China
Africa
Explore chapters and articles related to this topic
The Stomach
Published in E. George Elias, CRC Handbook of Surgical Oncology, 2020
Mucosa changes include dysplasia and metaplasia. Severe dysplasia and intestinal metaplasia are precancerous lesions. Severe dysplasias of the mucosa (grades III and IV) are usually found near benign gastric ulcers as well as cancers. Patients with nonspecific chronic gastritis may have mild to moderate dysplasia with no evidence of cancer, and these are not considered precancerous lesions. However, patients with severe dysplasia without gastric lesions should be closely monitored by frequent gastroscopy, as they have tenfold increase in risk of developing gastric carcinoma. However, in such cases, surgical resections are not warranted. On the other hand, atrophic gastritis (acquired or hereditary) may lead to intestinal metaplasia, which may result in severe dysplasia, then neoplasia. In some cases of gastric carcinoma, such dysplastic changes are not present. These carcinomas are usually of the diffuse type with genetic predisposition.
Endoscopic screening for upper gastrointestinal malignancy
Published in David Westaby, Martin Lombard, Therapeutic Gastrointestinal Endoscopy A problem-oriented approach, 2019
The epidemiological link between H. pylori infection and gastric cancer is now convincing. The World Health Organization consensus committee have concluded that there is sufficient evidence of the aetiological role. Virtually all infected patients will develop gastritis, leading to destruction and atrophy of gastric glands and other specialized cells. They are replaced by atrophic mucosa with intestinal metaplasia. The prevalence of atrophic gastritis increases by 2% annually in patients with Helicobacter infection, compared with 0.3% in the uninfected. There are many confounding factors, as treatment of patients who are infected with long-term acid suppression causes an increase in gastritis and intestinal metaplasia (Fig. 5.7). The hypothesis is that acid suppression changes the pattern of infection, with an antral gastritis being transformed to a gastric body gastritis, and this further suppresses acid secretion, increases inflammation and leads to atrophic gastritis. A large case control study in rural Japan showed by unconditional logistic regression analysis that H. pylori infection was associated with an increased odds ratio of 11 for men and 7 for women for the development of atrophic gastritis. In this study, diet, smoking and lifestyle were not related to atrophic gastritis. H. pylori infection also causes increased gastric cell proliferation and impaired secretion of vitamin C – factors that are improved after eradication of infection.
Stomach and duodenum
Published in Michael Gaunt, Tjun Tang, Stewart Walsh, General Surgery Outpatient Decisions, 2018
Carry out OGD and biopsy for detection of dysplasia and H. pylori. Vitamin B12 and folate levels may be low. Perform a Schilling test if atrophic gastritis is suspected. Measure serum gastrin levels and carry out a FBC for lymphocyte and eosinophil levels.
Gastric lesions in patients with autoimmune metaplastic atrophic gastritis: a retrospective study in a single center
Published in Scandinavian Journal of Gastroenterology, 2022
Haiyi Hu, Rongxue Li, Linlin Shao, Qian Zhang, Rui Xu, Shutian Zhang
All patients demonstrated atrophic gastritis affecting the corpus. All cases showed different extent of atrophy or intestinal metaplasia of background mucosa, including 18 cases of mild atrophic gastritis, 63 moderate and 54 severe atrophic gastritis. Intestinal metaplasia in the corpus was diagnosed in 108 cases. Pathological findings indicated a varying degree of gastric ECL cell hyperplasia in the fundus or corpus, of which, 51 cases showed linear hyperplasia, 67 cases in micronodular, 4 cases in dysplasia, 9 cases in adenomatoid and 4 cases in micro carcinoid. Pseudo pyloric metaplasia was found in 30 cases and pancreatic acinar metaplasia in 10 cases. A totalo f 132 cases had the sparing of the antral mucosa. Three cases with H. pylori infection had antral intestinal metaplasia.
Association between Vitamin B12 and Risk of Gastric Cancer: A Systematic Review and Meta-Analysis of Epidemiological Studies
Published in Nutrition and Cancer, 2022
Jianbo He, Hongjuan Fu, Cancan Li, Zhihui Deng, Hui Chang
Our analysis suggested that the relationship between vitamin B12 and gastric cancer may depend on Hp status, smoking, as well as cancer site. The explanation of the mechanism leading to the phenomenon found in our study is currently unclear. One possible reason is that long-term Hp infection is a factor to cause atrophic gastritis (AG) (42). AG is usually a benign process but can induce potentially life-threatening complications: anemia and carcinogenesis (43, 44). Recent studies and bioinformatics analysis have found that Transcobalamin (TCN1), a vitamin B12 binding protein, is abnormally expressed in AG patients. TCN1 can regulate cobalamin homeostasis and may be related to the occurrence of gastric tumors (45, 46). Previous studies have shown that large consumption of vegetables, fruits, vitamins, and antioxidants can reduce the risk of cancer including gastric cancer (47, 48). One potential reason why vitamin B12 is different from other vitamins may be that it comes entirely from food of animal origin. It is only a sign of eating animal protein. Studies have indicated that the risk of gastric cancer was associated with a high-fat diet (49, 50). Additionally, studies have shown that a diet with low animal protein and rich in fruits, vegetables, and fiber can reduce the risk of malignant transformation (51, 52).
Potential utility of nano-based treatment approaches to address the risk of Helicobacter pylori
Published in Expert Review of Anti-infective Therapy, 2022
Sohaib Khan, Mohamed Sharaf, Ishfaq Ahmed, Tehsin Ullah Khan, Samah Shabana, Muhammad Arif, Syed Shabi Ul Hassan Kazmi, Chenguang Liu
The transmission of H. pylori from person to person can occur through saliva, and it might be spread out through the excrement of food or water, untreated water, poor hygiene, and crowded conditions that largely contribute to the prevalence of H. pylori infection [49]. In brief, it is more likely to be transmitted within the household conditions as it enters the body through the oral cavity and travels to the digestive system, where it infects the stomach or the first part of the small intestine, thereby causing inflammation at the targeted area. The most peculiar characteristic of H. pylori is to survive in the harsh acidic environment of the stomach. It produces urease upon entering the stomach, which then reacts with urea to form ammonia and neutralizes the surrounding environment, consequently leads to the overproduction of the stomach acid (Figure 1) illustrates the invasion of H. pylori infection in the stomach that comprises of six steps; 1) movement of the pathogen through normal stomach lining (mucosa), 2) causing inflammation of the stomach lining (chronic gastritis), 3) loss of stomach cells and weakening of digestive system (atrophic gastritis), 4) transformation of the stomach lining (intestinal metaplasia), 5) initial stages of stomach cancer (dysplasia), and finally cause stomach cancer (gastric adenocarcinoma) [49].