ulcer(redirected from Buruli ulcer)
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ulcer, open sore or circumscribed erosion, usually slow to heal, on the skin or mucous membranes. It may develop as a result of injury; because of a circulatory disturbance, e.g., in varicose veins or after prolonged bed rest; or in association with such diseases as tuberculosis, syphilis, or leprosy. Corneal ulcers, which result from infection, allergy, or foreign objects in the eye, can cause visual impairment if not treated promptly. Some ulcers may develop into cancer. The underlying cause must be treated as well as the ulcerous lesion.
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 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.
a defect in the skin or mucous membrane resulting from tissue necrosis. Ulcers are frequently chronic in course and nonhealing, for example, trophic ulcers of the skin. They may be caused by prolonged mechanical (friction, pressure), thermal, chemical, and other actions on tissues, as well as by trophic disturbances of the nervous system, specific and nonspecific infections (tuberculosis, syphilis, leprosy, typhoid), and decomposition of a tumor. The development of an ulcer may also be fostered by metabolic disorders (for example, diabetes mellitus), chronic poisoning, vitamin deficiency, endocrinous disturbances, and exhaustion.
Ulcers vary in shape (round, oval, stellate), depth, and size. The base of an ulcer may be covered by granulations, a purulent deposit, or necrotic tissue. Deeply penetrating ulcers are dangerous because they destroy the walls of blood vessels and cause hemorrhages. If the course of the disease is favorable, the regenerative process is dominant and scarring occurs; however, recurrences are possible.
Treatment is directed toward curing the main disease. Physical therapy and any one of a variety of topical ointments and dressings may be prescribed. Surgery is required in refractory cases.
R. B. KAVTELADZE