Peptic Ulcer Disease (PUD for short) is the term used to describe wounds or sores that develop in the lining of the stomach (gastric ulcers) or in the lining of the upper part of the small intestine (duodenal ulcers). These ulcers can not only be uncomfortable causing you pain, but can also lead to other complications that may be dangerous. Ulcers can heal of their own accord but in the majority of people who do not get treatment, the ulcers tend to recur.
A peptic ulcer is a sore or break in the lining of any part within the digestive tract that contains concentrated gastric juice. The main components of gastric juice are water, mucus, hydrochloric acid, enzymes, and electrolytes. Ulcers most commonly occur in the first part of the small intestine below the stomach (duodenum), and can occur at the lower end of the esophagus or in the stomach.Most ulcers result from infection with bacteria called Helicobacter pylori (H. pylori).
Contrary to old beliefs, neither eating spicy food nor living a stressful life cause ulcers. H. pylori bacteria weaken the protective mucous coating of the esophagus, stomach, or duodenum, which then allows acid to get through to the sensitive lining beneath. Both acid and H. pylori irritate the lining and cause a sore (ulcer) to form.
It is unclear how these bacteria spread from person to person and why only a small percentage of those who have H. pylori within the stomach go on to develop peptic ulcers. Just because you have H. pylori bacteria populating your stomach does not mean you will get an ulcer, although most diagnosed with ulcers also have an H. pylori infection.
Another cause of ulcers is the regular use of pain medications called non-steroidal anti-inflammatory drugs (NSAIDs), which include aspirin and ibuprofen. Frequent or long-time use of NSAIDs, especially among the elderly population, can increase the risk of developing an ulcer. About 10% of Canadians will experience peptic ulcers at some point throughout their lives.
Hostile vs protective factor
“No gastric acid, no peptic ulcer” is a misconception. Excessive gastric acid secretion is only one factor in the pathogenesis of peptic ulcer disease. Decreased mucosal defense against gastric acid is another cause.
The integrity of the upper gastrointestinal tract is dependent upon the balance between “hostile” factors such as gastric acid, H. pylori, NSAIDs and pepsin, and “protective” factors such as prostaglandins, mucus, bicarbonate, and blood flow to mucosa affecting gastrointestinal mucosa.
Injury to gastric and duodenal mucosa develops when deleterious effects of gastric acid overwhelm the defensive properties of the mucosa. Inhibition of endogenous prostaglandin synthesis leads to a decrease in epithelial mucus, bicarbonate secretion, mucosal blood flow, epithelial proliferation, and mucosal resistance to injury.
Lower mucosal resistance increases the incidence of injury by endogenous factors such as acid, pepsin, and bile salts as well as exogenous factors such as NSAIDs, ethanol and other noxious agents
Other causes1. Use of non-steroid anti-inflammatory drugs (NSAID)
A small but important percentage of patients have adverse gastrointestinal events associated with NSAID use that results in substantial morbidity and mortality. Risk factors for the development of NSAID-associated gastric and duodenal ulcers include advanced age, history of previous ulcer disease, concomitant use of corticosteroids and anticoagulants, higher doses of NSAIDs, and serious systemic disorders. The concept of gastroduodenal mucosal injury has evolved from the notion of topical injury to concepts that involve multiple mechanisms.
NSAIDs initiate mucosal injury topically by their acidic properties. By diminishing the hydrophobicity of gastric mucus, endogenous gastric acid and pepsin may injure surface epithelium. Systemic effects of NSAIDs appear to play a predominant role through the decreased synthesis of mucosal prostaglandins.
The precursor of prostaglandins, arachidonic acid, is catalyzed by the two cyclo-oxygenase isoenzymes, cyclo-oxygenase-1 and cyclo-oxygenase-2. The gene for cyclo-oxygenase-1, the housekeeping enzyme, maintains the homeostasis of organs. Cyclo-oxygenase-2, the inflammatory enzyme, is inducible. Although NSAIDs can inhibit both pathways, only the gene for cyclo-oxygenase-2 contains a corticosteroid-responsive repressor element.
Literature suggests that the anti-inflammatory properties of NSAIDs are mediated through inhibition of cyclo-oxgenase-2, and adverse effects, such as gastric and duodenal ulceration, occur as a result of effects on the constitutively expressed cyclo-oxygenase-1.
H. pylori is prevalent among 22–63% of patients taking NSAIDs. Most studies do not show a significant difference in H. pylori prevalence between NSAID users and nonusers. Gastritis in patients on NSAID therapy appears to be related to underlying H. pylori rather than drug use.
The lower incidence of H. pylori among patients with gastric ulcers than those with duodenal ulcers is presumably the result of NSAID use. NSAIDs are more likely to cause gastric than duodenal ulcers. NSAIDs appear to cause ulcers by a mechanism independent of H. pylori based on the inhibition of prostaglandin synthesis.
2. Bacterium Helicobacter pylori.
H. pylori is the etiologic factor in most patients with peptic ulcer disease and may predispose individuals to the development of gastric carcinoma. H. pylori colonizes in the human stomach. The method of H. pylori transmission is unclear, but seems to be person-to-person spread via a fecal-oral route. The prevalence of H. pylori in adults appears to be inversely related to the socioeconomic status. It is also thought that water is a reservoir for transmission of H. pylori.
3. Gastrinoma (Zollinger-Ellison Syndrome)
The classic triad of Zollinger-Ellison syndrome involves peptic ulcers in unusual locations (i.e., the jejunum), massive gastric acid hypersecretion, and a gastrinproducing islet cell tumor of the pancreas (gastrinoma).
Gastrinoma in the pancreas appears in approximately 50% of patients. Another 20% of patients have it in the duodenum and others have it in the stomach, peripancreatic lymph nodes, liver, ovary, or small-bowel mesentery.
Zollinger-Ellison syndrome accounts for only 0.1% of all duodenal ulcer disease. One fourth of patients have this syndrome as part of the multiple neoplasia syndrome Type I (MEN I). Patients with gastrinoma may have intractable ulcer disease. Because gastrin is trophic to the gastric mucosa, endoscopy or x-ray may demonstrate hypertrophy of the gastric rugae. Patients may also experience diarrhea (including steatorrhea from acid inactivation of lipase) and gastroesophageal reflux. These symptoms are episodic in 75% of patients.
Hypercalcemia has a direct bearing on the gastric acid hypersecretory state found in patients with Zollinger-Ellison syndrome and MEN I. Intravenous calcium infusion in normal volunteers induces gastric acid hypersecretion. Additionally, calcium has been demonstrated in vivo and in vitro to stimulate gastrin release directly from gastrinomas.
Resolution of hypercalcemia (by parathyroidectomy) reduces the basal acid output and serum gastrin concentration in fasting gastrinoma patients and those with MEN I, suggesting that resolution of hypercalcemia plays an important role in the therapy of this subgroup of patients.
5. Genetic Factors
Genetic factors play a role in the pathogenes is of ulcer disease. The lifetime prevalence of developing ulcer disease in first-degree relatives of ulcer patients is about three times greater than the general population. Approximately 20–50% of duodenal ulcer patients report a positive family history; gastric ulcer patients also report clusters of family members who are likewise affected.
The literature reveals a strong positive correlation between cigarette smoking and the incidence of ulcer disease, mortality, complications, recurrences and delay in healing rates. Smokers are about two times more likely to develop ulcer disease than nonsmokers. Cigarette smoking and H. pylori are co-factors for the formation of peptic ulcer disease.
There is a strong association between H. pylori infection and cigarette smoking in patients with and without peptic ulcers. Cigarette smoking may increase susceptibility, diminish the gastric mucosal defensive factors, or may provide a more favorable milieu for H. pylori infection.
Numerous studies have revealed conflicting conclusions regarding the role of psychological factors in the pathogenesis and natural history of peptic ulcer disease. The role of psychological factors is far from established. Acute stress results in increases in pulse rate, blood pressure and anxiety, but only in those patients with duodenal ulcers did acute stress actually result in significant increases in basal acid secretion.
There is no clearly established “ulcer-type” personality. Ulcer patients typically exhibit the same psychological makeup as the general population, but they appear to perceive greater degrees of stress. In addition, there is no evidence that distinct occupational factors influence the incidence of ulcer disease.
8. Alcohol and Diet
Although alcohol has been shown to induce damage to the gastric mucosa in animals, it seems to be related to the absolute ethanol administered (200 proof). Pure ethanol is lipid soluble and results in frank, acute mucosal damage.
Because most humans do not drink absolute ethanol, it is unlikely there is mucosal injury at ethanol concentrations of less than 10% (20 proof). Ethanol at low concentrations (5%) may modestly stimulate gastric acid secretions; higher concentrations diminish acid secretion.
Though physiologically interesting, this has no direct link to ulcerogenesis or therapy. Some types of food and beverages are reported to cause dyspepsia. There is no convincing evidence that indicates any specific diet causes ulcer disease.
Epidemiologic studies have failed to reveal a correlation between caffeinated, decaffeinated, or cola-type beverages, beer, or milk with an increased risk of ulcer disease. Dietary alteration, other than avoidance of pain-causing foods, is unnecessary in ulcer patients.
The most common symptom of an ulcer is a burning pain in the upper abdomen, somewhere between the breastbone and the navel. The pain can last anywhere from a few minutes to several hours, often occurs between meals, and can awaken you from sleep. Food or antacids might temporarily relieve the discomfort. Less common symptoms of an ulcer include nausea, vomiting, lack of appetite, and weight loss.
There are three main complications of peptic ulcers: bleeding, perforation, and obstruction.
Bleeding may be the first and only symptom of an ulcer. Bleeding ulcers can cause vomiting of acidified blood that looks like ‘old coffee grounds’ and/or bowel movements that become tarry black. When an ulcer bleeds and continues to bleed without treatment, a person may become anemic and weak.
Perforation can occur when ulcers go untreated, as gastric juices can make a hole through (perforate) the stomach and/or duodenal lining, requiring surgery to close the opening.
Obstruction is a complication that can occur when chronic inflammation from the ulcer causes swelling and scarring. Over time, this scarring may close (obstruct) the outlet of the stomach, preventing the passage of food and causing vomiting and weight loss. Surgery is required to repair obstructions. It is important to contact a physician immediately if your ulcer symptoms worsen.
The most common tests used to check for the presence of an ulcer are:
Upper GI series
X-rays are taken after the patient swallows a special liquid to coat the esophagus, stomach, and upper part of the small intestine.
A physician passes a long flexible tube with a tiny video camera on the end (endoscope) through the patient’s mouth and down the esophagus to the stomach to look for the presence of inflammation or ulcers. If necessary, the physician removes a small sample of tissue (biopsy) for further testing.
Tests for H. pylori
There are several tests available to detect Helicobacter pylori infection. These include a simple breath test, checking the blood for antibodies to the bacteria, or examination of stomach biopsies.
Dietary and Lifestyle Modifications
Physicians often recommend lifestyle and dietary changes for persons with ulcers in addition to medications, until complete healing occurs. Patients should avoid certain foods and beverages such as chocolate, coffee, alcohol, fatty foods, peppermint, citrus fruits and juices, tomato products, pepper, mustard, and vinegar during healing.
Eating smaller meals that are more frequent may also control symptoms better. Smoking cessation is important, as smoking inhibits ulcer healing. You should also not take NSAIDs, such as aspirin or ibuprofen. Your physician will probably lift any dietary restrictions once your ulcers have healed.
The cause of your ulcer will determine the type of medical treatment that your physician recommends. If caused by NSAID use, then your doctor may discontinue prescribing NSAID medication, may suggest a different pain medication, or may continue NSAID use and add another medication to protect your stomach and duodenum, such as a proton pump inhibitor (PPI), which blocks stomach acid production.
If H. pylori infection is the cause of your ulcer, then your doctor may prescribe a treatment plan to kill the infection while reducing the acid in your stomach. Usually, this is a combination of one or more antibiotics (to kill the bacteria) plus a PPI. It is important to follow the treatment plan exactly as your doctor prescribes. This treatment can permanently cure 80-90% of peptic ulcers.
Some of the common antibiotic medications prescribed for treatment of ulcers caused by H. pylori infection include amoxicillin, clarithromycin, tetracycline, and metronidazole. It is important to take antibiotic prescriptions until they are complete. This helps prevent the growth of superbugs (more resistant bacteria) that might make subsequent infections more difficult to treat.
Usually a PPI is prescribed along with an antibiotic. The PPIs work by blocking an enzyme necessary for acid secretion. These include omeprazole (Losec®), lansoprazole (Prevacid®), pantoprazole sodium (Pantoloc®), esomeprazole (Nexium®), rabeprazole (Pariet®), pantoprazole magnesium (Tecta®), and dexlansoprazole