Home
Contact Us
Sitemap
AccessibilityGastric ulcers
A peptic ulcer is a deep lesion in the lining of the stomach (gastric ulcer) or duodenum (duodenal ulcer) that extends to the submucosa. It is caused in part by the erosive action of HCl and pepsin on the mucosa.
Prevalence
Approximately 15% of the Western population will suffer from an ulcer at sometime during their lives. Duodenal ulcers are approximately seven times more common than gastric ulcers, and whereas duodenal ulcers occur most frequently in men aged 20–50 years, gastric ulcers are more prevalent in men over 50 years of age.
Causes of gastric ulcers
Gastric ulcers can occur anywhere in the stomach, but are more commonly found on the lesser curvature of the stomach wall. Gastric ulcers are not normally caused by over secretion of acid or pepsin but arise due to reduced resistance of the stomach lining to gastric juice. Under normal conditions, the stomach mucosa is protected by mucus secretion from the surface mucous cells, local bicarbonate production, mucosal blood flow and prostaglandin-enhanced rapid renewal of damaged mucosal cells (Table 1). If this protective layer is not present, the mucosa is more susceptible to peptic damage.TABLE 1 – Factors that can contribute to the formation of gastric ulcers
| Aggressive | Defensive |
Excessive –
|
Reduced –
|
Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, interfere with the stomach’s ability to produce mucus and bicarbonate, and affect blood flow to the stomach and the capacity of the stomach to repair and renew cells. The combination of these effects can cause the stomach’s defence mechanisms to fail, increasing the likelihood of ulcers developing. Symptoms of gastric ulceration include vomiting and pain in the upper abdomen soon after eating.
Ulcer complications
Deep, penetrating ulcers may expose and erode the blood vessels in the muscle layers of the stomach and can result in internal haemorrhage requiring emergency treatment or surgery. Excess GI bleeding commonly results in anaemia or, rarely, fatal collapse. In some circumstances erosion occurs through the entire serosa, a condition known as a perforated ulcer. When this happens bacteria and partially digested food are able to pass into the peritoneal cavity, resulting in peritonitis. Perforation is more common with duodenal ulcers and occurs in men more than in women.
Lifestyle factors that contribute to ulcer formation
- Smoking increases the likelihood of developing an ulcer, as well as slowing the healing of existing ulcers and contributing to their recurrence
- Caffeine present in coffee (including decaffeinated), tea, soft drinks and foods stimulates acid production by the stomach and aggravates existing ulcers
- Alcohol consumption has not been proven as a risk factor for peptic ulcers, but they are more common in people with cirrhosis of the liver
- Stress is no longer considered a cause of ulcers; however, stress can increase the pain associated with existing ulcers
H. pylori and gastric ulcers
Although lifestyle and the effects of acid and pepsin on the sensitive mucosa undoubtedly contribute to ulcer formation, H. pylori infection is now considered to be the primary cause.
Helicobacter is a genus of spiral flagellated Gram-negative bacteria and is found in all regions of the stomach, but predominates in the antrum. Research has shown that the bacterium, combined with acid secretion, damages stomach and duodenal tissue causing inflammation (chronic gastritis) and ulcers. Indeed, the bacterium causes approximately 80% of gastric ulcers and more than 90% of duodenal ulcers,[Marshall & Warren, 1984] and because of this, has been classified by WHO as a Class I carcinogen.
A significant proportion of the world’s population is H. pylori-positive, with the incidence being higher in less developed countries, low socio-economic groups and the ageing population. The eradication of H. pylori (usually with anti-secretory agents such as proton pump inhibitors [PPIs] and antibiotics given together for 1–2 weeks as either dual or triple therapy) is a primary aim of therapy in this disease and usually results in complete healing of the ulcer.
For more information on H. pylori in peptic disease, see also:
http://digestive.niddk.nih.gov/ddiseases/pubs/hpylori/index.htm
http://www.gpnotebook.co.uk/simplepage.cfm?ID=1040580613&linkID=17540&cook=yes
http://www.npc.co.uk/MeReC_Bulletins/2001Volumes/pdfs/vol12no1.pdf
H. pylori and GORD
In contrast to the relationship between peptic disease and H. pylori infection, the contribution of H. pylori to the pathology of GORD has not been conclusively demonstrated,[O’Connor & Cunnane, 1994] and epidemiological studies have shown that patients with GORD have similar incidence rates of H. pylori infection as controls.[McNamara & O’Morain, 1999] Indeed, there is some evidence to suggest that H. pylori colonisation may protect from GORD.The most likely mechanisms for this are increased intragastric ammonia production and pangastritis with gastric atrophy and intestinal metaplasia, which both promote hypoacidity.[Richter, 1999]
Although H. pylori may aggravate reflux in some susceptible patients, its eradication with aggressive anti-secretory and antibiotic therapy often confers no advantage, and may exacerbate the disease. In addition, some studies have indicated that H. pylori may migrate to the body of the stomach during anti-secretory therapy with omeprazole, thus accelerating progression of gastritis to atrophy of the stomach mucosa.[Kuipers et al. 1996] Another study demonstrated that the predicted rank order for the presence of GORD and its complications (eg, peptic stricture and Barrett’s oesophagus) was highest in the H. pylori-positive patient population.[Graham & Yamaoka, 1998]
