Gastritis refers to inflammation caused by injury to the gastric epithelium, which is usually due to excessive alcohol consumption and prolonged use of nonsteroidal anti-inflammatory drugs. Millions of individuals worldwide suffer from this disease. However, the lack of safe and promising treatments makes it urgent to explore and develop leads from natural resources. Therefore, food as medicine may be the best approach for the treatment of these disorders. The present study described the protective effects of food-polydeoxyribonucleotides (f-PDRNs) in a rat model of gastric mucosal injury induced by HCl-EtOH. Administration of f-PDRN was performed with low-PRF002 (26 mg/kg/day), medium-PRF002 (52 mg/kg/day) and high-PRF002 (78 mg/kg/day) on the day of autopsy. The site of damage to the mucous membrane was also analysed. In addition, an increase in gastric juice pH, total acidity of gastric juice and decrease in gastric juice secretion were confirmed, and gastric juice secretion-related factors corresponding to the administration of f-PDRN were analysed. Administration of f-PDRN reduced the mRNA expression of histamine H2 receptor, muscarinic acetylcholine receptor M3, cholecystokinin 2 receptor and H⁺/K⁺ ATPase related to gastric acid secretion and downregulation of histamine, myeloperoxidase and cyclic adenosine monophosphate. In addition, it was histologically confirmed that the loss of epithelial cells and the distortion of the mucosa were recovered in the group in which f-PDRN was administered compared to the model group with gastric mucosa damage. In summary, the present study suggested that f-PDRN has therapeutic potential and may have beneficial effects if taken regularly as a food supplement.

• HCl‑EtOH
• cAMP
• food‑polydeoxyribonucleotides
• gastric mucosa

• Angiodysplasia
• Dieulafoy
• GAVE
• Gastric cancer
• Hemospray
• OTSC
• UGIB

The preventive effects of histamine 2 receptor antagonists vs. proton pump inhibitors on low-dose aspirin (LDA)-related gastroduodenal mucosal injury have not been fully investigated. We conducted a cross-sectional study to compare the prevalence of gastroduodenal ulcers or erosions in patients taking LDA with either 40 mg/day of famotidine or 15 mg/day of lansoprazole for at least three months.

Of 84 eligible patients, two taking 40 mg/day of famotidine and four taking 15 mg/day of lansoprazole refused to undergo upper gastrointestinal endoscopy. Ultimately, we performed upper gastrointestinal endoscopy in 78 patients taking either 40 mg/day of famotidine (group F, n = 31) or 15 mg/day of lansoprazole (group L, n = 47). The prevalence of gastroduodenal ulcers or erosions and the magnitude of gastric mucosal injury evaluated using modified Lanza scores were compared between the two groups.

No patients in either group had gastroduodenal ulcers. Gastroduodenal erosions were more prevalent in group F than in group L (48.4% vs. 17.0%, p = 0.005). The modified Lanza scores (mean ± SD) were significantly higher in group F than in group L (0.9 ± 1.3 vs. 0.3 ± 0.7, p = 0.007). A multivariate logistic regression analysis showed that the use of lansoprazole was negatively associated with gastroduodenal erosions.

This study suggests that 15 mg/day of lansoprazole may be more effective in preventing the development of LDA-related gastroduodenal erosions than 40 mg/day of famotidine. The preventive effects of these two regimens on the development of LDA-related gastroduodenal ulcers require further investigation.

• Disease management
• Endoscopic therapy
• Gastrointestinal endoscopy
• Nonvariceal bleeding
• Peptic ulcer bleeding
• Pharmacotherapy
• Upper gastrointestinal bleeding

• Anti-Inflammatory Agents, Non-Steroidal/adverse effects
• Disease Management
• Gastrointestinal Hemorrhage/chemically induced
• Gastrointestinal Hemorrhage/etiology
• Gastrointestinal Hemorrhage/microbiology
• Gastrointestinal Hemorrhage/therapy
• Helicobacter Infections/complications
• Hemostasis, Endoscopic
• Humans
• Risk Factors

• R24 CA095823 NCI NIH HHS

A clinical history of peptic ulcer has been reported to be associated with a high rate of ulcer recurrence in nonsteroidal anti-inflammatory drug (NSAID) users. Therefore, it is a very important issue to precisely know the previous history prior to NSAIDs administration. To clarify the possible difficulty to identify the history, we determined the sensitivity and diagnostic concordance of endoscopy for the identification of ulcer scars indicative of previous clinical history of peptic ulcer diseases.

The first study enrolled 200 consecutive patients with a clinical history of gastric or duodenal ulcers previously confirmed by esophagogastroduodenoscopy. The sensitivity of endoscopy for identifying scars was determined for these patients. In the second study, the extent of interobserver agreement was determined for 47 endoscopists who identified ulcer scars in endoscopic photographs of 30 sites of previous active gastric ulcers and 30 sites of previous active duodenal ulcers. The kappa coefficient of reliability was calculated to measure the interobserver agreement on the diagnosis of ulcer scars.

Out of 190 patients eligible for analysis, 104 (54.7%) were found to have gastric or duodenal ulcer scars on endoscopy; there were no gastric or duodenal ulcer scars seen in the remaining patients (45%). In the second study, the kappa values for endoscopic diagnosis of gastric and duodenal ulcer scars were 0.14 (95% CI 0.13-0.16) and 0.29 (95% CI 0.27-0.32), respectively. The addition of indigo-carmine chromoendoscopy did not provide a statistically significant improvement in diagnostic concordance in patients with gastric ulcer scar since the kappa value for chromoendoscopic diagnosis was 0.15; 95% CI 0.13-0.17 as low as for un-contrasted scars.

The sensitivity and concordance of endoscopic diagnosis of gastric and duodenal ulcer scars are not satisfactory for the use of endoscopy only to identify previous ulcer disease. To avoid the overlooking the previous clinical history of peptic ulcer diseases, the diagnosis of peptic ulcer scar has to be carefully done prior to NSAIDs administration.