[1] 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.

[2] H. pylori was first identified as causing peptic ulcers by Barry Marshall and Robin Warren in the late 20th century,[4] a discovery for which they received the Nobel Prize in 2005.

Medicines associated with peptic ulcer include NSAIDs (non-steroidal anti-inflammatory drugs) that inhibit cyclooxygenase and most glucocorticoids (e.g., dexamethasone and prednisolone).

[14] In people over the age of 45 with more than two weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by esophagogastroduodenoscopy.

Furthermore, typical ulcers tend to heal and recur, and as a result the pain may occur for few days and weeks and then wane or disappear.

The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few minutes to several hours, and it may be worse when the stomach is empty.

Also, sometimes the pain may flare at night, and it can commonly be temporarily relieved by eating foods that buffer stomach acid or by taking anti-acid medication.

[15] Taking nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin[24] can increase the risk of peptic ulcer disease by four times compared to non-users.

Risk of bleeding increases if NSAIDs are combined with selective serotonin reuptake inhibitor (SSRI), corticosteroids, antimineralocorticoids, and anticoagulants.

[15] Peptic ulcers caused by NSAIDs differ from those caused by H. pylori as the latter's appear as a consequence of inflammation of the mucosa (presence of neutrophil and submucosal edema), the former instead as a consequence of a direct damage of the NSAID molecule against COX enzymes, altering the hydrophobic state of the mucus, the permeability of the lining epithelium and mitochondrial machinery of the cell itself.

[28] Dietary factors, such as spice consumption, were hypothesized to cause ulcers until the late 20th century, but have been shown to be of relatively minor importance.

One of the reasons that blood tests are not reliable for accurate peptic ulcer diagnosis on their own is their inability to differentiate between past exposure to the bacteria and current infection.

Additionally, a false negative result is possible with a blood test if the person has recently been taking certain drugs, such as antibiotics or proton-pump inhibitors.

[38] To perform this exam, the person is asked to drink a tasteless liquid that contains the carbon as part of the substance that the bacteria breaks down.

The ulcer is a round to oval parietal defect ("hole"), 2–4 cm diameter, with a smooth base and perpendicular borders.

[citation needed] A gastric peptic ulcer is a mucosal perforation that penetrates the muscularis mucosae and lamina propria, usually produced by acid-pepsin aggression.

[39] Conditions that may appear similar include: Prevention of peptic ulcer disease for those who are taking NSAIDs (with low cardiovascular risk) can be achieved by adding a proton pump inhibitor (PPI), an H2 antagonist, or misoprostol.

[15] Although misoprostol is effective in preventing peptic ulcer, its properties of promoting abortion and causing gastrointestinal distress limit its use.

NSAID-associated ulcers heal in six to eight weeks provided the NSAIDs are withdrawn with the introduction of proton pump inhibitors (PPI).

However, there is a higher rate of complication for those who underwent surgery to patch the stomach bleeding site when compared to repeated endoscopy.

[41] Peptic ulcer disease had a tremendous effect on morbidity and mortality until the last decades of the 20th century when epidemiological trends started to point to an impressive fall in its incidence.

The reason that the rates of peptic ulcer disease decreased is thought to be the development of new effective medication and acid suppressants and the rational use of nonsteroidal anti-inflammatory drugs (NSAIDs).

[42] Helicobacter pylori was identified in 1982 by two Australian scientists, Robin Warren and Barry J. Marshall, as a causative factor for ulcers.

[43] In their original paper, Warren and Marshall contended that most gastric ulcers and gastritis were caused by colonization with this bacterium, not by stress or spicy food, as had been assumed before.

[44] The H. pylori hypothesis was still poorly received,[45] so in an act of self-experimentation Marshall drank a Petri dish containing a culture of organisms extracted from a person with an ulcer and five days later developed gastritis.

In 1997, the Centers for Disease Control and Prevention, with other government agencies, academic institutions, and industry, launched a national education campaign to inform health care providers and consumers about the link between H. pylori and ulcers.

This campaign reinforced the news that ulcers are a curable infection and that health can be greatly improved and money saved by disseminating information about H.

[47] In 2005, the Karolinska Institute in Stockholm awarded the Nobel Prize in Physiology or Medicine to Marshall and his long-time collaborator Warren "for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease."

Marshall continues research related to H. pylori and runs a molecular biology lab at UWA in Perth, Western Australia.

A 1998 New England Medical Journal study found that mastic gum, a tree resin extract, actively eliminated the H. pylori bacteria.