Peptic ulcer occurs in the mucous membrane of the intestinal tract. An estimated 90% of peptic ulcers are caused by infection with a bacterium, Helicobacter pylori, strains of which promote the formation of ulcers by causing an inflammtory response in the cells of the stomach wall, making it more susceptible to the hydrochloric acid secreted by the stomach. Most commonly, it occurs in the stomach (gastric ulcer) or at the beginning of the small intestine (duodenal ulcer, the most common form) and causes abdominal pain, especially between meals.
Infection with the H. pylori bacterium, which is also associated with some stomach cancer, is very common, but not all strains promote the formation of ulcers. Approximately 50% of those over 60 in developed countries are infected in developing countries the infection rate is much higher, and infection usually occurs earlier in life. Experts are as yet uncertain how the bacterium is spread. Around 20% of those infected develop ulcers. Peptic ulcer is found more frequently in men. Heavy aspirin or ibuprofen use and smoking increase the risk of ulcer development.
The connection of H. pylori infection with peptic ulcer was made in the early 1980s by Australian scientists Barry J. Marshall and J. Robin Warren. It previously was believed that peptic ulcers were caused by emotional stress, though since the early 1900s researchers had reported finding curved bacteria in the stomachs of dead patients with ulcers more often than in those without ulcers. Marshall and Warren were awarded the Nobel Prize in physiology or medicine in 2005 for their work. Treatment changed accordingly and now typically consists of antibiotics (such as clarithromycin or amoxicillin) plus metronidazole (Flagyl) and bismuth subsalicylate (e.g., Pepto-Bismol). For the relief of symptoms, drugs such as ranitidine (Zantac), famotidine (Pepcid), cimetidine (Tagamet), and omeprazole (Prilosec) may also be used. Hemorrhage or perforation of peptic ulcers requires emergency medical treatment.
The full set of genes (genome) of H. pylori was determined in 1997. This achievement will help researchers design new drugs to treat and prevent diseases caused by the bacterium.
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