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Biomedical subjects

B Tillenburg

Publications and source records attributed to B Tillenburg.

17 recordsLinked to original sources

[Insufficient validity of a rapid blood test for diagnosis of Helicobacter pylori infection].

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.

Adult↗

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↗

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↗

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↗

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↗

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↗

[Helicobacter pylori: pretherapeutic resistance status in Germany (Ruhr area)].

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.

Amoxicillin↗

[Ulcer healing through the elimination of Helicobacter pylori: is a week of therapy enough?].

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.

Adolescent↗

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.

Adolescent↗

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.

Adult↗

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.

Adult↗

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)

Adult↗

[Short-term triple therapy with pantoprazole, clarithromycin and metronidazole in eradication of Helicobacter pylori].

In a prospective study, thirty consecutive patients presenting with either H.pylori positive (histology and/or culture) ulcer disease (n = 17; acute ulcer: n = 11) or functional dyspepsia (n = 13) were treated over one week with pantoprazole 40 mg bd, clarithromycin 250 mg bd and metronidazole 400 mg bd. Four weeks after discontinuation of the study medication H.pylori eradication was assessed by means of an urease test, culture and histology. One patient had to be withdrawn from the study after one day because of a concomitant infectious disease requiring long-term antibiotic treatment. Another patient refused the final follow-up endoscopy. 28 patients completed the study without contravening the protocol. H.pylori infection was eradicated in 24 out of 28 patients (eradication rate: 86%; 95%-confidence interval: 57%-96%). Cure of bacterial infection was more frequently obtained in ulcer patients as compared to patients suffering from functional dyspepsia (94% vs 75%; p = 0.28). In 2 patients, treatment failure was associated with pretherapeutic resistance of H. pylori to either clarithromycin or metronidazole. Without antiulcer treatment beyond eradication therapy, ulcer healing was endoscopically confirmed after 5 weeks in 9 out of 10 patients available for follow-up (healing rate: 90%; 95%-confidence interval: 56%-100%). Seven patients reported mild adverse events that did not lead to discontinuation of the study medication (rate: 23%; 95%-confidence interval: 10%-42%). After cure of the infection, histology demonstrated a statistically highly significant improvement (p < 0.001) of both grade and activity of antrum and body gastritis.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Pyridinylmethylsulfinylbenzimidazoles↗

One-week low-dose triple therapy for the eradication of Helicobacter pylori infection.

OBJECTIVE: To evaluate the efficacy and safety of two 1-week low-dose triple therapy regimens for the treatment of Helicobacter pylori infection. PATIENTS AND METHODS: Eighty patients with H. pylori infection and peptic ulcer disease (n = 64) or functional dyspepsia (n = 16), with similar demographic and clinical characteristics, were treated for 1 week with either omeprazole 20 mg once in the morning and clarithromycin 250 mg and metronidazole 400 mg twice daily (OCM; n = 40) or with omeprazole 20 mg once in the morning and clarithromycin 250 mg and tetracycline 500 mg twice daily (OCT; n = 40). H. pylori infection was assessed by urease test, culture and histology performed before and 4 (or more) weeks after cessation of the eradication therapy. RESULTS: H. pylori infection was treated successfully in 38 out of 40 patients by OCM and in 26 out of 40 patients by OCT (95 versus 65%, respectively; P = 0.0015). The OCM regimen was well tolerated in all patients except for one who complained of epigastric pain. Three patients on the OCT regimen reported side effects (abdominal pain, diarrhoea, pruritus), two of whom discontinued the study medication after 1 day. CONCLUSIONS: The 1-week low-dose triple therapy comprising omeprazole, clarithromycin and metronidazole was highly effective in eradicating H. pylori and was well tolerated. The replacement of metronidazole by tetracycline resulted in a significant decrease in the eradication rate.

Adult↗

[Bleeding peptic ulcers--how can recurrent bleeding be prevented?].

Bleeding is the most frequent complication of peptic ulcer disease. Patients with a previous ulcer hemorrhage have a high risk for future bleeding episodes. Therefore, treatment aiming at ulcer prophylaxis is mandatory. Helicobacter pylori infection, acid/pepsin and intake of Aspirin or NSAIDs are the main causal factors involved in the pathogenesis of peptic ulcer disease. Ulcers induced by nonsteroidal anti-inflammatory drugs can be cured by gastric acid suppression (e.g. omeprazole) and prevented by withdrawal of the ulcerogenic substances or co-medication with omeprazole or misoprostol. Acid and Helicobacter pylori are necessary, albeit by themselves not sufficient factors in the causal web of the formerly idiopathic, gastritis-associated peptic ulcer disease of the stomach and the duodenum. Maintenance therapy with antisecretory drugs results in a marked decrease of ulcer recurrences and probably further ulcer complications after an index bleeding, but a definite cure of the ulcer disease is not feasible in the majority of patients. The proportion of patients remaining in remission is dependent on the degree of gastric acid suppression. Therefore, potent antisecretory drugs such as the proton pump inhibitor omeprazole should be used if a physician decides to initiate a long-term maintenance therapy. Several studies have demonstrated beyond doubt that cure of Helicobacter pylori eradication resulted in a stable remission of gastric and duodenal ulcer disease. In addition, a true reinfection after apparent eradication of the bacteria has been rarely observed in adults.(ABSTRACT TRUNCATED AT 250 WORDS)

Combined Modality Therapy↗

Validity of a novel biopsy urease test (HUT) and a simplified 13C-urea breath test for diagnosis of Helicobacter pylori infection and estimation of the severity of gastritis.

This prospective study was designed to validate a novel biopsy urease test as well as a simplified 13C-urea breath test for the detection of Helicobacter pylori. In addition, the hypothesis was tested that both the reaction velocity of the urease test and the 13CO2 excess of the urea breath test may allow a prediction of the severity of gastritis. Seventy dyspeptic patients with unknown H. pylori status were included. The H. pylori status was assessed by means of culture and histology after Warthin and Starry stain. One antral and one body biopsy specimen were separately analyzed by the novel biopsy urease test (HUT). Also, a 13C-urea breath test using 75 mg 13C-labelled urea and orange juice as test meal was performed in all patients. Forty-seven patients (67%) were H. pylori positive as judged from histology and culture. In 46 patients, H. pylori infection was also detected by the novel biopsy urease test and by the urea breath test as well (sensitivity 97.9%). False-positive results were not observed by either method (specificity 100%). Both the reaction velocity of the urease test and the 13CO2 excess of the breath test significantly correlated with H. pylori density and grade and activity of gastritis. The determination coefficients, however, indicated that both methods allow a reliable prediction of the severity of gastritis only in about 40-50% of the patients. In conclusion, the novel biopsy urease test and the simplified 13C-urea breath test proved to be highly accurate in diagnosing H. pylori infection. Despite a significant correlation, neither the reaction velocity of the urease test nor the 13CO2 excess of the breath test are clinically useful for the prediction of the severity of gastritis.

Adolescent↗