Whole body positron emission tomography/computed tomography (PET/CT) tumour staging with integrated PET/CT colonography: technical feasibility and first experiences in patients with colorectal cancer.

AIM: The aim of this study was to implement an imaging protocol for positron emission tomography/computed tomography (PET/CT) colonography and to combine this protocol with whole body PET/CT tumour staging for a single whole body examination for routine clinical use. SUBJECTS AND METHODS: A whole body PET/CT protocol for tumour staging and a protocol for PET/CT colonography were integrated into one examination. Fourteen prospective patients with suspected colorectal cancer underwent whole body PET/CT after aqueous bowel distension and pharmacological bowel relaxation. Colonoscopy and histopathology served as the standards of reference in all patients. RESULTS: The modified PET/CT examination detected all but one lesion in the colon. One additional lesion was detected in a patient with incomplete colonoscopy due to high grade luminal stenosis. One polyp with malignant conversion was identified with the modified PET/CT protocol. PET/CT colonography proved accurate in local lymph node staging and staged nine out of 11 patients correctly. Six additional extracolonic tumour sites were detected based on the whole body staging approach. CONCLUSION: Whole body PET/CT with integrated colonography is technically feasible for whole body staging in patients with colorectal cancer. Based on these initial diagnostic experiences, this integrated protocol may be of substantial benefit in staging patients with colorectal cancer, focusing on patients with incomplete colonoscopy and those with small synchronous bowel lesions.

Clonal relationship in multifocal non-Hodgkin's lymphoma of mucosa-associated lymphoid tissue (MALT).

To elucidate the progression of gastric marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) type, we analyzed a case presenting simultaneously with MALT lymphoma of the stomach and lung, and a gastric high-grade diffuse large lymphoma. The rearranged immunoglobulin heavy chain (IgH) variable regions were analyzed using a polymerase chain reaction (PCR)-based assay. Clonal relationship was shown between the gastric high-grade and the pulmonary low-grade lymphoma. The gastric MALT lymphoma was not related to the other manifestations. Translocation t(11;18) was not detected in the gastric high-grade lymphoma. MALT lymphomas at various locations and with different histologies may derive from a common precursor cell. Lymphomas at identical sites may have different stem cells.

High rate of post-therapeutic resistance after failure of macrolide-nitroimidazole triple therapy to cure Helicobacter pylori infection: impact of two second-line therapies in a randomized study.

BACKGROUND: The optimal second-line treatment after failed Helicobacter pylori therapy has not been established. AIMS: To ascertain whether quadruple therapy or triple therapy with omeprazole, clarithromycin and amoxicillin is the superior re-treatment after triple therapy containing a macrolide and a nitroimidazole, and to determine the impact of microbial in vitro resistance. METHODS: Patients after failed triple therapy were randomly allocated to one of two 1-week second-line treatments: omeprazole, 40 mg, clarithromycin, 500 mg, and amoxicillin, 1 g, all b.d.; or omeprazole, 20 mg b.d., bismuth subsalicylate, 600 mg q.d.s., metronidazole, 400 mg t.d.s., and tetracycline, 500 mg q.d.s. Post-therapeutic Helicobacter pylori status was assessed by 13C-urea breath test at least 4 weeks after treatment. RESULTS: The study was terminated after including 84 patients. H. pylori cure rates differed significantly: omeprazole-clarithromycin-amoxicillin: intention-to-treat, 43%; per protocol, 50%; omeprazole-bismuth subsalicylate-metronidazole-tetracycline: intention-to-treat, 68%; per protocol, 69%. The frequencies of resistance after first-line therapy were: metronidazole, 90%; clarithromycin, 71%; both combined, 68%. For clarithromycin resistance, H. pylori cure with omeprazole-clarithromycin-amoxicillin was 30% vs. 83% for clarithromycin susceptibility. CONCLUSIONS: Omeprazole-bismuth subsalicylate-metron- idazole-tetracycline was superior to omeprazole-clarithromycin-amoxicillin, but both therapies yielded unsatisfactory results. The high rate of post-therapeutic dual resistance has a negative impact on omepraz- ole-clarithromycin-amoxicillin, and probably also on omeprazole-bismuth subsalicylate-metronidazole-tetracycline, and limits the choice for second-line treatment.

[Insufficient validity of a rapid blood test for diagnosis of Helicobacter pylori infection]. / Unzureichende Validität eines Blutschnelltests zur Diagnose der Helicobacter-pylori-Infektion.

BACKGROUND AND AIM: Rapid blood tests for diagnosis of Helicobacter (H.) pylori infection enable to detect antibodies against H. pylori instantly without laboratory equipment. Primary aim: to validate the Helisal Rapid Whole Blood Test (HRBT) with endoscopic bioptic methods as reference. Secondary aim: to compare the HRBT with ELISA IgG serology. PATIENTS AND METHODS: The HRBT was performed in 145 consecutive dyspeptic patients (median age 59 years) before undergoing esophagogastroduodenoscopy including biopsies from gastric antrum and corpus. A positive H. pylori status was defined by a positive culture or the combination of a positive rapid urease test and a positive histology. Serum for ELISA IgG testing was available from 92 patients. RESULTS: The H. pylori status was positive in 66% of the patients. The sensitivity of the HRBT resulted at 80%, the specificity at 82%. The sensitivity of the HRBT for a positive ELISA test amounted to 87%, the specificity to 96%. CONCLUSIONS: The diagnostic validity of the HRBT is insufficient for clinical application. False test results add up by the general discrepancy between serological and bioptic methods and by diminished sensitivity compared to ELISA serology.

Helicobacter pylori increases the risk of peptic ulcer bleeding: a case-control study.

AIM: Aim of the present case-control study was to establish whether Helicobacter pylori increases the risk of ulcer bleeding. PATIENTS AND METHODS: All patients presenting with upper gastrointestinal bleeding between November 1994 and November 1995 were prospectively investigated and compared with hospital controls matched for age, sex, and race. We evaluated the frequency of Helicobacter pylori infection, intake of aspirin or non-steroidal anti-inflammatory drugs, use of alcohol, and smoking habits in patients and controls. RESULTS: Included in the study were 128 patients. In 72 patients, the source of bleeding was a peptic ulcer (duodenal ulcer: n = 33; gastric ulcer: n = 39). Ulcer patients were more frequently infected by Helicobacter pylori than controls (72% vs 42%; p < 0.001) while the incidence of infection was similar in patients with non-ulcer bleeding and controls (52% vs 46%; p = 0.59). Conditional multiple logistic regression analysis showed that Helicobacter pylori infection (odds ratio, 3.3 [Confidence interval, 1.5 to 7.0]; p = 0.002) and regular use of alcohol (odds ratio, 3.1 [Confidence interval, 1.0 to 9.0]; p = 0.041) increased the risk of peptic ulcer bleeding while previous intake of aspirin (> 100 mg) or non-steroidal anti-inflammatory drugs independently increased the risk of bleeding only in the case of gastric ulcer (odds ratio, 8.1 [Confidence interval 1.2 to 56.6]; p = 0.034). CONCLUSIONS: Helicobacter pylori infection increases the risk of peptic ulcer bleeding. Our results suggest that Helicobacter pylori and non-steroidal anti-inflammatory drugs are independent risk factors for peptic ulcer bleeding.

Effect of curing Helicobacter pylori infection on intragastric acidity during treatment with ranitidine in patients with duodenal ulcer.

BACKGROUND: In patients with duodenal ulcer cure of Helicobacter pylori infection resulted in a pronounced decrease in intragastric pH during treatment with omeprazole. AIM: To test the hypothesis that treatment of H pylori adversely affects the pH response to ranitidine. PATIENTS: Eighteen patients with duodenal ulcer who were infected with H pylori were studied. METHODS: Twenty four hour pH recordings were performed during treatment with ranitidine (300 mg) at night before and four to six weeks after cure of H pylori infection. Presence of H pylori was assessed by a rapid urease test, culture, histology, and a 13C urea breath test. Also, the fasting gastrin concentrations were measured before and after treatment for H pylori infection. RESULTS: Cure of H pylori infection resulted in a considerable improvement in both antral and corpus gastritis and a decrease in fasting gastrin concentrations. As a result of the cure the night time intragastric pH during treatment with ranitidine decreased (median pH 6.8 v 5.4; p = 0.007), whereas the acidity during the daytime was not affected. CONCLUSIONS: In patients with duodenal ulcer the intragastric pH during treatment with ranitidine depends on H pylori. However, the loss of effectiveness in altering pH seems to be less pronounced than previously found with omeprazole.

Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis.

BACKGROUND & AIMS: We have shown previously that cure of Helicobacter pylori infection leads to the disappearance of acid-neutralizing substances. Also, patients with ulcer after cure may gain weight. The aim of this study was to investigate whether cure of the infection increases the risk of reflux esophagitis. METHODS: Patients with duodenal ulcer without reflux esophagitis at the time of Helicobacter treatment were followed up prospectively after cure of the infection (n = 244) or after diagnosis of persisting infection (n = 216). All patients underwent endoscopy at 1-year intervals or when upper gastrointestinal symptoms recurred. H. pylori infection was assessed by rapid urease test and histology. RESULTS: The estimated incidence of reflux esophagitis within 3 years was 25.8% after cure of the infection and 12.9% when the infection was ongoing (P < 0.001). Patients who developed reflux esophagitis after the cure had a more severe body gastritis before cure (odds ratio, 5.5; 95% confidence interval [CI], 2.8-13.6), gained weight more frequently after cure (odds ratio, 3.2; 95% CI, 1.2-9.4), and were predominantly men (odds ratio, 3.6; 95% CI, 1.1-10.6). CONCLUSIONS: A considerable proportion of patients with duodenal ulcer treated for H. pylori will develop reflux esophagitis; risk factors are male sex, severity of corpus gastritis, and weight gain.

Efficacy of omeprazole one year after cure of Helicobacter pylori infection in duodenal ulcer patients.

OBJECTIVE: We have previously shown that, in duodenal ulcer patients, pH control by omeprazole is less pronounced after cure of Helicobacter pylori infection. The present study was designed to test the hypothesis that this response to omeprazole persists 1 yr after cure of H. pylori infection. METHODS: In 12 duodenal ulcer patients, intragastric acidity was measured with a glass electrode during treatment with omeprazole (20 mg) once daily before, and 4-6 wk and 1 yr after, cure of H. pylori infection. H. pylori infection was assessed by [13C]urea breath test, culture, histology (Warthin Starry stain), and rapid urease test. RESULTS: Cure of H. pylori infection resulted in a lowered pH during omeprazole treatment. This effect persisted after 1 yr. Median 24-h gastric pH before H. pylori treatment was 5.6; 4-6 wk after cure of the infection it was 2.9 (p = 0.003), and 1 yr after cure of the infection it remained unchanged (pH = 2.5; p = 0.5). Accordingly, twice as much time was spent above pH 3 and pH 4 before H. pylori treatment than 1 or 12 months after cure (percent of time > or = pH 3: 82.7 vs. 49.7 vs. 43.1; percent of time > or = pH 4: 72.7 vs. 38.3 vs. 26.4). CONCLUSION: In duodenal ulcer patients, cure of H. pylori infection resulted in a marked rapid and persistent decrease of the pH increasing effect of omeprazole. Therefore, H. pylori is a determinant of the pH achieved in response to omeprazole treatment in duodenal ulcer patients.

[Helicobacter pylori: pretherapeutic resistance status in Germany (Ruhr area)]. / Helicobacter pylori: Prätherapeutische Resistenzlage in Deutschland (Ruhrgebiet).

BASIC PROBLEM AND OBJECTIVE OF STUDY: The situation of pretherapeutical antimicrobial drug resistance of Helicobacter pylori has therapeutical implications. For this reason the present study was designed to evaluate the frequency of resistance in Germany. MATERIAL AND METHODS: A total of 201 H. pylori isolates cultured on the basis of biopsies taken by routine gastroscopies were tested for resistance by E-test. The antibiotics examined were amoxicillin, tetracycline, clarithromycin and metronidazole. For further analysis the last 101 patients were asked for demographical and clinical data that were evaluated for a correlation with metronidazole resistance. RESULTS: Pretherapeutical resistance against amoxicillin and tetracycline was not detected. The rate of drug resistance against clarithromycin came to 3% and against metronidazole to 29%. There was a higher incidence of metronidazole resistance in female patients (Odds ratio 1.71; p = n.s.). Reliable predictors for metronidazole resistance, however, could not be identified. CONCLUSIONS: About 30% of H. pylori isolates are pretherapeutically resistant to metronidazole. Resistance to clarithromycin is still rare, but further monitoring remains necessary to detect changes in the community.

One-week low-dose triple therapy for Helicobacter pylori is sufficient for relief from symptoms and healing of duodenal ulcers.

AIM: To test the hypothesis that 1-week low-dose triple therapy for H. pylori is sufficient for relief from dyspeptic symptoms and healing of duodenal ulcers. METHODS: Fifty-nine out-patients with duodenal ulcers and positive rapid urease test participated in this randomized, double-blind, two-centre study. All patients were treated for 1 week with omeprazole 20 mg b.d., clarithromycin 250 mg b.d. and metronidazole 400 mg b.d. In a double-blind fashion, patients were then randomly treated for another 3 weeks with either omeprazole 20 mg once daily or an identical-looking placebo. Patients were investigated endoscopically before treatment for H. pylori, after 2 weeks and after 4 weeks. H. pylori infection was assessed by a 13C-urea breath test at the time of enrollment and 4 weeks after cessation of any study medication. RESULTS: Fifty-two patients were included in the 'all patients treated' analysis of efficacy. The overall H. pylori cure rate was 96% (95% CI = 87-100%), with no difference between the treatment groups. After 2 weeks duodenal ulcer healing was confirmed in 91% (95% CI = 80-100%) of patients treated with omeprazole and in 76% (95% CI = 60-91%) in the placebo group (P = 0.14). After 4 weeks all ulcers had healed. Relief from dyspeptic symptoms and adverse events (13.8 and 16.7%) did not differ between the treatment groups. CONCLUSIONS: One-week low-dose triple therapy consisting of omeprazole, clarithromycin and metronidazole is a highly effective and well-tolerated approach to the cure of H. pylori infection in patients with a duodenal ulcer. Our data suggest that continuation of antisecretory drug therapy beyond anti-H. pylori therapy is actually excessive regarding relief from dyspeptic symptoms and healing of duodenal ulcers.

Efficacy of primed infusions with high dose ranitidine and omeprazole to maintain high intragastric pH in patients with peptic ulcer bleeding: a prospective randomised controlled study.

BACKGROUND: In healthy subjects, continuous infusions of high dose ranitidine and omeprazole produce high intragastric pH values. AIM: To test the hypothesis that both drugs also maintain high intragastric pH values in patients with bleeding ulcers. PATIENTS AND METHODS: In two parallel studies, 20 patients with bleeding duodenal ulcers and 20 patients with bleeding gastric ulcers were randomly assigned to receive either ranitidine (0.25 mg/kg/hour after a bolus of 50 mg) or omeprazole (8 mg/hour after a bolus of 80 mg) for 24 hours. Intragastric pH was continuously recorded with a glass electrode placed 5 cm below the cardia. RESULTS: Both drugs rapidly raised the intragastric pH above 6. During the second 12 hour period, however, the percentage of time spent below a pH of 6 was 0.15% with omeprazole and 20.1% with ranitidine (p = 0.0015) in patients with duodenal ulcer; in patients with gastric ulcer it was 0.1% with omeprazole and 46.1% with ranitidine (p = 0.002). CONCLUSIONS: Primed infusions of omeprazole after a bolus produced consistently high intragastric pH values in patients with bleeding peptic ulcers, whereas primed infusions with ranitidine were less effective during the second half of a 24 hour treatment course. This loss of effectiveness may be due to tolerance.

Intragastric pH during treatment with omeprazole: role of Helicobacter pylori and H. pylori-associated gastritis.

BACKGROUND: Omeprazole treatment produces lower intragastric pH values 4 weeks after cure of Helicobacter pylori infection than before. We therefore investigated the effect of healing H. pylori-associated gastritis on intragastric pH in the presence and in the absence of omeprazole therapy. METHODS: Before and on day 8 of omeprazole, 20 mg once daily, 24-h intragastric pH-recordings were performed in 14 subjects with H. pylori infection and repeated 4 and 52 weeks after cure of infection. Gastritis severity in corpus and antrum was graded by using a modified Sydney system. RESULTS: In the absence of omeprazole administration, median 24-h pH values before cure did not differ from those 4 and 52 weeks after cure. On day 8 of omeprazole administration, 24-h pH values were much higher before cure (median, 5.15; 95% confidence interval (CI), 4.3-6.0) than 4 weeks (3.6; 2.1-4.4; P < 0.001) and 52 weeks after cure (3.0; 2.1-4.4; P < 0.001). The activity of corpus and antral gastritis was not associated with the magnitude of H+ change induced by omeprazole. CONCLUSION: The increased pH produced by omeprazole during H. pylori infection is likely to be due to neutralizing substances produced by H. pylori and not to H. pylori-induced gastritis.

One-week triple therapy with omeprazole, amoxycillin and either clarithromycin or metronidazole for cure of Helicobacter pylori infection.

AIM: The present study was designed to evaluate the efficacy and tolerability of 1-week triple therapy regimens for Helicobacter pylori. METHODS: In two consecutive series, 120 patients with proven H. pylori infection and peptic ulcer disease or functional dyspepsia were treated with either omeprazole 20 mg b.d., amoxycillin 1 g b.d. and clarithromycin 250 mg b.d. (OAC; n = 60) or with omeprazole 20 mg b.d., amoxycillin 1 g b.d. and metronidazole 400 mg b.d. over 1 week (OAM; n = 60). H. pylori infection was assessed by rapid urease test, culture and histology before and 4 weeks after cessation of the eradication therapy. RESULTS: H. pylori eradication succeeded in 53 out of 60 patients by omeprazole-amoxycillin-clarithromycin (OAC) (88%; 95% CI 77-95%) and in 47 out of 60 patients by omeprazole-amoxycillin-metronidazole (OAM) (78%; 95% CI 66-88%) (P = 0.22). Nine patients of each group available for follow-up reported adverse events (15.0 and 15.5%, respectively) without necessity of discontinuation of the study medications. Serious adverse events were not observed. CONCLUSIONS: Simple and convenient 1-week triple therapies consisting of omeprazole, amoxycillin and either clarithromycin or metronidazole are sufficiently effective in eradicating H. pylori infection.

Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duodenal ulcer.

BACKGROUND & AIMS: Omeprazole is less effective in healthy subjects than in patients with duodenal ulcers. The aim of this study was to determine whether Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duodenal ulcers. METHODS: In 16 patients with duodenal ulcers, baseline intragastric acidity was measured before and 4-6 weeks after the cure of H. pylori infection. In 17 patients with duodenal ulcers, 24-hour pH metry was performed during treatment with 20 mg omeprazole once daily before as well as after eradication of H. pylori. Intragastric acidity was measured using a glass electrode placed 5 cm below the cardia. H. pylori infection was assessed by [13C] urea breath test, culture, histology, and rapid urease test. RESULTS: H. pylori eradication resulted in marked decrease of the pH-increasing effect of omeprazole (24-hour median gastric pH, 5.5 vs. 3.0; P<0.002) that was most pronounced during nighttime (median gastric pH, 6.4 vs. 2.1; P=0.001). On the other hand, baseline intragastric pH remained unchanged after eradication (median gastric pH, 1.0 vs. 1.1; P=0.5). CONCLUSIONS: In patients with duodenal ulcers treated with omeprazole, intragastric pH depends significantly on the presence or absence of H. pylori, whereas baseline pH remained unchanged after H. pylori eradication.

[Ulcer healing through the elimination of Helicobacter pylori: is a week of therapy enough?]. / Ulcusheilung durch Helicobacter-pylori-Eradikation: genügt eine Woche Therapie?

AIM OF STUDY: To test whether one week's triple therapy with omeprazole and two antibiotics is enough to induce healing of a peptic (gastric and/or duodenal) ulcer. PATIENTS AND METHODS: 112 Patients (73 males, 39 females; median age 55 [18-88] years) proven by culture or histology to have an Helicobacter (H.) pylori infection and uncomplicated peptic (gastroduodenal) ulcer. For one week they received omeprazole (20 mg once or twice daily) plus two antibiotics (clarithromycin/metronidazole, clarithromycin/tetracycline, clarithromycin/amoxycillin or amoxycillin/metronidazole) to eradicate H. pylori. No further anti-ulcer treatment was given subsequently. Healing of the ulcer and H. pylori status were checked by the urease test, culture and histology (endoscopic biopsy) 4 weeks later. RESULTS: The 5-week ulcer healing rate was 94.6% (95% confidence interval: 89-98%). Persisting ulcers (n = 6) were associated with either treatment with aspirin or nonsteroidal antiinflammatory drugs (n = 3), persistent H. pylori infection (n = 2) or persistent H. pylori infection plus treatment with aspirin (n = 1). The ulcer healing rate was significantly higher in patients with eradicated infection than in those with posttherapy persistence of H. pylori (97.0 vs. 76.9%; P = 0.02). There were no significant differences after 5 weeks between patients with duodenal and those with gastric ulcer (97.4 vs. 89.3%). CONCLUSIONS: One-week effective eradication treatment is adequate to induce healing of H. pylori-positive peptic ulcers. Anti-ulcer treatment after eradication of H. pylori should be considered only if the patient is receiving treatment with ulcerogenic drugs or continues to have symptoms.

Long-term consequences of Helicobacter pylori eradication: clinical aspects.

Helicobacter pylori is probably the most important factor in the pathogenesis of peptic ulcer disease in the absence of other precipitating factors, such as the intake of ulcerogenic drugs. Clinical studies have shown convincingly that eradication of H. pylori dramatically alters the long-term natural history of this chronic relapsing disorder, and that ulcer recurrences following eradication are rare. Available evidence also suggests that figures for H. pylori reinfection are low in adults in developed countries following eradication. In addition, H. pylori eradication may prevent peptic ulcer bleeding or rebleeding. Curing H. pylori infection significantly increases the quality of life of patients with duodenal ulcer disease and is, to date, the most cost-effective treatment in the long-term management of this disease. Ulcer patients presenting with recurrent dyspeptic symptoms after apparently successful eradication of H. pylori should be checked for ulcer and H. pylori recurrence, as well as for reflux oesophagitis, which has been shown to occur in about 9% of patients with duodenal ulcer disease and previously cured of H. pylori infection. We would also argue that H. pylori infection in young patients with dyspepsia should be treated, although this issue will remain controversial until well-designed, placebo-controlled studies establish the real benefits of eradication therapy in the long-term treatment of this disease.

Effect of curing Helicobacter pylori infection on intragastric pH during treatment with omeprazole.

It has been shown that omeprazole treatment produces higher intragastric pH values in Helicobacter pylori positive subjects than in H pylori negative subjects. This study aimed to investigate the effect of curing H pylori on the intragastric pH in both the presence and absence of omeprazole therapy. Twenty four hour intragastric pH recordings were performed before and after a one week course of omeprazole (20 mg once daily) in 18 H pylori positive subjects and were repeated after the infection had been cured. In the absence of omeprazole, the total 24 hour pH values before cure did not differ from those afterwards. During omeprazole treatment the 24 hour pH values were much higher before (median (95% CI) 5.4: 4.3, 6.0), than after cure of infection (3.6: 2.1, 4.4; p < 0.001). The omeprazole induced fall in H+ activity before cure of H pylori did not, however, differ from that afterwards. It is concluded that the apparently greater antisecretory effect of omeprazole during H pylori infection may be a result of the production of acid neutralising compounds by the H pylori. Although a direct interaction between H pylori and omeprazole cannot be excluded, it seems unlikely.

Omeprazole/amoxicillin versus triple therapy for Helicobacter pylori in duodenal ulcer disease: two-year follow-up of a prospective randomized study.

The present study was designed to compare the efficacy and tolerability of triple therapy and dual therapy for Helicobacter pylori in duodenal ulcer patients and to evaluate the long-term clinical course of ulcer disease. Forty duodenal ulcer patients with proven H. pylori infection were enrolled into the study and randomly treated with either triple therapy consisting of bismuth subsalicylate, metronidazole and tetracycline plus ranitidine or with dual therapy comprising omeprazole and amoxicillin. Patients were investigated clinically and endoscopically including assessment of H. pylori infection by means or rapid urease test, culture, histology and urea breath testing 4 weeks after cessation of eradication therapy, in 1-year intervals and when dyspeptic symptoms recurred. One patient of each group was lost during follow-up. H. pylori infection was cured by triple therapy in 84.2% and by dual therapy in 78.9% (p = 1.00). During follow-up, all patients with cure of H. pylori infection (n = 31) remained in stable remission with respect to duodenal ulcer disease, while 6 out of 7 patients persistently infected with H. pylori developed an ulcer relapse (p < 0.001). One patient with cured infection had had an episode of dyspeptic symptoms requiring pharmacotherapy and in another 3 patients mild refluxesophagitis without necessity of medical treatment had been detected on the occasion of a scheduled endoscopy. In the short-term, cure of the infection resulted in a marked reduction of the degree of antral gastritis and in a loss of activity in all but one patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Intragastric acidity as a predictor of the success of Helicobacter pylori eradication: a study in peptic ulcer patients with omeprazole and amoxicillin.

Omeprazole plus amoxicillin cures Helicobacter pylori infection. The hypothesis was tested that low acidity is a predictor of outcome. Fifty patients with relapsing or complicated, or both H pylori positive duodenal (n = 25) or gastric ulcer (n = 25) were randomly treated with either omeprazole 20 mg twice daily plus amoxicillin 1 g twice daily or with omeprazole 40 mg twice daily plus amoxicillin 1 g twice daily over two weeks. After one week of combined treatment, a 24 hour gastric pH measurement was performed in all patients. H pylori cure rate was 67%. Patients who later turned out to be cured had higher pH values during night time and after meals (p < 0.05). In an explorative analysis drug compliance, smoking, location of the ulcer (duodenum versus stomach), age, and grade of body gastritis were additional predictors of the outcome. Smoking (p = 0.006), compliance (p = 0.037), duodenal ulcer disease (p = 0.065), and young age (p = 0.021) were related to high acidity. In conclusion, the success of eradication treatment with omeprazole and amoxicillin in ulcer patients infected with H pylori depends on intragastric pH. Drug compliance, smoking habits, location of ulcer, age, and activity of body gastritis are other predictors and in part related to intragastric acidity.