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J Labenz

Publications and source records attributed to J Labenz.

At least 55 records · Page 3Linked to original sources
PubMed1999

Prevalence and clinical importance of Helicobacter pylori infection in patients after partial gastric resection for peptic ulcer disease. A prospective evaluation of Helicobacter pylori infection on 50 resected patients compared with matched nonresected controls.

UNLABELLED: There have been only a few surveys on the prevalence of persistent Helicobacter pylori (Hp) infection in patients who have undergone surgery for peptic ulceration. The aim of the study was to evaluate the prevalence and clinical importance of Hp infection after partial gastric surgery due to peptic ulcer disease. METHODS: We examined 50 patients who had partial gastric resection for peptic ulcer disease and years later underwent upper gastrointestinal (GI) endoscopy. 50 controls matched with respect to indication for GI endoscopy, age and gender were also studied. Three specimens from the fundus of gastric remnant were examined for Hp infection (histology and rapid urease test). The prevalence of Hp infection and pathology findings were compared between the two groups using chi-square statistics. RESULTS: 32 men and 18 women were examined (40 x BII, 10 x BI). The prevalence of Hp infection was 38% in the resected group compared to 60% in the control group (p = 0.015). We found a significant association (p = 0.0004) between Hp infection and endoscopic findings in the control group but not in the group of partially resected patients (p = 0.66). CONCLUSION: The prevalence of Hp infection in hospitalized patients with partial gastric resection is significantly lower than in matched controls. Hp infection does not play a significant pathogenic role in recurrent ulcer after partial gastric resection in these patients.

Adult↗
PubMed1999

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.

Adult↗
PubMed1998

Lack of effect of treating Helicobacter pylori infection in patients with nonulcer dyspepsia. Omeprazole plus Clarithromycin and Amoxicillin Effect One Year after Treatment (OCAY) Study Group.

BACKGROUND: It is uncertain whether treatment of Helicobacter pylori infection relieves symptoms in patients with nonulcer, or functional, dyspepsia. METHODS: We conducted a double-blind, multicenter trial of patients with H. pylori infection and dyspeptic symptoms (moderate-to-very-severe pain and discomfort centered in the upper abdomen). Patients were excluded if they had a history of peptic ulcer disease or gastroesophageal reflux disease and had abnormal findings on upper endoscopy. Patients were randomly assigned to seven days of treatment with 20 mg of omeprazole twice daily, 1000 mg of amoxicillin twice daily, and 500 mg of clarithromycin twice daily or with omeprazole alone and then followed up for one year. Treatment success was defined as the absence of dyspeptic symptoms or the presence of minimal symptoms on any of the 7 days preceding the 12-month visit. RESULTS: Twenty of the 348 patients were excluded after randomization because they were not infected with H. pylori, were not treated, or had no data available. For the remaining 328 patients (164 in each group), treatment was successful for 27.4 percent of those assigned to receive omeprazole and antibiotics and 20.7 percent of those assigned to receive omeprazole alone (P=0.17; absolute difference between groups, 6.7 percent; 95 percent confidence interval, -2.6 to 16.0). After 12 months, gastritis had healed in 75.0 percent of the patients in the group given omeprazole and antibiotics and in 3.0 percent of the patients in the omeprazole group (P<0.001); the respective rates of H. pylori eradication were 79 percent and 2 percent. In the group given omeprazole and antibiotics, the rate of treatment success among patients with persistent H. pylori infection was similar to that among patients in whom the infection was eradicated (26 percent vs. 31 percent). There were no significant differences between the groups in the quality of life after treatment. CONCLUSIONS: In patients with nonulcer dyspepsia, the eradication of H. pylori infection is not likely to relieve symptoms.

Adolescent↗
PubMed1998

Does Helicobacter pylori status affect nonsteroidal anti-inflammatory drug-associated gastroduodenal pathology?

There are two lines of thought regarding the interrelationship between the damaging effects of Helicobacter pylori and those of nonsteroidal anti-inflammatory drugs (NSAIDs) on the gastroduodenal mucosa. First, both pathogenic factors exert a damaging effect on the mucosa, and therefore an additive, or even synergistic, effect occurs, leading to aggravation of mucosal damage. Second, mutual antagonism exists, leading to one of the pathogenic factors actually deriving some protection from the damaging potential of the other. Microscopically, H. pylori- and NSAID-associated gastritis are recognized as two separate entities. Furthermore, pathologically, the mechanisms of mucosal damage of the two factors have important differences; for example, H. pylori increases the synthesis of prostaglandins, whereas NSAIDs inhibit prostaglandin synthesis. The role of H. pylori infection in patients with NSAID-associated peptic ulcers has been addressed recently in two large, randomized, multicenter trials. From these studies, it appears that antisecretory drugs are more effective in H. pylori-positive peptic ulcer patients taking NSAIDs than in H. pylori-negative patients taking these drugs. The studies, however, do not provide any evidence that H. pylori infection reduces the pathogenic effects of NSAIDs. Other studies, however, have shown protection against NSAID-associated gastroduodenal damage in H. pylori-negative patients. Thus, there are no firm conclusions on the role of H. pylori infection in patients with NSAID-associated peptic ulcers. Based on the available data, however, practical considerations and guidelines are listed.

Animals↗
PubMed1998

Increased risk for Helicobacter pylori recurrence by continuous acid suppression: a randomized controlled study.

BACKGROUND AND AIMS: Acid hyposecretion may enhance Helicobacter pylori colonization. We tested the hypothesis that maintenance therapy with ranitidine after cure of Helicobacter pylori infection increases the risk of recurrence of infection. PATIENTS AND METHODS: Sixty-six patients with duodenal ulcer and cured Helicobacter pylori infection were randomly assigned to 12 months maintenance treatment with ranitidine 150 mg daily (group A) or no treatment (group B). Follow-up consisted of clinical and endoscopic controls with biopsies for histology and rapid urease test every 4 months. RESULTS: Six patients, 3 in each group, were lost to follow up. Helicobacter pylori recurrence occurred in 9 patients in group A and in 2 patients in group B (30% versus 7%; p < 0.05). Duodenal ulcer recurred in one patient in group A and in 2 in group B, all three patients were reinfected with Helicobacter pylori. A corpus-predominant gastritis was observed in all reinfected patients in group A but in none in group B. CONCLUSIONS: Long-term inhibition of gastric acid secretion after eradication of Helicobacter pylori increases the risk of recurrence of infection. Our data imply that gastric acid not only influences the pattern of Helicobacter pylori localization in gastric mucosa, but also plays a key role in preventing recurrence of infection with Helicobacter pylori.

Adult↗
PubMed1997

[Helicobacter pylori--when and how do gastroenterologists treat themselves? A clinical and practical survey].

OBJECTIVE: To determine how often gastroenterologists know their own Helicobacter pylori status, how they diagnose the infection and what consequences they draw from the findings. METHODS: Between November 1995 and March 1996 questionnaires were sent to gastroenterologists in hospitals (592, with five not reached) or private practice in Germany (431, 12 not reached), with a response rate of 24.4% and 55.4%, respectively. RESULTS: Of the 375 respondents 27 were female; the average age was 47.6 +/- 7.8 years. 151 knew their own H. pylori status (40.3%), with an infection rate of 55.6%. Most of the doctors had used noninvasive diagnostic tests (serology: 18.5%, breath test: 37.7%, serology + breath test 2.0%). 54 doctors (among them three without prior testing) had treated themselves between 1992 and 1995, ulcer or dyspepsia having been the most common indication (in 60%). Between 1992 and 1994 omeprazole plus amoxycillin was the most common form of treatment, while in 1995 a triple regimen with omeprazole and two antibiotics was most common during 1995. Either regimen was well tolerated in 85% of those treated, but about a quarter of doctors reported difficulties in compliance. Only half of the participants tested the result of treatment, similar numbers using either the breath test (n = 14) or biopsy (n = 13) for confirmation. CONCLUSIONS: A significant percentage of gastroenterologists in Germany knew their own H. pylori status. However, the diagnostic procedures and indications for treatment often did not respond to recommended guidelines. The frequency of treatment and the regimen used mirrored the improved knowledge of the significance of H. pylori infection and the development of antibacterial treatment during the last few years.

Adult↗
PubMed1997

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.

Adult↗
PubMed1997

Doubling the omeprazole dose (40 mg b.d. vs. 20 mg b.d.) in dual therapy with amoxycillin increases the cure rate of Helicobacter pylori infection in duodenal ulcer patients.

BACKGROUND: Several studies have shown that dual therapy with omeprazole and amoxycillin may cure Helicobacter pylori infection. However, the optimum dose of omeprazole has still to be established. METHODS: An international, randomized, double-blind multicentre trial was conducted in patients with duodenal ulcers to compare the H. pylori cure rates obtained by dual therapy consisting of either omeprazole 20 mg b.d. plus amoxycillin 750 mg b.d. or omeprazole 40 mg b.d. plus amoxycillin 750 mg b.d. for 2 weeks. Dual therapy was followed by omeprazole 20 mg once daily for 2 weeks. Before entering the trial and 4 weeks after cessation of treatment H. pylori infection was assessed by histology and a 13C-urea breath test. RESULTS: 381 patients were randomized into the study, of whom 345 were evaluable for the all-patients-treated analysis of efficacy and 378 were valid for the evaluation of safety. Histology results showed that H. pylori infection was cured in 64 out 174 patients treated with omeprazole 20 mg b.d. plus amoxycillin and in 102 out of 171 patients treated with omeprazole 40 mg b.d. plus amoxycillin (37% vs. 60%; P < 0.001). Both treatment regimens were well tolerated, with adverse events reported by 29 (15.2%) and 35 patients (18.7%), respectively. CONCLUSIONS: This study has shown that dual therapy with amoxycillin 750 mg b.d. and omeprazole 40 mg b.d. is superior to dual therapy with amoxycillin and omeprazole 20 mg b.d. in patients with H. pylori-positive duodenal ulcers. Thus, a true dose-response relationship exists between omeprazole and treatment success. However, a combination of omeprazole with two of amoxycillin, clarithromycin and nitroimidazole is a preferable alternative for routine clinical use.

Amoxicillin↗
PubMed1997

Efficacy and tolerability of a one-week triple therapy consisting of pantoprazole, clarithromycin and amoxycillin for cure of Helicobacter pylori infection in patients with duodenal ulcer.

BACKGROUND: Previous studies have shown that one-week triple therapy consisting of omeprazole, clarithromycin and amoxycillin may cure Helicobacter pylori infection in the vast majority of patients. The present study was designed to test the hypothesis that a triple therapy with pantoprazole, clarithromycin and amoxycillin cures the infection in > or = 80% of duodenal ulcer patients infected with H. pylori. METHODS: In an open two-centre study, 60 duodenal ulcer patients were treated with pantoprazole 40 mg b.d., clarithromycin 500 mg b.d. and amoxycillin 1 g b.d. for 1 week. During the second week patients received pantoprazole 40 mg once in the morning. We assessed H. pylori infection before treatment and 4 weeks after cessation of the study medication by a rapid urease test, histology after Warthin-Starry stain and a 13C-urea breath test. RESULTS: Sixty patients (42 males, mean age 47.4 years) entered the trial. All patients were infected with H. pylori. One patient was withdrawn from the study because of allergy to penicillin and six patients were protocol violators. H. pylori infection was cured in 47 out of 53 patients who completed the trial according to the protocol (89%; 95% CI: 80-97%) and in 49 of 60 patients included in the trial (82%; 95% CI: 72-92%). Four weeks after the last administration of study drugs, 55 out of 60 ulcers had healed (92%). Twenty-nine patients reported 51 adverse events that were mostly mild to moderate. CONCLUSIONS: One-week triple therapy consisting of pantoprazole, clarithromycin and amoxycillin is a simple and effective approach to the cure of H. pylori infection in patients with duodenal ulcer. In those patients who took the drugs as prescribed the H. pylori cure rate was 89%, with the lower 95% confidence limit being 80%.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

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.

Anti-Bacterial Agents↗
PubMed1997

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.

Adult↗
PubMed1997

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.

Adult↗
PubMed1997

Focal inflammatory infiltrations in gastric biopsy specimens are suggestive of Crohn's disease. Crohn's Disease Study Group, Germany.

BACKGROUND: Crohn's disease is a systemic inflammatory disease that may involve all regions of the gut. METHODS: Thirty-six patients with Crohn's disease and 36 age- and sex-matched control patients were prospectively evaluated by upper endoscopy. Biopsy specimens were taken from the oesophagus, duodenum, and 10 locations in the antrum and corpus. RESULTS: Granulomas were found in four patients (11.13%) with Crohn's disease but in none of the control patients (P > 0.5). In 23 of 36 patients (63.9%) with Crohn's disease focal inflammatory infiltrations were found, as compared with 7 of 36 (19.4%) of the controls (P < 0.001). For focal inflammatory infiltrations, an odds ratio of 7.33 (2.55-21.38) was calculated, which increased to 20.04 (4.07-98.45) when only specimens from the angulus were considered. Helicobacter pylori infection was present in 13 of 36 controls (36.1%) and in 3 of 36 patients (8.3%) with Crohn's disease (P = 0.009). CONCLUSION: These data suggest that Crohn's disease is typically associated with focal inflammatory infiltrations of the gastric mucosa.

Adult↗
PubMed1997

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.

Adult↗