Peptic ulcer disease is characterized by variable degrees of inflammation involving
gastric (gastritis) and duodenal linings (duodenitis), caused when gastric acid (gastric
juice) penetrates the protective mucus barrier. Depending on the severity of disease,
patients may develop superficial erosions limited to the most inner layer of the stomach
or duodenum (mucosa) or deep, penetrating ulcers involving the entire gastric or duodenal
wall.
It is estimated that 4 million Americans have peptic ulcer disease.
The most common cause for peptic ulcer disease is infection with a spiral shaped
bacterium called Helicobacter pylori (H. pylori). H. pylori lives within the protective
mucus layer that coats the gastric lining (mucosa). This organism can weaken the mucus
layer and allow the damaging gastric juice to irritate the gastric lining resulting in
acute or chronic inflammation (gastritis). It is not currently known how this organism is
spread, but it appears to be transmitted from person to person through close contact and
by ingesting contaminated food or water. H. pylori gastritis is one of the most common
infections in the world, more common in the developing than the industrialized (Western)
countries. In the United States, 20% of the young adults and about 50% of the patients
older than 60, are infected. The infection appears to be acquired in the childhood and
remains throughout the life, until cured by antibiotic treatment.
The next most common cause for peptic ulcer disease is long-term use of pain relieving
drugs (aspirin, Advil, Motrin, Aleve, Ketoprofen, and others, collectively named NSAIDs -
Non Steroidal Anti-Inflammatory Drugs). These drugs can damage the gastric or duodenal
mucosa by two mechanisms: 1) they block the release of a cytoprotective substance
(prostaglandin) from the inflammatory cells in the stomach, and 2) they can induce direct
damage by lodging within the gastric or duodenal mucosa. When used sporadically and in
small amount, the NSAIDs can cause minimal or no tissue damage, especially if taken with
large quantities of water (at least 8 oz), with food, milk or antiacids. However, when
used regularly or in large quantities, these drugs can lead to chronic gastritis and
ulcers.
Other causes of gastritis include excessive alcohol use (hemorrhagic gastritis), reflux
of bile into the stomach (bile reflux gastritis), antibodies produced by the immune system
against certain cells in the gastric mucosa (autoimmune gastritis) and stress.
The most common symptom of ulcer is gnawing or burning pain in the upper abdomen. The
pain may come and go for several days or weeks, starts about 2-3 hours after a meal, may
occur in the middle of the night, and is relieved by food or antiacid medication.
Other symptoms include nausea, vomiting, bloating, belching, poor appetite, weight
loss.
Emergency signs and symptoms that should prompt a visit to the physician include sharp,
sudden and persistent stomach pain, bloody or black stools and bloody or black (similar to
coffee ground) vomitus. These signs may indicate serious complications such as perforated
ulcer, bleeding ulcer or narrowing (stenosis) of the gastric outlet.
Several tests are routinely recommended for the diagnosis of gastric or duodenal ulcer:
upper gastrointestinal series (X-ray of the esophagus, stomach and duodenum) and/or upper
endoscopy. The X-rays are taken after drinking a white, milky liquid (barium) that coats
the lining of the digestive organs allowing to see any defect in the lining that indicates
the presence of ulcer. During the upper endoscopy a thin tube equipped with a video camera
(endoscope) is placed in the esophagus, stomach and duodenum. The images captured by the
camera are transmitted to a video monitor and examined by the endoscopist during the
procedure. An ulcer appears like a defect (hole) in the mucosal lining, that could be
covered by blood or have a clean, white base. During the same procedure, tiny tissue
fragments (biopsies) can be removed from the diseased area and sent to the pathology lab
for microscopic examination and diagnosis.
Once a diagnosis of peptic ulcer disease is confirmed, additional tests are necessary
to determine the cause of the ulcer, because different types of ulcers are treated
differently.
Blood tests are usually ordered to check for the presence of antibodies against H.
pylori. A positive test indicates that the patient came in contact, recently or in the
past, with the bacterium, but it doesn't necessarily indicate current infection.
Breath test for H. pylori is an effective diagnostic test, performed in the doctor's
office, during which the patient drinks a solution of urea (a chemical compound that is
metabolized by an enzyme called urease, secreted by H. pylori). This compound is marked
with a special carbon atom, which is released in the blood when the urease breaks down the
urea. The blood carries the carbon to the lungs, where the patient exhales it. This test
is very accurate and if positive, indicates the presence of current infection with H.
pylori.
Stool tests detect the presence of H. pylori bacteria in the fecal material and if
positive, indicate the presence of current infection.
The tissue tests use mucosal samples (biopsies) removed during upper endoscopy, for the
diagnosis of H. pylori. One test (rapid urease test, Pyloritek) detects the urease enzyme
produced by H. pylori. Another test consists of examination of the tissue under the
microscope and uses special stains that highlight the microorganisms.
The clinical course may be prolonged and can be complicated by bleeding, acute
perforation and peritonitis, or narrowing of the gastric outlet leading to vomiting and
weight loss. Another rare complication is gastric cancer.
The treatment of peptic ulcer disease depends on the specific causes and may require
lifestyle changes (stop smoking and alcohol use, limit the intake of spicy foods), medical
treatment or, rarely, surgery.
The medical treatment in the case of H. pylori gastritis is aimed at killing the
bacteria, reducing the gastric acid and protecting the gastric lining. Antibiotics that
are routinely used for killing H. pylori include metronidazole, tetracycline,
clarithromycin and amoxicillin. Antiacid medication is used in conjunction with antibiotic
therapy in order to decrease the amount of gastric acid, help heal the ulcer and reduce
the gastric pain. The most potent acid-suppressing drugs are the proton pump inhibitors
such as omeprazole, lansoprazole, esomeprazole and pantoprazole. The mucosal protectors
(bismuth subsalicylate) are used to protect the stomach lining from the damaging effect of
the gastric acid.
These agents must be used in combination in order to be effective in eradication of H.
pylori infection. The most commonly used regimen called the triple therapy, involves two
antibiotics and either an acid suppressor or a mucosal protector taken daily for two
weeks.
Surgery may be needed for those patients in whom the ulcers fail to heal or develop
complications (bleeding, perforation or obstruction). During the surgery, the surgeon my
remove the ulcer together with a narrow rim of tissue, or, depending on the size and
location of the ulcer, may remove the entire lower portion of the stomach together with
part of the duodenum.
Patients that have peptic ulcer disease due to long standing treatment with pain
relievers (NSAIDs) should substitute their current drugs with different pain-relief
medications that are not as damaging to the gastric or duodenal lining (for example,
acetaminophen). In addition, they should consult with their doctor regarding adding a
mucosal protective drug to their regular anti-inflammatory treatment.
Additional information about gastric disorders:
National Digestive
Diseases
The American
Gastroenterological Association
Mayo Clinic
Helicobacter pylori Foundation
