An ulcer is an open sore. The word peptic means that the cause of the problem is due to acid. The two most common types of peptic ulcer are called gastric ulcers and duodenal ulcers. These names refer to the location where the ulcer is found. Gastric ulcers are located in the stomach. Duodenal ulcers are found at the beginning of the small intestine known as the duodenum. A person may have both gastric and duodenal ulcers at the same time. 5-10% of the U.S. population develops peptic ulcer disease (PUD). PUD has 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.
Abdominal pains are the most common symptoms. A burning sensation is felt in the stomach region between the breastbone and the belly button. This pain is often felt when the stomach is empty, between meals generally, but it can occur at any time. The pain last anywhere from a few minutes to several hours. Others symptoms of PUD include nausea, vomiting of blood, heartburn, bloating, and loss of appetite and unexplained weight loss which happens in severe causes.

First of the distinct causes of PUD is the bacterium Helicobacter pylori (previously named as Campylobacter pylori) which lives on the mucous lining of the stomach. The enzyme urease is produced by the bacterium which divides urea into ammonia and carbon dioxide. While shielding the bacterium form the acidity of the stomach, the ammonia also damages the protective mucous layer and the underlying gastric cells. H pylori also produce catalase, an enzyme that may protect the microbe from engulfing and ingesting neutrophils, plus several adhesion protein that allow the bacterium to attach itself to gastric cells. Symptoms of an H. pylori infection include gastritis, indigestion (dyspepsia) and signs of bleeding in the digestive tract. Transmission of H. pylori is unknown but it is believed it may spread from person to person through fecal-oral or oral-oral routes. It may also be transmitted by contaminated water sources. H. pylori are becoming less common in the UK as living standards are improving. H. pylori infection is acquired predominantly in childhood.
Another common cause of PUD is the regular use of pain medications called non-steroidal anti-inflammatory drugs (NSAIDs), which include aspirin, ibuprofen, naproxen, ketoprofen, meloxicam and celecoxib. Risk of NSAIDs-induced ulcer is high when one is age 60 and above because the stomach lining becomes fragile with age. Past experiences of internal bleeding increase the risk of PUD. Taking steroid medications such as prednisone and blood thinners are among the risk factors of NSAIDs-induced ulcer. Excessive consumption of alcohol and tobacco is also a high risk factor of PUD. Taking large doses of NSAIDs and other medications containing aspirin over long period of time is another risk factor. NSAIDs are known to have certain side effects such as heartburn.
Zollinger Ellison Syndrome (ZES) can also develop into PUD. People who have ZES develop tumours known as gastrinomas in the pancreas and duodenum. The gastrinomas caused by ZES secrete the hormone gastrin. Because gastrin creates excessive stomach acid. A person with ZES may have only one gastrinoma or have several. It’s believed that approximately, one-quarter of ZES patients also have a genetic disorder known as multiple endocrine neoplasia type 1, which causes tumours in the pituitary and parathyroid glands. Another complication of ZES is that in up to two-thirds of cases, gastrinomas are cancerous.
These malignant gastrinomas can spread to other parts of the body, including the liver, lymph nodes, spleen, bones, or skin. ZES do not have symptoms but when symptoms occur, they are similar to that of PUD such as heartburn, abdominal pain, bleeding and nausea. Research has proven that alcohol abuse is high risk factor of ZES. ZES is treated by reducing the amount of acid your stomach produces. Medications called proton pump inhibitors are usually prescribed. These drugs, which include omeprazole, lansoprazole, pantoprazole and esomeprazole curb the production of stomach ulcers and allow the ulcers to heal. Also medications known as H2-blockers, such as cimetidine could be prescribed. However, these medications do not work as well to reduce stomach acids. In severe cases, surgery is undergone for the peptic ulcer and to remove the gastrinoma. However, only 20-25% of patients that undergo surgery are cured. For cancerous tumours, radiation and chemotherapy may be offered.
PUD can be diagnosed by taking the urea breath test which a test is taken to detect the presence of H. pylori. It is not advised to take any antibiotics or proton pump inhibitors 2 weeks prior to the test. The stool antigen test can be also taken to check for the H. pylori. This test is taken to look for H. pylori in excreted faeces. Research has proven that the stool antigen test like the urea breath test is influenced by proton pump inhibitors. In a study conducted in Japan to investigate the effects of proton pump inhibitor treatment on the stool antigen treatment using the TestMate pylori enzyme immunoassay. 28 patients were assessed in this study of which 16 were men and 12 women with mean age (63.1 ±5.9) years and age range of 25-84 years, underwent stool antigen test and urea breath test before and after the administration of proton pump inhibitors (PPI). With standards set on the urea breath test, the sensitivity, specificity and the agreement of the stool antigen test in all 28 patients were 95.2%, 71.4%, and 89.3%, respectively, before PPI administration, and 88.9%, 90.9%, and 89.3%, respectively, after PPI treatment. Mean values of urea breath test were 23.98% ± 5.33% before and 16.19% ± 4.75% after PPI treatment and, in 15 patients treated for 4 weeks or more, were significantly lower after than before the 4 weeks of PPI treatment. It was concluded that the stool antigen test was equally sensitive to the urea breath test, making it a useful and reliable diagnostic method, even during PPI administration.
Gastrointestinal endoscopy is the more advance way of treating ulcers. Gastrointestinal endoscopy has undergone a remarkable expansion in its capabilities as a result of sophisticated technological advances in recent years. New imaging technologies, novel ablation and resection techniques, cutting-edge endoscope development and creative extraluminal applications have taken gastrointestinal endoscopy to an exciting new level. An update on some of these advances is presented for the physician audience.