Head-to-head comparison of H2-receptor antagonists and proton pump inhibitors in the treatment of erosive esophagitis: A meta-analysis

Aim: To systematically evaluate the efficacy of H2-receptor antagonists (H2RAs) and proton pump inhibitors in healing erosive esophagitis (EE). Methods: A meta-analysis was performed. A literature search was conducted in PubMed, Medline, Embase, and Cochrane databases to include randomized controlled head-to-head comparative trials evaluating the efficacy of H2RAs or proton pump inhibitors in healing EE. Relative risk (RR) and 95% confidence interval (CI) were calculated under a random-effects model. Results: RRs of cumulative healing rates for each comparison at 8 wk were: high dose vs standard dose H2RAs, 1.17 (95%CI, 1.02-1.33); standard dose proton pump inhibitors vs standard dose H2RAs, 1.59 (95%CI, 1.44-1.75); standard dose other proton pump inhibitors vs standard dose omeprazole, 1.06 (95%CI, 0.98-1.06). Proton pump inhibitors produced consistently greater healing rates than H2RAs of all doses across all grades of esophagitis, including patients refractory to H2RAs. Healing rates achieved with standard dose omeprazole were similar to those with other proton pump inhibitors in all grades of esophagitis. Conclusion: H2RAs are less effective for treating patients with erosive esophagitis, especially in those with severe forms of esophagitis. Standard dose proton pump inhibitors are significantly more effective than H2RAs in healing esophagitis of all grades. Proton pump inhibitors given at the recommended dose are equally effective for healing esophagitis. © 2005 The WJG Press and Elsevier Inc. All rights reserved.published_or_final_versio

Helicobacter pylori infection is associated with increased expression of macrophage migratory inhibitory factor - by epithelial cells, T cells, and macrophages - in gastric mucosa

The macrophage migratory inhibitory factor (MIF) plays a pivotal role in inflammatory and immune diseases; however, its role in gastrointestinal diseases has not been clarified. This study intended to determine the expression of MIF, by gastric epithelial cells, T cells, and macrophages, in Helicobacter pylori-induced gastritis. Sixty-four patients (30 males, 34 females; mean age, 47 years) referred for upper endoscopy were recruited. Biopsy specimens from the gastric antrum and corpus were obtained for (1) detection of H. pylori and histological examination, (2) single and double immunostaining to test for expression of MIF protein in epithelial cells, T cells, and macrophages, and (2) in situ hybridization for expression of MIF mRNA within the lamina propria. In mucosal specimens from each of the 2 sites, both the percentage of MIF + epithelial cells and the numbers of MIF mRNA+ inflammatory cells, MIF+ T cells, and MIF+ macrophages were significantly higher in H. pylori-positive patients than in H. pylori-negative patients. Overall, the percentage of MIF+ epithelial cells and the numbers of MIF mRNA+ cells, MIF+ T cells, and MIF+ macrophages were higher in the antrum than in the corpus. The percentage of MIF+ epithelial cells and the numbers of MIF mRNA+ cells, MIF+ T cells, and MIF+ macrophages increased in chronic gastritis, but, in the absence of H. pylori infection, this increase disappeared for all except MIF+ T cells. Therefore, H. pylori infection is associated with increased expression of the MIF protein and MIF mRNA in gastric epithelial and inflammatory cells; along with other cytokines, MIF may play a significant role in gastric inflammation related to H. pylori infection.published_or_final_versio

Macrophage migration inhibitory factor stimulated by Helicobacter pylori increases proliferation of gastric epithelial cells

Aim: Helicobacter pylori (H pylori) is associated with increased gastric inflammatory and epithelial expression of macrophage migration inhibitory factor (MIF) and gastric epithelial cell proliferation. This study aimed at determining whether H pylori directly stimulates release of MIF in monocytes, whether the cag pathogenicity island (PAI) is involved for this function, and whether MIF stimulated by H pylori increases gastric epithelial cell proliferation in vitro. Methods: A cytotoxic wild-type H pylori strain (TN2), its three isogenic mutants (TN2Δcag, TN2ΔcagA and TN2ΔcagE) were co-cultured with cells of a human monocyte cell line, THP-1, for 24 h at different organism/cell ratios. MIF in the supernatants was measured by an ELISA. Cells of a human gastric cancer cell line, MKN45, were then co-cultured with the supernatants, with and without monoclonal anti-MIF antibody for 24 h. The cells were further incubated for 12 h after addition of 3H-thymidine, and the levels of incorporation of 3H-thymidine were measured with a liquid scintillation counter. Results: The wild-type strain and the isogenic mutants, TN2ΔcagA and TN2ΔcagE, increased MIF release at organism/cell ratios of 200 /1 and 400/1, but not at the ratios of 50/1 and 100/1. However, the mutant TN2Δcag did not increase the release of MIF at any of the four ratios. 3H-thymidine readings for MKN-45 cells were significantly increased with supernatants derived from the wild-type strain and the mutants TN2ΔcagA and TN2ΔcagE, but not from the mutant TN2Δcag. Moreover, in the presence of monoclonal anti-MIF antibody, the stimulatory effects of the wild-type strain on cell proliferation disappeared. Conclusion: H pylori stimulates MIF release in monocytes, likely through its cag PAI, but not related to cagA or cagE. H pylori-stimulated monocyte culture supernatant increases gastric cell proliferation, which is blocked by anti-MIF antibody, suggesting that MIF plays an important role in H pylori-induced gastric epithelial cell proliferation. © 2005 The WJG Press and Elsevier Inc. All rights reserved.published_or_final_versio

Expression of Ki-67 and Bcl-2 in gastric epithelial cells: role of antralization in gastric carcinogenesis

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Low dose 13C-Urea breath test (13C-UBT) with citrate is equally reliable for the detection of Helicobacter pylori infection in Chinese

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Expression of macrophage migration inhibitory factor in Helicobacter pylori-induced gastritis and peptic ulcer disease

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Non-H. pylori, non-NSAID duodenal ulcers: clinical and endoscopic characteristics

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Increased serum levels and epithelial expression of macrophage migration inhibitory factor in gastric cancer

This journal suppl. contain abstracts of the 8th Medical Research Conference, Medical Science Group, Queen Mary Hospital, Hong Kongpublished_or_final_versio

Antralization at the edge of proximal gastric ulcers: Does Helicobacter pylori infection play a role?

Aim: To determine the prevalence of antralization at the edge of proximal gastric ulcers, and the effect of H. pylori eradication on the mucosal appearances. Methods: Biopsies were taken from the antrum, body and the ulcer edge of patients with benign proximal gastric ulcers before and one year after treatment. Gastric mucosa was classified as antral, transitional or body type. H. pylori positive patients received either triple therapy, or omeprazole. Results: Patients with index ulcers in the incisura, body or fundus (n=116) were analyzed. Antral-type mucosa was more prevalent at the ulcer edge in H. pylori-positive patients than H. pylori-negative patients (93 % vs 60 %, OR=8.95, 95 %CI: 2.47-32.4, P=0.001). At one year, there was a significant reduction in the prevalence of antralization (from 93 % to 61 %, P=0.004) at the ulcer edge in patients with H. pylori being eradicated. However, there was no difference in the prevalence of antralization at the ulcer edge in those with persistent infection. Conclusion: H. pylori infection is associated with antralization at the edge of proximal gastric ulcers, which may be reversible in some patients after eradication of the infection.published_or_final_versio

Effects of Primary Metronidazole and Clarithromycin Resistance to Helicobacter pylori on Omeprazole, Metronidazole, and Clarithromycin Triple-Therapy Regimen in a Region with High Rates of Metronidazole Resistance

The aim of this study was to investigate the effect of metronidazole resistance (MtzR) and clarithromycin resistance (CIaR) on the eradication rate for omeprazole, clarithromycin, and metronidazole triple-therapy regimen and on the development of posttherapy drug resistance in a region of high rates of MtzR. One hundred ninety-six Helicobacter pylori isolates were recovered from patients with duodenal ulcer, gastric ulcer, or nonulcer dyspepsia during upper endoscopy. The prevalences of MtzR, ClaR, and dual resistance were 37.8%, 13.8%, and 8.7%, respectively. The intention-to-treat eradication rates for metronidazole-susceptible (87.2% vs. 67.6%; P = .001) and clarithromycin-susceptible (86.4% vs. 40.7%; P < .001 ) strains were significantly higher than the rates for resistant strains. Multiple logistic regression analysis implicated younger age (<40 years old), MtzR, ClaR, and the diagnosis of nonulcer dyspepsia as independent factors that predicted treatment failure. The rates of posttreatment MtzR, ClaR, and dual resistance were 88%, 88%, and 75%, respectively. MtxR and ClaR significantly affected the success of eradication therapy. Posttreatment rates of resistance were high and were related to the presence of pretreatment antibiotic resistance.published_or_final_versio