ABSTRACT
A 25-year-old Japanese female was referred to our clinic for the investigation of moderate iron-deficiency anemia and epigastralgia. Endoscopic examination showed diffuse mucosal nodules in the gastric body resembling nodular gastritis, but this pattern was not observed in the antrum. Histology of the gastric biopsies taken from the gastric body showed mild atrophic mucosa with chronic active inflammation. Some of the biopsy specimens showed deposition of patchy, band-like subepithelial collagen. Four years later, the patient showed no clinical symptoms and signs. A follow-up endoscopic examination showed similar findings, which mimicked pseudopolyposis or a cobblestone-like appearance. The biopsy specimens from the depressed mucosa between the nodules revealed a thickened subepithelial collagen band with no improvement, which led to a diagnosis of collagenous gastritis. Treatment with oral administration of proton-pump inhibitors and histamine-2-receptor antagonists had proved ineffective. To make a correct diagnosis of collagenous gastritis, we should determine the characteristic endoscopic findings and take biopsies from the depressed mucosa between the nodules.
ABSTRACT
Numerous cellular and molecular events have been described in development of gastric cancer. In this article, we overviewed roles of Helicobacter pylori (H pylori) infection on some of the important events in gastric carcinogenesis and discussed whether these cellular and molecular events are reversible after cure of the infection. There are several bacterial components affecting gastric epithelial kinetics and promotion of gastric carcinogenesis. The bacterium also increases risks of genetic instability and mutations due to NO and other reactive oxygen species. Epigenetic silencing of tumor suppressor genes such as RUNX3 may alter the frequency of phenotype change of gastric glands to those with intestinal metaplasia. Host factors such as increased expression of growth factors, cytokines and COX-2 have been also reported in non-cancerous tissue in H pylori-positive subjects. It is noteworthy that most of the above phenomena are reversed after the cure of the infection. However, some of them including overexpression of COX-2 continue to exist and may increase risks for carcinogenesis in metaplastic or dysplastic mucosa even after successful H pylori eradication. Thus, H pylori eradication may not completely abolish the risk for gastric carcinogenesis. Efficiency of the cure of the infection in suppressing gastric cancer depends on the timing and the target population, and warrant further investigation.
Subject(s)
Cell Transformation, Neoplastic , Helicobacter Infections/physiopathology , Helicobacter pylori/physiology , Stomach Neoplasms/microbiology , Stomach Neoplasms/pathology , Animals , Cell Transformation, Neoplastic/genetics , Core Binding Factor Alpha 3 Subunit/genetics , Core Binding Factor Alpha 3 Subunit/physiology , Cyclooxygenase 2/physiology , Cytokines/physiology , Epigenesis, Genetic , Gastric Mucosa/microbiology , Gastric Mucosa/pathology , Gene Expression Regulation, Neoplastic , Genetic Predisposition to Disease , Helicobacter Infections/therapy , Humans , Membrane Proteins/physiology , Metaplasia/pathology , Nitric Oxide/physiology , Reactive Oxygen Species/metabolism , Stomach Neoplasms/genetics , Stomach Neoplasms/prevention & control , Tumor Suppressor Protein p53/physiology , VirulenceABSTRACT
BACKGROUND AND AIMS: Helicobacter pylori infection is associated with peptic ulcers; however, it is unclear whether the bacterium delays ulcer healing. We investigated the influence of H. pylori on ulcer healing in mice. We also examined the influence of H. pylori infection on angiogenesis. METHODS: An acetic acid ulcer was made in male BALB/c mice. Three days later (day 0), the animals were inoculated with H. pylori SS1 strain. The healing process of the ulcer was examined macroscopically and microscopically on days 0, 6 and 9. The index of angiogenesis was also determined using carmine dye injection. RESULTS: On day 0, angiogenesis began at the ulcer margin while the mucosal epithelia had not yet regenerated. On days 6 and 9, angiogenesis and epithelial regeneration developed and ulcer size reduced. These phenomena were significantly suppressed in mice infected with H. pylori. CONCLUSION: Helicobacter pylori infection significantly suppressed angiogenesis and delayed ulcer healing. These results indicate that H. pylori plays an important role in ulcer healing.
Subject(s)
Gastric Mucosa/blood supply , Helicobacter Infections/physiopathology , Helicobacter pylori/physiology , Neovascularization, Physiologic , Peptic Ulcer/physiopathology , Wound Healing/physiology , Acetic Acid/toxicity , Animals , Helicobacter Infections/microbiology , Indicators and Reagents/toxicity , Male , Mice , Mice, Inbred BALB C , Models, Animal , Peptic Ulcer/chemically induced , Peptic Ulcer/microbiologyABSTRACT
We report the case of a 69-year-old female with unresectable gastric cancer (T3, N2, P3, H0, Stage IVb) accompanied by peritoneal dissemination, diagnosed on laparotomy. UFT/low-dose cisplatin (CDDP) combination chemotherapy was performed after surgery. UFT 300 mg/day was administered orally every day, and CDDP 10 mg was injected intravenously every week. Chemotherapy was continued for ten months with a total dose of CDDP of 380 mg, but was stopped after oral mucositis developed as a side effect. Seven months after the chemotherapy was started, endoscopy revealed that the gastric cancer tumors had disappeared and the gastric mucosa was intact. Gastric cancer recurrence occurred 2 years and 2 months after chemotherapy was started. Low-dose CDDP/5-FU chemotherapy and TS-1 chemotherapy were performed, but no effects were observed. The patient died 3 years and 6 months after the start of initial chemotherapy, and was treated as an outpatient for 3 years while maintaining a good quality of life. UFT/low-dose CDDP combination chemotherapy offers promise as an effective tool in the clinical management of advanced gastric cancer with peritoneal dissemination.
