| Verrucosa gastritis (VG, or chronic erosive gastritis, varioform gastritis) is a independent disease with special endoscopic and pathologic signs. It is different from peptic ulcer and commonly chronic gastritis. The clinical features are short of peculiarities. With the universal using of fibrous gastroscopy, it is cognized increasingly, exactly its etiology. Verrucosa gastritis is associated with many factors, for example, helicobacter pylori (HP) infection, acidity, bile countercurrent, hypersusceptibility and so on. Maybe HP infection is the main etiological factors for VG. The mechanism is complicated. First, HP plants in stomach through mouth to mouth spreading route, then traverses the exterior mucous layer by the figure of twist and the power of flagellums. It can parasitize the surface of gastric epithelium and release many kinds of pathogenic factors. Ultimately the gastric mucosa can be lesioned. Under endoscopy, we can see hyperaemia, edema, partial apophysis, punctual putrescence, et al. But the exact mechanism is not very clear and needs more investigations. We explored the relationship of HP infection and VG by detecting the HP infection incidence.Recently the prognosis of VG has become the focus of people's attention. Many scholars think VG is one of high-risk precancerous diseases. The persistent inflammation and epithelium hyperplasia can cause gastric cancer (GC). But the exact pathology is rarely reported. Now it has been known that carcinogenesis and development is a pathological process of multifactor and multistep alteration. The process is from atrophic gastritis, intestinal metaplasia, dysplasia to GC. It is based on the activation of pro-oncogene and the inhibition of suppressor oncogene. HP infection is the startup factor. So we studied the relationship of VG and GC from three aspects: pro-oncogene activation, suppressor oncogene inhibition, HP infection. We detected the proteins P21 and P53. P21 is the expressive product of ras oncogene. It involves in message transmission and regulates cell cycle. Its activation can disturb cell metabolism, signal transmission and cell division, which can result in abnormal differentiation, pathological karyokinesis and cell cancerization. The generation and development of GC are related to P21. P53 is the expressive product of P53 tumour suppressor gene. P53 includes two types: wild-type and mutant-type. Mutant P53 can be detected in most of human carcinomas. One side, wild P53 involves in the regulation of cell cycle by restraining G1 to S and inhibits cell division and proliferation. The other side, P53 induces cell apoptosis with the help of many kinds of oncogene and growth factors. So wild P53 is called tumour suppressor gene. As wild P53 mutates, wild-type transforms into mutant-type. Mutant P53 not only loses the ability of inhibiting cancer, but also can induce cancerization. It has been known that the abnormal expression of P53 is related to GC and detecting P53 carries much weight in diagnosing GC.41 cases of VG (testing group), 21 cases of chronic superficial gastritis (CSG, comparing group), 20 cases of GC(comparing group) were selected by endoscopy. Each group was divided into HP positive and HP negative subgroup again. All patients were diagnosed according to the Gastritis Diagnosis Criterions of 1996 New Sydney System and Diagnosis and Therapy Criteria of Common Carcinoma in China. Immunohistochemical staining was used to detect the expressions of P21 and P53 in tissue specimens. Rapid urease test was used to detect HP in all samples. The tissue samples were taken by enoscopy, fixed in 10% formalin, embedded in paraffin and sectioned. The sections were stained with immunohistochemistry. Slices were examined under the microscope. The tissue samples were considered to be positive for gene expression only when there were nuclear (P53) or nuclear/cytoplasm/cell membrane (P21) staining brown-yellow. Each specimen was observed in ten high-time-fields(×400). Counting the positive cells, it is positive if the... |
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