Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease.

BACKGROUND: It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. AIMS: To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. METHODS:. Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. RESULTS: Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001). CONCLUSIONS:. The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.     

Hypersecretory duodenal ulcer and Helicobacter pylori infection: for-year follow-up study

Background. About 10% of duodenal ulcer patients are characterized by gastric acid hypersecretion with normal gastrin values. Relapsing duodenal ulcer after Helicobacter pylori cure has been related to high acid output and maintenance antisecretory therapy has been suggested in hypersecretory duodenal ulcer patients. The role of Helicobacter pylori infection and the effects of Helicobacter pylori cure in hypersecretory duodenal ulcer patients still remain to be fully studied.Aim. To study: a) whether gastric acid hypersecretion “per se” is a risk factor for duodenal ulcer recurrence; b) whether maintenance antisecretory therapy is necessary after eradication in hypersecretory duodenal ulcer patients.Patients. The study population comprised 8 hypersecretory duodenal ulcer patients, selected from a population of 79 Helicobacter pylori-positive duodenal ulcer patients.Methods. Hypersecretory duodenal ulcer patients were followed-up for at least 4 years after eradication. Gastric acid secretion was measured again 12 months after Helicobacter pylori eradication. Gastroscopy with histology was performed 3, 6, 12 and 36 months after treatment, ¹³C-urea breath test after 42 months; clinical questionnaires were completed every 6 months.Results. After eradication, despite a not significantly reduced high acid output (median value of basal acid output and pentagastrin-stimulated acid output, respectively, 23.1 mEg/h and 64. 1 mEg/h before treatment vs 16 mEg/h and 49.7 mEq/h 12 months after treatment), all patients were free from symptoms, none of them had duodenal ulcer relapse or complications (7/8 before treatment), or needed antisecretory maintenance therapy, except for one patient taking non-steroidal anti-inflammatory drugs.Conclusions. These findings, obtained in a selected population of hypersecretory duodenal ulcer patients with long-term follow-up, suggest that after successful Helicobacter pylori eradication gastric acid hypersecretion “per se” is not able to determine the recurrence of duodenal ulcer.     

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients

Background. Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either, whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients.Aims. To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status.Patients and methods. A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination.Results. There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum.Conclusion. Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.     

Impairment of gastric secretion modulation in duodenal ulcer and in long-term PPI treatment: quantitative morphologic findings and pathophysiologic implications

Helicobacter pylori affects gastric secretion. This functional effect might have a morphometric counterpart. Therefore, the gastric cell secretory compartment was morphometrically assessed in different pathophysiologic conditions related to Helicobacter pylori infection. Nineteen Helicobacter pylori-positive nonduodenal ulcer subjects, 15 omeprazole chronically treated subjects, and 19 duodenal ulcer patients were studied against 19 controls. Somatostatin, gastrin, enterochromaffin-like, and parietal cell density was assessed in gastric biopsies. No differences in any cell type density were found between Helicobacter pylori-positive nonduodenal ulcer subjects and controls. On the contrary, differences were significant when comparing omeprazole and duodenal ulcer patients to controls (higher density of gastrin, enterochromaffin-like, and parietal cells, lower density of somatostatin cells). In duodenal ulcer a reversion to control values followed Helicobacter pylori eradication and ulcer healing. A direct linear correlation between enterochromaffin-like, gastrin, and parietal cell density was demonstrated. An almost complete map of mucosal cells involved in gastric secretion is provided by this study. The cell density pattern, identical to the omeprazole group, points to an impaired feedback control of secretion in duodenal ulcer. The reversion to control values after Helicobacter pylori eradication and ulcer healing demonstrates the pathogenetic role of Helicobacter pylori–host interaction in these changes.     

Cure of Helicobacter pylori-positive active duodenal ulcer patients: double-blind, multicentre, 12-month study comparing a two-week dual vs a one-week triple therapy

Aims. To compare a two-week dual therapy to a one-week triple therapy for the healing of duodenal ulcer and the eradication of the Helicobacter pylori infection.Patients and Methods. A total of 165 patients with active duodenal ulcer were enrolled in the study. At entry, endoscopy, clinical examination and laboratory tests were performed. Histology and the rapid urease test were used to diagnose Helicobacter pylori infection. Patients received either lansoprazole 30 mg plus amoxycillin 1 g bid for two weeks (two-week, dual therapy) or lansoprazole 30 mg plus amoxycillin 1 g plus tinidazole 500 mg bid for one week plus lansoprazole qd for an additional week (one-week, triple therapy). Two and twelve months after cessation of therapy, endoscopy and clinical assessments were repeated.Results. Duodenal ulcer healing and Helicobacter pylori eradication were both significantly greater (p<0. 0001) in the triple therapy group (healing: 98.6%; Helicobacter pylori cure rate: 72.6%) than in the dual therapy group (healing: 77.3%; Helicobacter pylori cure rate: 33.3%). Ulcers healed more frequently in Helicobacter pylori-cured than in Helicobacter pylori-not cured patients (94.9% vs. 77.2%; p<0.0022). After one year, Helicobacter pylori eradication was re-confirmed in 46/58 patients previously treated with the triple therapy and in 10/40 patients treated with the dual therapy (p<0.0001). Only three duodenal ulcer relapses were observed throughout follow-up: all were in Helicobacter pylori-not cured patients.Conclusions. Triple therapy was more effective than dual both in curing Helicobacter pylori infection and healing active duodenal ulcers. The speed of ulcer healing obtained after only 7 days of antibiotics and 14 days of proton pump inhibitors confirmed that longer periods of anti ulcer therapy were not necessary. Helicobacter pylori -not cured patients had more slowly healing ulcers which were more apt to relapse when left untreated.     

Medium- and high-dose omeprazole plus amoxicillin for eradication ofHelicobacter pylori in duodenal ulcer disease

The purpose of the present study was to investigate theHelicobacter pylori eradication potency of combined amoxicillin-omeprazole treatment in patients with duodenal ulcer disease and to compare the efficacy of two omeprazole and amoxicillin doses concerningH. pylori eradication, ulcer healing, pain relief, and safety. Ninety patients with activeH. pylori-positive (culture and/or histology) duodenal ulcer disease were randomly treated with either omeprazole 20 mg twice a day plus amoxicillin 1 g twice a day (group I,N=30), omeprazole 40 mg twice a day plus amoxicillin 1 g twice a day (group II,N=30), or omeprazole 40 mg twice a day plus amoxicillin 1 g three times a day (group III,N=30) over two weeks, followed by ranitidine at bedtime for another four weeks. The overall proportion ofH. pylori eradication was 83% and of ulcer healing 92% without statistically significant differences between the study groups. Complete pain relief occurred after a median of one day in all groups. Six patients complained of side effects during the therapy phase, which led to therapy discontinuation in one female patient. In conclusion, omeprazole plus amoxicillin is a highly effective and well-tolerated therapy regimen to eradicateH. pylori in duodenal ulcer disease. In addition, the results suggest that there is no clear dose-response relation between the dosages of omeprazole and amoxicillin used in this study on the one hand and theH. pylori eradication rates on the other.     

Gastric emptying andHelicobacter pylori infection in duodenal ulcer disease

The pathogenetic link betweenHelicobacter pylori gastritis and duodenal ulcer is still unknown. Fast gastric emptying of liquids might be important in the pathogenesis of gastric metaplasia of the duodenum and duodenal ulcer through an increased exposure of the duodenum to gastric acid. InH. pylori-infected subjects, an abnormal gastric emptying could affect urea breath test results and correlate with the histological gastritis. This study was performed to evaluate the gastric emptying of liquids in duodenal ulcer patients withH. pylori infection and the possible relation between the bacterial load, gastric emptying, and urea breath test results. Seventeen duodenal ulcer patients withH. pylori gastritis and 15 healthy volunteers were studied by a combined [¹⁴C]octanoic acid and [¹³C]urea breath test to evaluate gastric emptying rate andH. pylori status simultaneously. Endoscopy with antral biopsies was performed in all duodenal ulcer patients. Duodenal ulcer patients withH. pylori infection have a normal liquid gastric emptying that is unrelated with the histological severity of gastritis. The urea breath test results and the gastric emptying parameters do not correlate with histology. A significant correlation between the gastric emptying and the urea hydrolysis rate is found. It is concluded thatH. pylori infection in duodenal ulcer patients is not associated with abnormally fast liquid gastric emptying, and this finding should be taken into account when a causal link betweenH. pylori infection and duodenal ulcer disease is searched for. The correlation between gastric emptying and urea hydrolysis rate explains why no conclusions on intragastric bacterial load can be drawn from the urea breath test results.This study was presented in part as an oral communication at the Annual Meeting of the American Gastroenterological Association, May 1994, New Orleans, and published in abstract form inGastroenterology 106:A160, 1994.     

Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output >10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence ofHelicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis).Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P<0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found amongHelicobacter pylori-positive compared toHelicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr wereHelicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence ofHelicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.     

Effect of Helicobacter pylori Eradication on 24-Hour Gastric pH and Duodenal Gastric Metaplasia

Published data on the regression of the extent of duodenal gastric metaplasia (DGM) after the eradication of Helicobacter pylori infection and the normalization of the organism-induced alterations in gastric physiology are scanty and controversial. Therefore, we decided to assess the circadian pattern of gastric acidity and the degree of DGM before and one year after H. pylori eradication in a group of duodenal ulcer patients. Fifteen consecutive H. pylori-positive patients with endoscopically proven duodenal ulcer were recruited for this study. The diagnosis of H. pylori infection was based on CLO-test and histology, and DGM was assessed on four bulb biopsies taken before and one year after H. pylori eradication. At the same time, gastric pH was measured by 24-hr continuous intraluminal recording. H. pylori eradication was ascertained by means of concomitant negative CLO-test and histology performed both four weeks after the end of the eradicating treatment and at the one-year endoscopic control. After successful cure, all patients discontinued any antiulcer medication. The mean 24-hr gastric pH was 1.7 ± 0.4 before and 1.6 ± 0.4 after one year of H. pylori eradication (P = 0.75). DGM improved in three cases, worsened in four cases, and was unchanged in eight cases at the one-year control (P = 0.87). No correlation was found between 24-hr gastric pH and DGM (P = NS) both at baseline and one year after eradication. Our results show that neither circadian gastric acidity nor DGM change significantly one year after H. pylori eradication in duodenal ulcer patients. Thus, the disappearance of H. pylori infection does not determine any increase in gastric pH and any reversal of gastric-type epithelium in the duodenum.     

Effects of Omeprazole and Eradication of Helicobacter pylori on Gastric and Duodenal Mucosal Enzyme Activities and DNA in Duodenal Ulcer Patients

Vetvik K, Schrumpf E, Mowinckel P, Aase S, Andersen K-J. Effects of omeprazole and eradication of Helicobacter pylori on gastric and duodenal mucosal enzyme activities and DNA in duodenal ulcer patients. Scand J Gastroenterol 1994;29:995-1000.

Background: Duodenal and gastric content of mucosal enzymes in duodenal ulcer (DU) patients differs from that of controls. The purpose of this study has been to examine the effect of omeprazole and eradication of Helicobacter pylori on mucosal enzymes in DU patients

Methods: The enzyme activities of seven gastric and duodenal mucosal marker enzymes from the brush border, lysosomes, and mitochondria have been studied. In study I the measurements were made in 29 patients with an active DU before and after 14 days of omeprazole treatment. In study II 22 duodenal ulcer patients were given bismuth subnitrate, oxytetracycline, and metronidazole (triple therapy) for 2 weeks to eradicate H. pylori. Biopsy specimens were taken from the duodenum and the stomach for enzyme measurements and histologic assessment. In study II additional specimens were obtained from the prepyloric region for urease tests and culture of H. pylori.

Results: The ulcer healing rates were more than 90% after both omeprazole and triple therapy. H. pylori was eradicated in 86% after triple therapy. The activities of the brush-border enzymes lactase, neutral-α-glucosidase, alkaline phosphatase, leucyl-β-naphthylami-dase, and γ-glutamyltransferase (γ-GT) increased significantly in the duodenal bulb and the descending duodenum during treatment with omeprazole. No changes in duodenal enzyme activity were detected after triple therapy, whereas a significant fall in γ-GT and acid phosphatase activities was seen in the stomach. The mucosal DNA in the gastric antrum decreased both after treatment with omeprazole and after triple therapy.

Conclusions: A similar decrease in mucosal DNA of the gastric antrum was demonstrated after both omeprazole and triple therapy with bismuth subnitrate, oxytetracycline, and metronidazole. Omeprazole also affects the content of duodenal mucosal enzymes, whereas triple therapy particularly affects the gastric mucosal enzyme activity.     

Does Helicobacter pylori eradication depend on the period of amoxicillin treatment? A retrospective study

In this study, the effect of different periods of amoxicillin (AMPC) treatment on the eradication rate of Helicobacter pylori in 173 patients with peptic ulcers (gastric ulcer, 109; duodenal ulcer, 64) was investigated. AMPC (1.5 g/day) was administered for 2, 4, or 6 weeks with omeprazole (20 mg/day) and plaunotol (240 mg/day), a mucoprotective drug, for 8 weeks. The H. pylori eradication rate was 46.7% for 2 weeks' treatment, 83.4% for 4 weeks' treatment, and 100% for 6 weeks' treatment. The eradication rate had a good correlation with the period of AMPC treatment. The healing rates of peptic ulcer at 4 and 8 weeks were 93.3% and 100%, respectively, in the 2-week group, 98.0% and 99.3% in the 4-week group, and 85.7% and 100% in the 6-week group. The recurrence rate of gastric and duodenal ulcers was 3.5% and 0% respectively, in the patients in whom H. pylori was eradicated and 30.0% and 40%, respectively, in the patients in whom H. pylori was not eradicated for 12 months after the H. pylori eradication treatment. Adverse effects of this regimen were observed in 5 (2.9%) of the 173 patients. Diarrhea was observed in 3 patients and eruption in 2. These adverse effects disappeared within a few days after only AMPC was withdrawn. Therefore, these may be caused by AMPC. The eradication rate of H. pylori depends on the period of AMPC treatment. This regiment, AMPC (1.5 g/day) + omeprazole (20 mg/day) + plaunotol (240 mg/day), is safe and well tolerated for eradication of H. pylori. Received Oct. 17, 1996; accepted June 27, 1997     

Gastric metaplasia of regenerating duodenal mucosa and deformity of duodenal bulb: A correlative study

The correlation between the presence and degree of gastric metaplasia of regenerating duodenal mucosa and the deformity of duodenal bulb was studied. Based on the endoscopically morphological patterns of bulb, the duodenal ulcers were divided into three types: type I, with a normal-shaped bulb; type II, with a mildly deformed bulb; and type III, with a markedly deformed bulb. A total of 159 patients with active duodenal ulcers were scheduled to be treated with H₂-receptor antagonists. Of these patients, 124 proved to have a healed duodenal ulcer 4 weeks after initial treatment upon follow-up endoscopic examinations. Two biopsies were taken from the centre of the ulcer scar when the ulcer was found to be healed for light microscopic study. Histologically, the degree of gastric metaplasia was divided into three grades: grades 0, 1 and 2. The results show that a healed duodenal ulcer with a normal-shaped bulb is not frequently accompanied by gastric metaplasia. However, a healed ulcer with a markedly deformed bulb has a high incidence and degree of gastric metaplasia, which may be easily colonized by Helicobacter pylori and thus develop an environment of easy recurrence. Therefore, a cycle of healing and recurrence may exist in patients with a duodenal ulcer and a markedly deformed bulb. Eradication of H. pylori may be the best way to break this cycle.     

Helicobacter pylori and gastric acid output in peptic ulcer disease

Helicobacter pylori is associated with peptic ulcer, and a causal relationship has been postulated. We investigated the association betweenHelicobacter pylori and gastric acid output. Two hundred forty-one patients were studied: 173 with duodenal ulcer, 51 with gastric ulcer (41 corpus, 10 prepyloric), and 17 with combined gastric and duodenal ulcer. In 194 patients (80%),Helicobacter pylori could be demonstrated histologically from gastric antral biopsies. The presence or absence ofHelicobacter pylori was not influenced by age, sex, or use of tobacco or analgesics. Patients with duodenal ulcer or combined gastric and duodenal ulcer had similar gastric acid outputs irrespective of the presence or absence ofHelicobacter pylori. However, gastric ulcer patients withHelicobacter had higher basal and maximal acid outputs when compared to patients withoutHelicobacter (mean basal output: 4.1 mmol/hr vs 2.4,P<0.05; mean maximal output 19.5 mmol/hr vs 14.4,P<0.05). AlthoughHelicobacter pylori is associated with both gastric ulcer and duodenal ulcer, its significance may be different in the two diseases.     

Duodenal gastric metaplasia and Helicobacter pylori infection in high and low duodenal ulcer-prevalent areas in India

Background: Previous reports, based on surgery, showed duodenal ulcer (DU) to be more common in the rice‐eating areas of southern India than in the northern wheat‐eating areas. Aims: Does this difference persist? Can it be explained by risk factors other than diet? Methods: A total of 20 053 records from patients undergoing endoscopy for dyspepsia, and 590 endoscopy patients from two northern and two southern centers in India were studied prospectively. Records were scrutinized to determine the relative incidence of DU and non‐ulcer dyspepsia in wheat‐ and rice‐eating areas. Age, sex, length of history, smoking and medication were recorded. Three antral biopsies and one from each duodenal quadrant were taken. A rapid urease test was carried out on one of the antral biopsies; the others were examined for Helicobacter pylori, gastritis, duodenitis and duodenal gastric metaplasia. Results: The difference in diet‐associated prevalence persisted. No differences in smoking, Helicobacter pylori infection or duodenal gastric metaplasia were found between the two regions, but all three were more common in DU than in non‐ulcer dyspeptic patients from both dietary areas. Conclusions: The dietary differences between the regions remain the only factor to account for the differences in DU prevalence. A strong interrelationship between duodenal gastric metaplasia and cigarette smoking is demonstrated.     

Randomised study ofefficacy of Omeprazole and clarithromycin with either amoxycillin or metronidazole in the eradication of Helicobacter pylori in screened primary care patients

Background. Population Helicobacter pylori screening and treatment has been advocated as a means of reducing mortality from gastric cancer. The optimum Helicobacter pylori eradication therapy to use in this setting is uncertain.Aims. To compare efficacy of seven days of omeprazole, clarithromycin and either metronidazole, or amoxycillin in Helicobacter pylori positive subjects detected by population screening.Patients. Helicobacter pylori positive patients from the placebo group of a population screening and treatment trial were invited to take part in the investigation.Methods. Patients were randomised to receive either omeprazole, clarithromycin and metronidazole or omeprazole, clarithromycin and amoxycillin, and Helicobacter pylori eradication was verified with a ¹³C-urea breath test at least four weeks after completion of therapy.Results. A total of 221 patients took part in the study and 210 completed the protocol. Treatment was successful in 93/111 (84%) patients allocated to omeprazole, clarithromycin and metronidazole and in 96/110 (87%) allocated to omeprazole, clarithromycin and amoxycillin in an intention-to-treat analysis (p=0.46). Per protocol eradication rates were 93/107 (87%) in the metronidazole, and 96/103 (93%) amoxycillin group (p=0.129).Conclusions. There was no significant difference between the two regimens. The eradication rates achieved are comparable with previous studies in both dyspepsia and peptic ulcer patients.     

Helicobacter pylori eradication improves gastric histology and decreases serum gastrin, pepsinogen I and pepsinogen II levels in patients with duodenal ulcer

Background and Aim: The aim of this study was to assess the gastric histopathology and serum gastrin‐17 and pepsinogens profiles in patients with duodenal ulcer before and after Helicobacter pylori eradication in a population with a very high prevalence of H. pylori. At the same time we assessed the role of H. pylori density on these variables. Methods: Eighty Caucasian patients with H. pylori–associated duodenal ulcer before treatment and 1 year after randomized eradication were studied. Among patients with unsuccessful eradication two groups were distinguished according to the data obtained after treatment: the group with negative rapid urease test and decreased bacterial density according to morphological score (partial elimination group); the group with positive rapid urease test and high bacterial density (failed eradication group). Results: One year after successful eradication, serum levels of gastrin‐17, pepsinogen I and pepsinogen II decreased. Similar changes of serum pepsinogen I and pepsinogen II levels were observed in patients with partial elimination of H. pylori infection. In the group with successful eradication, inflammation, activity, atrophy and number of lymphoid follicles in the antral mucosa fell. In the group with partial elimination, antral mucosa activity and H. pylori score reduced. Other morphological changes were statistically non‐significant. Conclusion: Patients with duodenal ulcer after successful eradication have improvement of morphological and functional characteristics of gastric mucosa.     

Effect of omeprazole on duodenal ulcer-associated antral gastritis andHelicobacter pylori

This study set out to investigate the effects of omeprazole or ranitidine on the progression of antral gastritis andHelicobacter pylori in patients with active duodenal ulcer. A double-blind, double-dummy trial was performed in 270 patients, 241 of whom were studied histologically for the presence ofH. pylori. Patients were randomized to receive omeprazole, 10 mg every morning, omeprazole, 20 mg every morning, or ranitidine, 150 mg twice a day, for four weeks. Endoscopy was performed on entry and at weekly intervals during the study; at least two antral biopsies were taken on each occasion to assess the activity and degree of chronic inflammation, as reflected by the degree of polymorphonuclear leukocyte infiltration and mononuclear cell infiltration, respectively. Biopsy specimes also were assessed histologically forH. pylori. The sex, age and maximal acid output were comparable in the three treatment groups. The percentages of patients showing an improvement in the activity of gastritis in the four consecutive weeks of treatment were 9%, 40%, 51%, and 53% for omeprazole, 10 mg (N=78); 14%, 42%, 49%, and 53% for omprazole, 20 mg (N=81); and 2%, 23%, 30%, and 33% for ranitidine, 150 mg twice a day (N=82) (life table analysis gaveP<0.01 for both omeprazole regimens compared with ranitidine). The degree of chronic inflammation showed similar changes. The density ofH. pylori decreased significantly after treatment with omeprazole, 10 mg or 20 mg, (both,P<0.00001) but not with ranitidine. The reduction in bacterial density was significantly higher (P<0.003) in those who showed improvement of gastritis than in those who did not. We conclude that effective acid inhibition with omeprazole improves antral gastritis and is accompanied by a reduction in antral bacterial density, suggesting that both acid andH. pylori may be involved in the pathogenesis of antral gastritis.     

Comparison of lansoprazole and omeprazole in the short-term management of duodenal ulcers in Taiwan

Lansoprazole is a novel H +/K + -ATPase inhibitor which exhibits a very potent and long-acting suppression of acid secretion. The object of this randomized, controlled trial was to compare duodenal ulcer healing rates after 4 weeks of treatment with a once-daily regimen of either 30 mg lansoprazole or 20 mg omeprazole. Of a total of 111 patients 57 received lansoprazole, whereas 54 received omeprazole. In intention-to-treat analysis at 4 weeks, 89.5% patients showed ulcer healing following treatment with lansoprazole compared with 83.3% of patients treated with omeprazole. Per protocol analysis indicated that 96.1% of patients treated with lansoprazole showed ulcer healing, compared with 93.6% of patients treated with omeprazole (NS). Age, smoking or ulcer size did not affect the ulcer healing rate. Both agents could effectively and quickly resolve ulcer symptoms. The Helicobacter pylori clearance was seen in 36 (73.5%) patients in the lansoprazole group and in 40 (80%) patients in the omeprazole group after four weeks of treatment (NS). In addition, both agents led to hypergastrinaemia, by approximately 1.6 fold. Adverse side effects included a few occurrences of reversible skin rash and constipation. It is concluded that lansoprazole elicits an adequate healing response and resolves symptoms of duodenal ulcer as well as omeprazole. Furthermore, lansoprazole is well tolerated with a few adverse side effects.     

Influence of cure of Helicobacter pylori infection on gastric acidity and gastroesophageal reflux: study by 24-h pH monitoring in patients with gastric or duodenal ulcer

Background Whether or not the eradication of Helicobacter pylori is a risk factor for reflux esophagitis (RE) is a question at issue. To find an answer, it is necessary to clarify the influence of H. pylori eradication on the mechanism of RE.Methods The authors investigated the influence of H. pylori eradication on gastric acidity and gastroesophageal reflux in ten gastric ulcer (GU) patients and ten duodenal ulcer (DU) patients by 24-h simultaneous determination of pH in the stomach and esophagus.Results Though the results indicated enhanced gastric acidity in GU patients at night after H. pylori eradication, no such influence was observed in DU patients. No significant changes in gastroesophageal reflux occurred in GU or DU patients before and after H. pylori eradication. RE after H. pylori eradication occurred in only one patient, with GU. This patient had several risk factors for RE, such as obesity, male sex, and dietary habits to add to the increase in gastric acidity at night that occurred after H. pylori eradication. No increase in gastroesophageal reflux occurred in any DU patients or in the other GU patients that demonstrated enhanced gastric acidity at night after H. pylori eradication.Conclusions The cure of H. pylori infection does not, by itself, cause RE in patients who have few other risk factors for RE.     

Effect of the eradication ofHelicobacter pylori on duodenal ulcer healing and ulcer relapse: Randomized controlled study in Japan

To investigate the effect of the eradication ofHelicobacter pylori on the healing and relapse of duodenal ulcers. 50 patients with active duodenal ulcer andH. pylori infection were randomly allocated to two treatment groups. One group (cimetidine group) received cimetidine 400mg twice daily for 6 weeks and the other group (double-therapy group) received 300mg amoxicillin granules and 250 mg metronidazole thrice daily for 2 weeks, in addition to the same regimen of cimetidine as the cimetidine group. Forty-two patients completed the study. After confirmation of ulcer scar, all patients were followed up for 6 months while receiving treatment with teprenone, an agent that does not affect acid secretion or the eradication ofH. pylori. The healing rates at 6 weeks were 90% in the cimetidine group and 95.5% in the double-therapy group.H. pylori eradication occurred in 0% of the cimetidine group and in 73.7% of the double-therapy group (P-0.004). The cumulative relapse rates in the two groups at 6 months were 64.3% and 11.1%, respectively (P=0.0007). In the double-therapy group, the cumulative relapse rate at 6 months in the patients in whomH. pylori persisted was 50% (2/4); the rate was 0% (0/14) in the patients in whomH. pylori had been eradicated (P=0.005). Histological gastritis significantly improved compared with the baseline in the double-therapy group, but no such improvement was seen in the cimetidine group. White scarring was found in 7.1% of the cimetidine group and in 83.3% of the double-therapy group after 6 months (P=0.0001). The eradication ofH. pylori markedly decreased the relapse rate in duodenal ulcer patients, and it significantly improved both the grade of gastritis and the quality of the ulcer scar.