pylori) infection is the most important risk factor for gastric cancer (GC) development through the Correa's gastric carcinogenesis cascade. pylori eradication alone does not eliminate GC, as pre-neoplastic lesions (atrophic gastritis, intestinal metaplasia and dysplasia) may have already developed in some patients. It is therefore necessary to identify patients at high-risk for gastric cancer after H. pylori eradication to streamline the management plan. If the patients have not undergone endoscopy with histologic assessment, the identification of certain clinical risk factors and non-invasive testing (serum pepsinogen) can predict the risk of atrophic gastritis. For those with suspected atrophic gastritis, further risk stratification by endoscopy with histologic assessment according to validated histologic staging systems would be advisable. Patients with higher stages may require long-term endoscopic surveillance. Apart from secondary prevention to reduce deaths by diagnosing GC at an early stage, identifying medications that could potentially modify the GC risk would be desirable. Gastritis is inflammation of the gastric mucosa caused by any of several conditions, including infection (Helicobacter pylori), drugs (NSAIDs, alcohol), stress, and autoimmune phenomena (atrophic gastritis). Many cases are asymptomatic, but dyspepsia and GI bleeding sometimes occur. Treatment is directed at the cause but often includes acid suppression and, for Helicobacter pylori infection, antibiotics. Gastritis is classified as erosive gastritis or nonerosive gastritis based on the severity of mucosal injury. It is also classified according to the site of involvement (ie, cardia, body, antrum). Gastritis can be further classified histologically as acute or chronic based on the inflammatory cell type. No classification scheme matches perfectly with the pathophysiology; a large degree of overlap exists. Some forms of gastritis involve acid-peptic and Helicobacter pylori Infection" Chronic gastritis implies some degree of atrophy (with loss of function of the mucosa) or metaplasia. Lasix bodybuilding dosage Buy stromectol in uk How does kamagra oral jelly work Home Q & A Questions Has anyone experienced bouts. Has anyone experienced bouts of gastritis after long term use of Metformin, 850 2x daily? I've been taking. I'm still shaking my head over my own idiocy in not making the connection between metformin and my revived GI problems until now In February 2013, just before my. I've been on regular-release metformin since November last year and although I did have a few bowel troubles with them to begin with, everything. Digestive disorders (diarrhoea, vomiting) represent the most common metformin side-effects (around 30%) with this first-line drug treatment for type 2 diabetes. In healthy individuals, metformin affects glucose, vitamin B12 and the digestive uptake of bile salts. In the colon, it acts locally by modifying glucose cell metabolism. Different pathophysiological hypotheses have been proposed to explain the metformin-induced diarrhoea and vomiting, which can sometimes cause the patient to stop an effective treatment. These theories include stimulation of intestinal secretion of serotonin, changes in incretin and glucose metabolism, and bile-salt malabsorption. However, none of these hypotheses can be considered an adequate pathophysiological explanation of metformin digestive side-effects. In addition, there is a lack of experimental data to explain these highly patient-dependent adverse effects. Erosive gastritis is more severe than nonerosive gastritis. This form involves both inflammation and wearing away (erosion) of the stomach lining. The cells that produce mucus to protect the stomach lining from acid are missing or are damaged. Erosive gastritis typically develops suddenly (called acute erosive gastritis) but may develop slowly (called chronic erosive gastritis), usually in people who are otherwise healthy. Nonerosive gastritis is characterized by changes in the stomach lining that range from wasting away (atrophy) of the stomach lining to transformation of stomach tissue into another type of intestinal tissue (metaplasia). Often, several types of white blood cells accumulate in the stomach and cause varying degrees of inflammation. The white blood cells may cause inflammation in the entire stomach or only in certain parts. Less commonly, radiation, viral infections (such as cytomegalovirus), and direct injuries (such as by the insertion of a nasogastric tube) can cause erosive gastritis. 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