J Ho

A sensitive guaiac faecal occult blood test is less useful than an immunochemical test for colorectal cancer screening in a Chinese population

Background : Colorectal cancer screening by guaiac faecal occult blood test has been shown to reduce the incidence and mortality of colorectal cancer in Western populations. The optimal faecal occult blood test, whether guaiac or immunochemical, for colorectal cancer screening in the Chinese population remains to be defined.

EFFECT OF OMEPRAZOLE ON DUODENAL ULCER-ASSOCIATED ANTRAL GASTRITIS AND HELICOBACTER 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.

Differential Helicobacter pylori infection rates in two contrasting gastric cancer risk regions of South China

Background: Carriers of Helicobacter pylori are believed to have a three‐ to six‐fold increased risk of developing gastric cancer. We have recently conducted a simultaneous cross‐sectional population study on the prevalence of H. pylori infection in a cohort of asymptomatic adult volunteers in two contrasting gastric cancer risk regions of South China, Hong Kong and Changle of Fujian. Their mean annual gastric cancer mortality has been approximately 7.5 and 75/100 000 population, respectively, since the beginning of the last decade. The aim of this study was to evaluate if H. pylori prevalence bears any relationship to gastric cancer mortality rates in these two southern regions of China.

Triple therapy for Helicobacter pylori eradication is more effective than long-term maintenance antisecretory treatment in the prevention of recurrence of duodenal ulcer: a prospective long-term follow-up study.

: The effectiveness of Helicobacter pylori eradication treatment and long term acid suppression maintenance in the natural course of duodenal ulcer has not been directly compared.

Comparison of lansoprazole-based triple and dual therapy for treatment of Helicobacter pylori-related duodenal ulcer: An Asian multicentre double-blind randomized placebo controlled study

: In Asian countries with limited resources, clarithromycin‐based triple therapy may not be readily available. There are also few direct comparisons of different regimens in Asia.

Nonsteroidal Antiinflammatory Drugs Could Reverse Helicobacter pylori-Induced Apoptosis and Proliferation in Gastric Epithelial Cells

It remains controversial whether the harmfuleffects of Helicobacter pylori (Hp) and nonsteroidalantiinflammatory drugs (NSAIDs) are additive. We studiedthe effects of Hp (virulent and nonvirulent strains) and NSAIDs, alone or in combination, onapoptosis and proliferation of gastric epithelial cellsin nonulcer dyspepsia (NUD) patients. Forty-four (25Hppositive and 19 Hp-negative) consecutive Chinese NUD patients with rheumatoid arthritis who hadtaken continuously NSAIDs for more than three monthswere recruited for this study. Another 41 (20Hp-positive and 21 Hp-negative) NUD patients not on anyNSAIDs were included as controls. All patientsunderwent a gastroscopy examination and gastricbiopsies. Hp infection was confirmed by CLOtest, anti-HpELISA, and [13C]urea breath test. The CagAstatus was determined by the anti-CagA antibody assay. The degree ofgastritis, apoptosis, and proliferation indices weredetermined with H&E staining, terminal uridinedeoxynucleotidyl nick end-labeling (TUNEL), andproliferating cell nuclear antigen (PCNA) immunostainingmethods, respectively. A significantly higher apoptosiswas observed in subjects who had Hp infection or hadbeen consuming NSAIDs when compared with the controls. Unlike NSAID-treated subjects, patients with Hpinfection were shown to have significantly enhanced cellproliferation. However, the increased apoptosis andproliferation in Hp-positive subjects were reversed by also taking NSAIDs. No correlation was foundbetween apoptosis and proliferation in all the studygroups. There was no association found between CagAexpression or degree of gastritis with cellproliferation or apoptosis. It was demonstrated at thecellular level that NSAIDs could abrogate apoptosis orproliferation effects induced by Hp. Furthermore, thelatter effects appeared not to be influenced by the virulent nature of the Hp strains.

Persistence of Campylobacter pyloridis despite healing of duodenal ulcer and improvement of accompanying duodenitis and gastritis

Campylobacter pyloridis has been associated with antral gastritis and duodenal ulcer. To study the pathogenetic role of these organisms in duodenal ulcer, endoscopic biopsies, two from the first part of duodenum, four from antrum, and four from body and fundus, were taken before and after four weeks of cimetidine treatment (1.2 g/day) from 67 patients with active duodenal ulcer. The biopsies were examined for the presence and severity of any inflammation by two independent pathologists in the absence of any clinical information and for the occurrence and density ofCampylobacter pyloridis by culture and Warthin-Starry stain. Before treatment, inflammation was present in 71.1, 100, and 25.8%, while the organisms were present in 34.3, 91.0, and 79.1% of the duodenal, antral, and fundal biopsies, respectively. With complete healing of duodenal ulcer, inflammation was present in 48.9, 98.2, and 30.2%, while the organisms were present in 25, 76.7, and 63.3% of the respective mucosae. With ulcer healing, duodenitis became significantly milder (P<0.05). With improvement of gastritis and duodenitis, there was no significant change in the occurrence and density ofCampylobacter pyloridis. These findings indicate that healing of duodenal ulcer is not influenced by the presence ofCampylobacter pyloridis, which is frequently found in the gastroduodenal mucosa of patients with duodenal ulcer, but does not appear to be associated with mucosal inflammation except in the antrum.

Effect of sucralfate and cimetidine on duodenal ulcer-associated antral gastritis and Campylobacter pylori☆

The course of gastritis and Campylobacter pylori was studied in a single-blind randomized trial comparing cimetidine 200 mg three times a day and 400 mg at night and sucralfate 1 g four times a day orally for four weeks in 140 patients with proved duodenal ulcer. At least two antral biopsies were performed during endoscopy before entry and at the end of four weeks. The activity and the degree of chronic inflammation, as assessed histologically by the degree of infiltration of, respectively, polymorphs and chronic inflammatory cells, were graded blindly by two pathologists as nil, mild, moderate, or severe. The density of C. pylori, as assessed after Warthin-Starry stain, was similarly graded. Ulcer-healing rates were comparable in the cimetidine (73.2 percent) and sucralfate (79.7 percent) groups. Improvement of the activity of gastritis occurred significantly (p less than 0.05) more frequently in the sucralfate (33.3 percent) than in the cimetidine group (18.3 percent), and remained so (p less than 0.05) when only patients with healed ulcer were compared. The density of C. pylori decreased significantly in the sucralfate group after treatment (p less than 0.01) but not in the cimetidine group. The 12-month ulcer relapse rates were significantly (p less than 0.05) lower by life-table analysis in patients healed with sucralfate than in those healed with cimetidine and were unaffected by either the density of Campylobacter in either group or the improvement of the gastritis. It is concluded that sucralfate improves duodenal ulcer-associated antral gastritis and decreases the density of C. pylori, and that factors other than bacterial density and antral gastritis may be responsible for the advantage of sucralfate over cimetidine in ulcer relapse.

Pathogenetic role of Helicobacter pylori in duodenal ulcer disease. Multivariate analysis of factors affecting relapse.

The pathogenesis of duodenal ulcer disease is multifactorial and the contribution of Helicobacter pylori in relation to the other factors to the release of duodenal ulcer is unknown. To investigate this, we studied 147 patients with endoscopically proven healed ulcers. These patients were randomized to receive either placebo, misoprostol 200 micrograms or misoprostol 300 micrograms four times daily, and clinical, personal, physiological and endoscopic characteristics were obtained prospectively. Endoscopy was performed at the active phase of the ulcer and when the ulcer healed. Biopsies were taken from the antrum to assess histologically for: (1) the activity of gastritis as assessed by the degree of polymorph infiltration, (2) the degree of chronic inflammation by the degree of chronic inflammatory cells infiltration and degree of mucosal degeneration, and (3) bacteriologically for the presence of H. pylori. The severity of the gastritis and the bacterial density were graded independently by two pathologists. The patients were assessed at two-month intervals for 12 months or until the ulcer relapsed. The results demonstrated that the relapse rates of duodenal ulcer were similar in the three treatment groups. The relapse rate was higher in the group with higher density of the bacteria (P less than 0.05). The degree of gastritis did not affect the relapse rate of duodenal ulcer in either the placebo or misoprostol group or in all patients combined. Stepwise logistic regression analysis identified that increased duodenal inflammation, male sex, early-onset disease, and H. pylori adversely affected relapse of the ulcer. We conclude that multiple factors affect the relapse of duodenal ulcer and H. pylori is one of them.

Helicobacter pylori in Meckel’s diverticulum with heterotopic gastric mucosa in a population with relatively high H. pylori prevalence rate

Background: Helicobacter pylori (H. pylori) colonize only foveolar gastric‐type mucosa and are associated with active chronic gastritis and peptic ulcer. The aim of this study was to investigate whether H. pylori can also be found in Meckel’s diverticulum which contains heterotopic gastric mucosa.