Gastric cancer can occur as a result of many factors. It occurs twice as commonly in males as females. Estrogen may protect women against the development of this form of cancer. Infections Helicobacter<unk>  infection is an essential risk factor in 65–80% of gastric cancers, but only 2% of people with H.<unk>  infections develop stomach cancer. The mechanism by which H.<unk>  induces stomach cancer potentially involves chronic inflammation, or the action of H.<unk>  virulence factors such as CagA. It was estimated that Epstein–Barr virus is responsible for 84,000 cases per year. AIDS is also associated with elevated risk. Smoking Smoking increases the risk of developing gastric cancer significantly, from 40% increased risk for current smokers to 82% increase for heavy smokers. Gastric cancers due to smoking mostly occur in the upper part of the stomach near the esophagus. Some studies show increased risk with alcohol consumption as well. Diet Sequence of 123-iodine human scintiscans after an intravenous injection: (from left) after 30 minutes, 20 hours, and 48 hours - a high and rapid concentration of radio-iodine is evident in gastric mucosa of the stomach, in salivary glands, oral mucosa, and the periencephalic and cerebrospinal fluid (left). In the thyroid gland, I-concentration is more progressive, also in the reservoir (from 1% after 30 minutes to 5.8% after 48 hours, of the total injected dose). Dietary factors are not proven causes, and the association between stomach cancer and various foods and beverages is weak. Some foods including smoked foods, salt and salt-rich foods, red meat, processed meat, pickled vegetables, and brackens are associated with a higher risk of stomach cancer. Nitrates and nitrites in cured meats can be converted by certain bacteria, including H.<unk> , into compounds that have been found to cause stomach cancer in animals. Fresh fruit and vegetable intake, citrus fruit intake, and antioxidant intake are associated with a lower risk of stomach cancer. A Mediterranean diet is associated with lower rates of stomach cancer, as is regular aspirin use. Obesity is a physical risk factor that has been found to increase the risk of gastric adenocarcinoma by contributing to the development of gastroesophageal reflux disease (GERD). The exact mechanism by which obesity causes GERD is not completely known. Studies hypothesize that increased dietary fat leading to increased pressure on the stomach and the lower esophageal sphincter, due to excess adipose tissue, could play a role, yet no statistically significant data have been collected. However, the risk of gastric cardia adenocarcinoma, with GERD present, has been found to increase more than 2 times for an obese person. There is a correlation between iodine deficiency and gastric cancer. Genetics About 10% of cases run in families, and between 1 and 3% of cases are due to genetic syndromes inherited from a person's parents such as hereditary diffuse gastric cancer. A genetic risk factor for gastric cancer is a genetic defect of the CDH1 gene known as hereditary diffuse gastric cancer (HDGC). The CDH1 gene, which codes for E-cadherin, lies on the 16th chromosome. When the gene experiences a particular mutation, gastric cancer develops through a mechanism that is not fully understood. This mutation is considered autosomal dominant, meaning that half of a carrier's children will likely experience the same mutation. Diagnosis of hereditary diffuse gastric cancer usually takes place when at least two cases involving a family member, such as a parent or grandparent, are diagnosed, with at least one diagnosed before the age of 50. The diagnosis can also be made if at least three cases occur in the family, in which case age is not considered. The International Cancer Genome Consortium is leading efforts to identify genomic changes involved in stomach cancer. A very small percentage of diffuse-type gastric cancers (see Histopathology below) arise from an inherited abnormal CDH1 gene. Genetic testing and treatment options are available for families at risk. Other Other risk factors include diabetes, pernicious anemia, chronic atrophic gastritis, Menetrier's disease (hyperplastic, hypersecretory gastropathy), and intestinal metaplasia. In addition, Foxp3 polymorphism (rs3761548) might contribute to gastric cancer development through influencing Treg cell activity.
complications of Helicobacter pylori
medical cause of Gastritis
symptoms of Helicobacter pylori
medical cause of Peptic ulcer disease
complications of Crohn's disease
complications of Peptic ulcer disease
symptoms of Crohn's disease
complications of Campylobacteriosis