dyspepsia referred for endoscopy to a tertiary centre. A salivary IgG ELISA antibody assay was performed using the Helisal Helicobacter pylori (IgG) assay kit, and at least four gastric biopsies were obtained. H pylori infection was confirmed by demonstration of the organism on Warthin-Starry silver stain (sensitivity 85%, specificity 55%). The prevalence of infection with H pylori was 30%. When the analysis was redone, excluding those treated with eradication therapy, the results were similar (sensitivity 86%, specificity 58%). The positive predictive value of the assay was 45% and the negative predictive value was 90%. Despite the ease of sampling, the assay used has limited diagnostic utility, lacking the predictive value to indicate which patients referred with dyspeptic symptoms to a tertiary care setting are infected with H pylori.     

Chronic pancreatitis and neoplasia: correlation or coincidence

Renal biopsy specimens from patients with membranous nephropathy (MN) were studied using immunohistochemical labelling to clarify the aetiological significance of Helicobacter pylori antigen in this disease. Sixteen specimens were examined, from 7 male and 9 female MN patients. Renal specimens from patients with diabetic nephropathy and IgA nephropathy, and from autopsied patients without renal diseases were obtained as controls. Immunohistochemical labelling was performed using one polyclonal antibody and three monoclonal antibodies against H. pylori. Specimens from 11 of the MN patients revealed granular deposits along the glomerular capillary walls, which reacted positively with polyclonal antibody after trypsin pretreatment. None of the control specimens revealed positive labelling. The MN specimens showed no positive reaction with the primary antibody, which had been treated for immunoabsorption testing using sonicated H. pylori. We also determined H. pylori status in these MN patients histologically and/or serologically. Of the 11 patients whose glomeruli were positive for anti-H. pylori antibody, 7 were suitable for analysis, and all were regarded as positive for H. pylori infection. These results suggest that the presence of a specific antigen in the glomeruli of patients with MN and H. pylori infection may be involved in the pathogenesis of MN.     

Midazolam improves postoperative epidural analgesia with continuous infusion of local anaesthetics

BACKGROUND: A number of triple drug regimens using proton pump inhibitors and two antibiotics have been evaluated in the West and reported to achieve Helicobacter pylori eradication rates of over 90%. In developing countries however, these combinations have neither been well evaluated, nor the optimum treatment for H. pylori infection well defined. AIM: To compare the combination of a proton pump inhibitor with a nitroimidazole and another antibiotic in eradicating H. pylori infection and healing duodenal ulcer. METHODS: Sixty consecutive patients with active duodenal ulcer who were positive for H. pylori (by rapid urease test and 14C-urea breath test) were randomized into three treatments groups: (1) LAS (n=21): lansoprazole 30 mg o.m., amoxycillin 500 mg q.d.s. and secnidazole 2 g on alternate days for 2 weeks; (2) LCS (n=18): lansoprazole 30 mg o.m., clarithromycin 500 mg b.d. and secnidazole 2 g on alternate days for 1 week; (3) LPS (n=21): lansoprazole 30 mg o.m., pefloxacin 400 mg o.m. and secnidazole 2 g on alternate days for 2 weeks. Urease and breath tests were performed at 0, 6 and 12 weeks to check for H. pylori eradication. RESULTS: Intention-to-treat eradication rates were as follows: LAS 86%, LCS 83%, LPS 71%; the overall ulcer healing rate was 90% at 6 weeks. CONCLUSIONS: High H. pylori eradication rates were achieved using the amoxycillin- and clarithromycin-based therapies. Fewer side-effects, better compliance and low cost favoured the amoxycillin-based therapy.     

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.     

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.     

Urease-specific monoclonal antibodies prevent Helicobacter felis infection in mice

Experiments were performed to determine the antigenic specificity of a monoclonal antibody (immunoglobulin A [IgA] 71) previously demonstrated to neutralize the ability of Helicobacter felis to colonize mice. Immunoprecipitation of radiolabeled H. felis outer membrane proteins with IgA 71 revealed specificity for a 62-kDa protein. Another of our monoclonal antibodies, IgG 40, precipitated a protein of similar molecular weight. IgA 71 but not IgG 40 also precipitated purified recombinant H. pylori urease. The antigenic specificity of both antibodies was confirmed to be urease by the ability of each to select Escherichia coli clones expressing the H. felis urease genes. The two antibodies were shown to bind nonoverlapping epitopes in a competition enzyme-linked immunosorbent assay. Both IgA 71 and IgG 40 could effectively neutralize H. felis infectivity by incubating the bacteria with the antibodies prior to oral administration to naive mice. The mechanism of protection does not appear to be inhibition of urease activity, as IgA 71 does not inhibit the conversion of urea to ammonia by H. pylori urease in vitro. These results support a protective role for the secretory humoral immune response in Helicobacter immunity and provide further evidence that the urease enzyme can serve as a protective antigen.