Under the Microscope/Prof William Reville: Peptic ulcers occur in the lining of the stomach or duodenum and are common. About one in 10 people develop an ulcer at some time.
About two-thirds of all ulcers are caused by a bacterium called Helicobacter pylori, or H pylori for short. Most other ulcers are caused by prolonged use of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen. Heavy drinking of alcohol and stress can contribute to peptic ulcers. H pylori can also initiate the most common form of stomach cancer. Peptic ulcers can be successfully treated.
H pylori is an ancient organism but it has been disappearing from the developed world over the past century because of improved hygiene and increased use of antibiotics. As H pylori has declined, the rates of peptic ulcers and stomach cancers have gone down, but, unexpectedly, diseases of the oesophagus have dramatically increased. Evidence indicates that the rise in oesophageal disease is related to the decline in H pylori. The story is told by Martin Blaser in Scientific American, February 2005.
The system of channels through which food passes, from its entry in the mouth to the final stage of the excretion of the indigestible part of it at the anus, is called the alimentary tract. The food passes from the mouth through the oesophagus into the stomach, then into the duodenum (the start of the small intestine) and through the small intestine and the large intestine to the anus. The gastrointestinal (GI) tract extends from and includes the stomach and down through the intestines. The environment inside the stomach is very acidic. Food passes from the stomach on into the small intestine from where much of it, in digested form, is absorbed into the body.
The inner wall of the alimentary canal is coated with a layer of mucus. This serves the two-fold purpose of a lubricant and a protective barrier for the underlying cells that line the alimentary tract. The protective function of the mucus layer is particularly important in the stomach whose contents are very acidic, and also in the duodenum. H pylori has found a home in the protective mucus layer of the stomach and, sometimes, the duodenum. Both H pylori and NSAIDs can weaken the protective lining allowing the corrosive acid to reach the stomach or duodenal wall.
H pylori infection is common. In the USA, about 20 per cent of people aged less than 40 and half of those more than 60 have H pylori infection. However, most infected people do not develop ulcers.
Infection rates with H pylori are much greater in less-developed regions of the world. The reasons for the differences are hygiene standards and use of antibiotics. In developing countries, 70 to 100 per cent of children are infected with H pylori by age 10 and most remain infected for life. Fewer than 10 per cent of US-born children carry H pylori.
As infections by H pylori have declined in developed countries, so too has the incidence of peptic ulcers and stomach cancer. However, since the 1970s epidemiologists have noted a dramatic increase in oesophageal disease in developed countries, particularly cancer and gastroesophageal reflux disease, a chronic disorder involving regurgitation of acidic stomach contents into the oesophagus.
The contents of the stomach are extremely acidic, but yet H pylori can live there.
However, the bacterium can tolerate only so much acid, and Blaser proposes that the bacterium and the host live in a situation regulated by negative feedback controls. These feedbacks ensure that the bacterium does not do too much harm to the host and the host does not damage the bacterium by secreting too much acid into the stomach. In effect, the bacterium regulates the degree of acidity of the stomach. But, if H pylori is absent, as is increasingly becoming the case in developed countries, the stomach is not regulated to maintain moderate levels of acidity. The resulting swings of stomach acidity may be central to the rise in oesophageal diseases, which are apparently triggered by exposure of the oesophagus to highly acid stomach contents.
William Reville is associate professor of biochemistry and director of microscopy at UCC