Premedication with pronase or N-acetylcysteine improves visibility during gastroendoscopy: An endoscopist-blinded, prospective, randomized study

AIM: To assess the efficacy of premedicaton with pronase or N-acetylcysteine (NAC) at 20 min before upper gastrointestinal (UGI) endoscopy and to determine whether pronase or NAC pretreatment influences the reliability of the rapid urease test. METHODS: A total of 146 patients were prospectively and randomly assigned into the study groups according to different premedications before endoscopy. One endoscopist assessed mucosal visibility (MV) with scores ranged from 1 to 4 at four sites in the stomach. The sum of the MV scores from these four locations was defined as the total mucosal visibility (TMV) score. Identification of H pylori was performed using CLO test, histology, and serology. RESULTS: The Group with pronase premedication had a significantly lower TMV score than did the groups with gascon and gascon water (P < 0.001 and P < 0.01, respectively). The group with NAC had a significantly lower TMV score than the group with gascon (P < 0.01) and a trend of a lower MV score than the group with gascon water (P = 0.06). The TMV score did not significantly differ between the group with pronase and the group with NAC (P = 0.39 and P = 0.14, respectively). The sensitivity and specificity of the CLO test were 92.5% and 93.9%, respectively, in groups premedicated with pronase and NAC together.CONCLUSION: Premedication with pronase or NAC at 20 min before UGI endoscopy improves the mucosal visibility of the stomach. Neither pronase nor NAC produces any obvious interference with the CLO test for the identification of H pylori infection.

Protective effects of Ginkgo biloba extract on the ethanol-induced gastric ulcer in rats

AIM: To evaluate the preventive effect of Ginkgo bilobaextract (GbE) on ethanol-induced gastric mucosal injuries in rats.METHODS: Female Wistar albino rats were used for the studies. We randomly divided the rats for each study into five subgroups: normal control, experimental control, and three experimental groups. The gastric ulcers were induced by instilling 1 mL 50% ethanol into the stomach. We gaveGbE 8.75, 17.5, 26.25 mg/kg intravenously to the experimental groups respectively 30 min prior to the ulcerative challenge. We removed the stomachs 45 min later. The gastric ulcers,gastric mucus and the content of non-protein sulfhydryl groups (NP-SH), malondialdehyde (MDA), c-Jun kinase (JNK) activity in gastric mucosa were evaluated. The amount of gastric juice and its acidity were also measured. RESULTS: The findings of our study are as follows: (1)GbE pretreatment was found to provide a dose-dependent protection against the ethanol-induced gastric ulcers in rats; (2) the GbE pretreatment afforded a dose-dependent inhibition of ethanol-induced depletion of stomach wall mucus, NP-SH oontents and increase in the lipid peroxidation (increase MDA) in gastric tissue; (3) gastric ulcer induced by ethanolproduced an increase in JNK activity in gastric mucosawhich also significantly inhibited by pretreatment with GbE;and (4) GbE alone had no inhibitory effect on gastric secretionin pylorus-ligated rats.CONCLUSION: The finding of this study showed that GbE significantly inhibited the ethanol-induced gastric lesions in rats. We suggest that the preventive effect of GbE may be mediated through: (1) inhibition of lipid peroxidation;(2) preservation of gastric mucus and NP-SH; and (3)blockade of cell apoptosis.

Eradication of Helicobacter pylori significantly reduced gastric damage in nonsteroidal anti-inflammatory drug-treated Mongolian gerbils

AIM: To examine the effect of eradication of Helicobacter pyloriprior to usage of NSAIDs, by investigating gastric inflammatory activity, myeloperoxidase (MPO) activity,prostaglandin (PG) E2 synthesis in H pylori-infected, and H pylori-eradicated gerbils followed by administration of indomethacin and rofecoxib.METHODS: Six-week-old male gerbils were orally inoculated with H pylori. Seven weeks later, anti-H pyloritriple therapy and vehicle were given to gerbils respectively and followed for 2 wk. We examined the area of lesions, gastric inflammatory activity, PGE2 synthesis and MPO activity in the stomach.RESULTS: In indomethacin and rofecoxib-treated gerbils,the following results were obtained in H pylori-infected group vs Hpylori-eradicated group respectively: hyperplasia area of the stomach (mm2): 82.4±9.2 vs 13.9±3.5 (P＜0.05),30.5±5.1 vs 1.3±0.6 (P＜0.05); erosion and ulcer area (mm2):14.4±4.9 vs0.86±0.5 (P＜0.05), 1.3±0.6 vs0.4±0.3 (P＜0.05);score of gastritis: 7.0±0.0 vs3.6±0.5 (P＜0.05), 7.0±0.0 vs2.7±0.5 (P＜0.05); MPO activity (μmol H2O2/min/g tissue):104.7±9.2 vs9.0±2.3 (P＜0.05), 133.5±15.0 vs2.9±0.7(P＜0.05); PGE2 synthesis (pg/mg wet weight/min): 299.2±81.5vs 102.8±26.2 (P＜0.05), 321.4±30.3 vs 11.9±4.8 (P＜0.05).CONCLUSION: Eradication of H pylori reduced gastric damage of NSAID-treated Mongolian gerbils. Rofecoxib caused less severe gastric damage than indomethacin in H pylori-eradicated gerbils.

Anti-Helicobacter pylori therapy significantly reduces Helicobacter py/ori-Induced gastric mucosal damage in Mongolian gerbils

AIM: To investigate the effectiveness of 4 d' anti-Helicobacter pyloritherapy on the H pylori-infected Mongolian gerbils based on physiological and pathological changes.METHODS: We used 6-wk-old male gerbils orally inoculated with H pylori (ATCC43504, 2x108 CFU/mL).Seven weeks after H pylori inoculation, the animals of study group received 4 d' anti-H pylori triple therapy (H pylorieradicated group). Seven days later, all animals of the H pylori-eradicated and control groups (H pylori-infected& H pylori-uninfected groups) were sacrificed. We examined gastric mucosal lesions macroscopically, studied gastritis microscopically and determined the stomach weight ratio, myeloperoxidase (MPO) activity and prostaglandin (PG) E2 level.RESULTS: The results showed that both macroscopic and histological gastric damages were significantly less in H pylori-eradicated group than H pylori-infected group.Stomach weight ratio, MPO activity and PGE2 levels were significantly higher in H pylori-infected group than those in the other two groups.CONCLUSION: Four days' anti-H pylori therapy was effective in the improvement of H pylori-induced gastric lesions in Mongolian gerbils.

Deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer: A correlated study

AIM: To investigate the correlation among the presence and degree of gastric metaplasia of duodenal regenerating mucosa, the deformity of bulb and the recurrence of duodenal ulcer.METHODS: A total of 99 patients with duodenal ulcer were treated with H2-antagonist with or without antimicrobial therapy. All patients received follow-up endoscopic examinations 6 wk after treatment. When the ulcer(s) were noted to be healed, two biopsies were taken from the ulcer scar for histological study of gastric metaplasia, and 4 biopsies were taken from antrum for Helicobacter pylori(H pylori) study. Out of these cases,44 received further follow-up endoscopic examinations after 3, 6 and 12 mo respectively for studying the recurrence rate of duodenal ulcers. The correlation among ulcer recurrence, degree of gastric metaplasia of regenerating mucosa, bulbar deformity, and colonization of Hpylori in the stomach was then studied.RESULTS: The results showed that there was a strong correlation between the deformity of duodenal bulb and the degree of gastric metaplasia of regenerating duodenal mucosa. The recurrence rate of duodenal ulcer had a significant difference between patients with and without Hpyloricolonization in the stomach (P＜0.001). The greater the degree of gastric metaplasia of duodenal regenerating mucosa, the higher the recurrence rate of duodenal ulcer (P= 0.021). The more deformed the duodenal bulb, the higher the incidence of recurrence of duodenal ulcer (P = 0.03).CONCLUSION: There is a correlation among deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer.A more severely deformed duodenal bulb is closely related to a greater extent of gastric metaplasia. Both factors contribute to the recurrence of duodenal ulcer.