J. J. Misiewicz

Eradication of Helicobacter pylori with clarithromycin and omeprazole.

Clarithromycin, a new and well tolerated, acid stable macrolide antibiotic, has a similar antimicrobial spectrum to erythromycin but a better in vitro MIC90 (0.03 microgram/l-1) against Helicobacter pylori (H pylori). This study aimed at determining the eradication rate using clarithromycin 500 mg thrice daily and omeprazole 40 mg daily for two weeks. Patients were given an endoscopy and H pylori status assessed by antral culture (microaerobic conditions, for up to 10 days), antral and corpus histology tests (haematoxylin and eosin/Gimenez stains), and 13C-urea breath test (13C-UBT, European standard protocol, positive result = excess delta 13CO2 excretion > 5 per mil). Compliance was assessed by returned tablet counts. H pylori clearance at the end of treatment and eradication four weeks after finishing treatment were assessed by the 13C-UBT. Seventy three patients (54 men, median age 45 years) with duodenal ulcers (n = 42) or duodenitis/non-ulcer dyspepsia (n = 31) all with a positive 13C-UBT (mean (SEM) excess delta-13CO2 excretion = 26.6 (4.9) per mil) and either positive antral histology (n = 72) or positive antral culture (n = 35) were studied. Before treatment 2/27 (7%) isolates of H pylori were resistant to clarithromycin and five isolates were resistant to metronidazole. In 70/73 (96%) the 13C-UBT was negative immediately after finishing treatment. Four weeks later the 13C-UBT was negative in 57/73 (mean (SEM) excess delta 13CO2 excretion = 1.2 (0.3) per mil, eradication rate = 78%). Forty eight (66%) patients experienced a metallic taste while taking the tablets. Although four (5%) patients, however, could not complete the course of treatment, in only one of these four was H pylori not eradicated. These results show that duel therapy with clarithromycin and omeprazole is well tolerated. With an eradication rate of 78% it is an effective treatment for metronidazole resistant H pylori and may be an alternative to standard triple therapy.

One week eradication regimen for Helicobacter pylori.

Although Helicobacter pylori is both a frequent cause of gastritis and an important factor in duodenal ulcer recurrence, no treatment regimen exists that is completely safe and effective. We have studied a short eradication regimen of tripotassium dicitrato bismuthate 120 mg four times daily and amoxycillin 500 mg four times daily for seven days with metronidazole 400 mg five times daily for three days (days 5-7). 106 patients with peptic ulceration and non-ulcer dyspepsia, who were also infected with H pylori, were entered into the study. H pylori was successfully eradicated in 76/106 (72%) patients (median follow-up 9.3 months). The rate of eradication was higher among patients with metronidazole-sensitive H pylori (40/43, 93%). In 17/30 patients in whom eradication failed, pretreatment metronidazole-resistant strains were subsequently isolated. Side-effects were mild, the commonest (24/106, 24%) being taste disturbance with metronidazole. A one-week eradication regimen is a safe, effective, cheap, and well-tolerated treatment for metronidazole-sensitive H pylori.

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

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

Relation between gastric acid output, Helicobacter pylori, and gastric metaplasia in the duodenal bulb.

BACKGROUND: Factors that determine gastric metaplasia in the duodenal bulb are ill defined. It is more common and extensive in the presence of high acid output and possibly in the presence of Helicobacter pylori. However, no quantitative relation between acid output and the extent of gastric metaplasia has been demonstrated and its relation to H pylori is uncertain. AIM: To determine the relation between H pylori infection and acid output and the presence and extent of gastric metaplasia in the duodenal bulb. subjects: H pylori positive and negative patients with duodenal ulcer and healthy controls were studied. METHODS: Quadrantic duodenal bulb biopsy specimens were taken and the presence and extent of gastric metaplasia determined using a computer enhanced image intensifier. Basal and stimulated acid outputs were measured. RESULTS: gastric metaplasia was significantly (p < 0.05 more common and significantly (p < 0.05) greater in extent in patients with duodenal ulcer than in controls. Neither the prevalence or extent of gastric metaplasia was affected by H pylori status. There were significant (p < 0.01) direct correlations between acid output and extent of gastric metaplasia. CONCLUSIONS: Prevalence and extent of gastric metaplasia are not related to H pylori in controls, or in patients with duodenal ulcer. Rather, high acid response to gastrin may be more important.

Lansoprazole, clarithromycin and metronidazole for seven days in Helicobacter pylori infection

Background: This study determines the efficacy and safety of a 1‐week triple therapy regimen of lansoprazole, clarithromycin and metronidazole in an area with a high prevalence of pre‐treatment metronidazole‐resistant strains of Helicobacter pylori.

Recurrence of duodenal ulcer after Helicobacter pylori eradication is related to high acid output

Background: Helicobacter pylori eradication reduces the recurrence of duodenal ulcers. It is unclear why duodenal ulcers rarely recur in the absence of reinfection with H. pylori or NSAID treatment.

Eradication of Helicobacter pylori with lansoprazole and clarithromycin.

Background: Helicobacter pylori eradication with omeprazole and clarithromycin varies between 40 and 80%. The dose, frequency and duration of treatment may account for these differences. Lansoprazole, a recently introduced proton pump inhibitor, is a more potent H. pylori bacteriostat in vitro than omeprazole. The aim of this open, comparative, randomized study was to investigate the efficacy and safety of lansoprazole 30 mg once or twice a day (and for 2 vs. 4 weeks) plus clarithromycin 500 mg t.d.s. for 2 weeks, in the eradication of H. pylori.

Two-week eradication regimen for metronidazole-resistant Helicobacter pylori

At present there is no generally accepted treatment regimen for eradicating metronidazole‐resistant Helicobacter pylori. This study determines the eradication rate after treatment with 40 mg omeprazole o.m. and 500 mg amoxycillin q.d.s. for 14 days, with 120 mg tripotassium dicitrato bismuthate q.d.s. for the first week (Days 1–7) and 750 mg ciprofloxacin b.d. for the second week (Days 8–14). Thirty patients (16 male, mean age 45 years, range 16–80 years) with duodenal ulcers (n= 18) or non‐ulcer dyspepsia (n= 2) and metronidazole‐resistant H. pylori detected by histology, culture, in vitro sensitivity tests and a positive 13C‐urea breath test entered the study. Follow‐up was by 13C‐urea breath test at the end of treatment and at 1, 3, 6, and 12 months. Eradication was denned as a negative 13C‐urea breath test at least 1 month after finishing treatment. H. pylori was successfully eradicated in 21/30 (71%) patients (median follow‐up 10.2 months, range 4–12 months). A pre‐treatment ciprofloxacin‐resistant strain was isolated in 1/9 patients in whom eradication failed. Of 30 patients 29 completed the 2‐week regimen; one patient experienced dizziness after 3 days of treatment. The most common side‐effect was increased stool frequency (n= 6). This 2‐week treatment regimen for metronidazole‐resistant H. pylori is well tolerated and achieves an eradication rate of 70%.

Parietal cells in the duodenal bulb and their relation to Helicobacter pylori infection.

AIM: To investigate the prevalence, and relation to Helicobacter pylori, of parietal cells in the duodenal bulb using a monoclonal antibody directed against H+,K(+)-ATPase (HK12.18). METHODS: Twenty six patients with duodenal ulcer disease and 16 healthy controls were studied. H pylori status was determined by gastric histology and culture and by the 13C-urea breath test. Four biopsy specimens were taken from the duodenal bulb and stained with HK12.18. The presence/absence and number of parietal cells in the duodenal bulb were assessed blindly by a histopathologist. RESULTS: The overall prevalence of parietal cells in the duodenal bulb was 31% (13/42) and was similar in patients with duodenal ulcer and in controls, and in H pylori positive and negative subjects. The median (range) number of parietal cells in the duodenal bulb was 7.5 (4-20) parietal cells/subject, and was similar in all four groups. CONCLUSIONS: The prevalence of parietal cells in the duodenal bulb (31%) is notably higher than previously reported in endoscopic studies, and is in keeping with reports from studies on necropsy/operative specimens. There was no difference in the prevalence or number of parietal cells in the duodenal bulb between patients with duodenal ulcer and controls, regardless of H pylori status. These findings suggest that parietal cells in the duodenal bulb do not contribute to the pathogenesis of duodenal ulcer.