The VacA gene encodes for vacuolating cytotoxin, but its mechanism of causing peptic ulcers is unclear. Such stomach mucosal inflammation can be associated with hyperchlorhydria (increased stomach acid secretion) or hypochlorhydria (reduced stomach acid secretion). Inflammatory cytokines inhibit the parietal cell acid secretion. H. pylori also secretes certain products that inhibit hydrogen potassium ATPase; activate calcitonin gene-related peptide sensory neurons, which increases somatostatin secretion to inhibit acid production by parietal cells; and inhibit gastrin secretion. This reduction in acid production causes gastric ulcers. On the other hand, increased acid production at the pyloric antrum is associated with duodenal ulcers in 10% to 15% of H. pylori infection cases. In this case, somatostatin production is reduced and gastrin production is increased, leading to increased histamine secretion from the enterochromaffin cells, thus increasing acid production. An acidic environment at the antrum causes metaplasia of the duodenal cells, causing duodenal ulcers.Human immune response toward the bacteria also determines the emergence of peptic ulcer disease. The human IL1B gene encodes for Interleukin 1 beta, and other genes that encode for tumour necrosis factor (TNF) and Lymphotoxin alpha also play a role in gastric inflammation. NSAIDs
Taking nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin can increase the risk of peptic ulcer disease by four times compared to non-users. The risk of getting a peptic ulcer is two times for aspirin users. Risk of bleeding increases if NSAIDs are combined with selective serotonin reuptake inhibitor (SSRI), corticosteroids, antimineralocorticoids, and anticoagulants.
Other conditions that produce similar symptoms include stomach cancer, coronary heart disease, and inflammation of the stomach lining or gallbladder inflammation.Diet does not play an important role in either causing or preventing ulcers. Treatment includes stopping smoking, stopping use of NSAIDs, stopping alcohol, and taking medications to decrease stomach acid. The medication used to decrease acid is usually either a proton pump inhibitor (PPI) or an H2 blocker, with four weeks of treatment initially recommended. Ulcers due to H. pylori are treated with a combination of medications, such as amoxicillin, clarithromycin, and a PPI. Antibiotic resistance is increasing and thus treatment may not always be effective. Bleeding ulcers may be treated by endoscopy, with open surgery typically only used in cases in which it is not successful.Peptic ulcers are present in around 4% of the population. New ulcers were found in around 87.4 million people worldwide during 2015. About 10% of people develop a peptic ulcer at some point in their life. Peptic ulcers resulted in 267,500 deaths in 2015, down from 327,000 in 1990. The first description of a perforated peptic ulcer was in 1670, in Princess Henrietta of England. H. pylori was first identified as causing peptic ulcers by Barry Marshall and Robin Warren in the late 20th century, a discovery for which they received the Nobel Prize in 2005. Signs and symptoms
Signs and symptoms of a peptic ulcer can include one or more of the following:
abdominal pain, classically epigastric, strongly correlated with mealtimes.