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MirelaStancu, MD

Definition

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.

Epidemiology

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.

Symptoms

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.

Diagnosis

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.

Clinical Course and Complications

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.

Treatment Options

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.

More Information

Additional information about gastric disorders:

National Digestive Diseases

The American Gastroenterological Association

Mayo Clinic

Helicobacter pylori Foundation

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  • 1. MirelaStancu, MD Definition 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. Epidemiology 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. Symptoms 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
  • 2. indicate serious complications such as perforated ulcer, bleeding ulcer or narrowing (stenosis) of the gastric outlet. Diagnosis 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. Clinical Course and Complications 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. Treatment Options 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,
  • 3. 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. More Information Additional information about gastric disorders: National Digestive Diseases The American Gastroenterological Association Mayo Clinic Helicobacter pylori Foundation << PREVIOUS | HOME Healthcare Professionals Patients and General Public