v H. pylori and Peptic Ulcer What is a peptic ulcer? A peptic ulcer is a sore on the lining of the stomach or duodenum, which is the beginning of the small intestine. Peptic ulcers are common: One in 10 Americans develops an ulcer at some time in his or her life. One cause of peptic ulcer is bacterial infection, but some ulcers are caused by long-term use of nonsteroidal antiinflammatory agents (NSAIDs), like aspirin and ibuprofen. In a few cases, cancerous tumors in the stomach or pancreas can cause ulcers. Peptic ulcers are not caused by stress or eating spicy food, but these can make ulcers worse. What is H. pylori? Helicobacter pylori (H. pylori) is a type of bacteria. Researchers believe that H. pylori is responsible for the majority of peptic ulcers. H. pylori infection is common in the United States: About 20 percent of people under 40 years old and half of those over 60 years have it. Most infected people, however, do not develop ulcers. Why H. pylori does not cause ulcers in every infected person is not known. Most likely, infection depends on characteristics of the infected person, the type of H. pylori, and other factors yet to be discovered.

Researchers are not certain how people contract H. pylori, but they think it may be through food or water. Researchers have found H. pylori in the saliva of some infected people, so the bacteria may also spread through mouth-to-mouth contact such as kissing.

How does H. pylori cause a peptic ulcer?

H. pylori weakens the protective mucous coating of the stomach and duodenum, which allows acid to get through to the sensitive lining beneath. Both the acid and the bacteria irritate the lining and cause a sore, or ulcer.

H. pylori is able to survive in stomach acid because it secretes enzymes that neutralize the acid. This mechanism allows H. pylori to make its way to the “safe” area—the protective mucous lining. Once there, the bacterium’s spiral shape helps it burrow through the lining.

What are the symptoms of an ulcer?

Abdominal discomfort is the most common symptom. This discomfort usually

Other symptoms include

Some people experience only very mild symptoms, or none at all.

Emergency Symptoms

If you have any of these symptoms, call your doctor right away:

They could be signs of a serious problem, such as

How is an H. pylori-related ulcer diagnosed?

Diagnosing an Ulcer   To see whether symptoms are caused by an ulcer, the doctor may do an upper gastrointestinal (GI) series or an endoscopy. An upper GI series is an x ray of the esophagus, stomach, and duodenum. The patient drinks a chalky liquid called barium to make these organs and any ulcers show up more clearly on the x ray. An endoscopy is an exam that uses an endoscope, a thin, lighted tube with a tiny camera on the end. The patient is lightly sedated, and the doctor carefully eases the endoscope into the mouth and down the throat to the stomach and duodenum. This allows the doctor to see the lining of the esophagus, stomach, and duodenum. The doctor can use the endoscope to take photos of ulcers or remove a tiny piece of tissue to view under a microscope. This procedure is called a biopsy. If an ulcer is bleeding, the doctor can use the endoscope to inject drugs that promote clotting or to guide a heat probe that cauterizes the ulcer.

Diagnosing H. pylori

If an ulcer is found, the doctor will test the patient for H. pylori. This test is important because treatment for an ulcer caused by H. pylori is different from that for an ulcer caused by NSAIDs.

H. pylori is diagnosed through blood, breath, stool, and tissue tests. Blood tests are most common. They detect antibodies to H. pylori bacteria. Blood is taken at the doctor’s office through a finger stick.

Urea breath tests are an effective diagnostic method for H. pylori. They are also used after treatment to see whether it worked. In the doctor’s office, the patient drinks a urea solution that contains a special carbon atom. If H. pylori is present, it breaks down the urea, releasing the carbon. The blood carries the carbon to the lungs, where the patient exhales it. The breath test is 96 percent to 98 percent accurate.

Stool tests may be used to detect H. pylori infection in the patient’s fecal matter. Studies have shown that this test, called the Helicobacter pylori stool antigen (HpSA) test, is accurate for diagnosing H. pylori.
Tissue tests are usually done using the biopsy sample that is removed with the endoscope. There are three types:

In diagnosing H. pylori, blood, breath, and stool tests are often done before tissue tests because they are less invasive. However, blood tests are not used to detect H. pylori following treatment because a patient’s blood can show positive results even after H. pylori has been eliminated.

How are H. pylori peptic ulcers treated?

Drugs Used to Treat H. pylori

Peptic UlcersAntibiotics: metronidazole, tetracycline, clarithromycin, amoxicillinH2 blockers: cimetidine, ranitidine, famotidine, nizatidine, Proton pump inhibitors: omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprozoleStomach-lining protector: bismuth subsalicylate.

H. pylori peptic ulcers are treated with drugs that kill the bacteria, reduce stomach acid, and protect the stomach lining. Antibiotics are used to kill the bacteria. Two types of acid-suppressing drugs might be used: H2 blockers and proton pump inhibitors.

H₂ blockers work by blocking histamine, which stimulates acid secretion. They help reduce ulcer pain after a few weeks. Proton pump inhibitors suppress acid production by halting the mechanism that pumps the acid into the stomach. H₂ blockers and proton pump inhibitors have been prescribed alone for years as treatments for ulcers. But used alone, these drugs do not eradicate H. pylori and therefore do not cure H. pylori-related ulcers. Bismuth subsalicylate, a component of Pepto-Bismol, is used to protect the stomach lining from acid. It also kills H. pylori.

Treatment usually involves a combination of antibiotics, acid suppressors, and stomach protectors. Antibiotic regimens recommended for patients may differ across regions of the world because different areas have begun to show resistance to particular antibiotics.

The use of only one medication to treat H. pylori is not recommended. At this time, the most proven effective treatment is a 2-week course of treatment called triple therapy. It involves taking two antibiotics to kill the bacteria and either an acid suppressor or stomach-lining shield. Two-week triple therapy reduces ulcer symptoms, kills the bacteria, and prevents ulcer recurrence in more than 90 percent of patients.

Unfortunately, patients may find triple therapy complicated because it involves taking as many as 20 pills a day. Also, the antibiotics used in triple therapy may cause mild side effects such as nausea, vomiting, diarrhea, dark stools, metallic taste in the mouth, dizziness, headache, and yeast infections in women. (Most side effects can be treated with medication withdrawal.) Nevertheless, recent studies show that 2 weeks of triple therapy is ideal.

Early results of studies in other countries suggest that 1 week of triple therapy may be as effective as the 2-week therapy, with fewer side effects.

Another option is 2 weeks of dual therapy. Dual therapy involves two drugs: an antibiotic and an acid suppressor. It is not as effective as triple therapy.

Two weeks of quadruple therapy, which uses two antibiotics, an acid suppressor, and a stomach-lining shield, looks promising in research studies. It is also called bismuth triple therapy.

Can H. pylori infection be prevented?

No one knows for sure how H. pylori spreads, so prevention is difficult. Researchers are trying to develop a vaccine to prevent infection.

Why don’t all doctors automatically check for H. pylori?

Changing medical belief and practice takes time. For nearly 100 years, scientists and doctors thought that ulcers were caused by stress, spicy food, and alcohol. Treatment involved bed rest and a bland diet. Later, researchers added stomach acid to the list of causes and began treating ulcers with antacids.

Since H. pylori was discovered in 1982, studies conducted around the world have shown that using antibiotics to destroy H. pylori cures peptic ulcers. The prevalence of H. pylori ulcers is changing. The infection is becoming less common in people born in developed countries. The medical community, however, continues to debate H. pylori’s role in peptic ulcers. If you have a peptic ulcer and have not been tested for H. pylori infection, talk to your doctor.

Points to Remember

Complications

Both gastric and duodenal ulcers can lead to four types of complications: perforation, hemorrhage, penetration of the ulcer into adjacent organs, and gastric outlet obstruction. The overall, yearly complication rate ranges between 2 and 5 percent. Five percent of all ulcer patients will experience perforation during their lifetime, the rate being higher in men than in women. On the average, 15 percent of patients die from their perforation.The death rate from perforated ulcers stays constant until age 60 years and then shows a sharp rise; perforation is more common in gastric than in duodenal ulcer. Bleeding is three to four times more common than perforation. Similar to perforation, bleeding occurs more often in men than women. One-fourth of all bleeding ulcers need to be operated on, and approximately 10 percent of patients with bleeding ulcers die from this complication.The incidence and death rates of bleeding ulcers show an age-related rise.

An ulcer may erode through the entire thickness of the gastric or duodenal wall into adjacent abdominal organs. Such a penetration without leakage of intestinal contents into the peritoneal cavity can involve the pancreas, bile ducts, liver, and the small or large intestine. The percentage of penetrating ulcers is between 5 and 10 percent for gastric and duodenal ulcers, respectively. These numbers are based on estimates derived from surgical patients and postmortem examinations.The exact prevalence is not known because, unlike perforation, peritonitis does not serve as a hallmark of the event, and penetrating ulcers can seal off like any uncomplicated ulcer. Penetration may become diagnosed only by the acute onset of associated complications such as pancreatitis, cholangitis, or diarrhea of undigested food. In other instances, endoscopic biopsies taken from a deep ulcer unexpectedly reveal liver or pancreatic tissue.

Duodenal ulcers give rise to pyloric stenosis far more often than gastric ulcers. Overall, this is a relatively rare complication, affecting fewer than 2 percent of all patients. Pyloric stenosis slows healing and promotes recurrence of gastric ulcers. Stenosis of the duodenal bulb has been reported to delay healing of duodenal ulcer.

A peptic ulcer comes to be noted only if it causes symptoms or leads to a complication. Because 50 percent of all ulcers may occur in asymptomatic patients and are not included in the denominator, complication rates expressed as a fraction of acute ulcers may be largely inflated. Hospitalization occurs mostly for complicated peptic ulcer, and hospital discharge data reflect the rates of complicated ulcers, unless a peptic ulcer was diagnosed incidentally during workup for other diseases. Surgery for peptic ulcer disease is done in the case of life-threatening complications. Chronic disabling ulcer disease that has been shown refractory to previous medical therapy represents a smaller fraction of ulcers requiring surgery.

Disability and Mortality

Although duodenal ulcer is about twice as common as gastric ulcer, 50 percent more individuals become disabled or die from a gastric rather than a duodenal ulcer. One reason is that, on the average, patients with a gastric ulcer are older than those with a duodenal ulcer. In addition, gastric ulcer patients are more frequently operated on because the ulcer responds less to drug therapy than a duodenal ulcer and, in some cases, gastric cancer is considered a diagnostic possibility. However, only during the first 2 years following the initial diagnosis does the death rate of ulcer patients exceed the average death rate of the general population. Thereafter, peptic ulcer does not significantly influence life expectancy. Most mortality from peptic ulcer disease occurs secondary to complication or surgery for peptic ulcer. Death rates, therefore, reflect the incidence of complicated ulcers and surgery for peptic ulcer disease.

v Environmental Risk Factors

Smoking

Gastric and duodenal ulcers affect smokers twofold more often than nonsmokers. Smoking delays ulcer healing and promotes relapse. Both types of ulcer are adversely affected by cigarette smoking, the negative influence being more pronounced in duodenal than in gastric ulcer. As yet, it is not well understood how smoking exerts its unfavorable influence. The mechanisms that have been discussed include weakening of the mucosal defense by reducing prostaglandin synthesis,impairment of bicarbonate delivery to the duodenal bulb, increase in pepsin secretion, and reduction of mucosal blood flow.

NSAIDs and Peptic Ulcers

A peptic ulcer is a sore that forms in the lining of the stomach or the duodenum (the beginning of the small intestine). An ulcer can cause a gnawing, burning pain in the upper abdomen; nausea; vomiting; loss of appetite; weight loss; and fatigue. Most peptic ulcers are caused by infection with the bacterium Helicobacter pylori (H. pylori). But some peptic ulcers are caused by prolonged use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen sodium.

Normally the stomach has three defenses against digestive juices: mucus that coats the stomach lining and shields it from stomach acid, the chemical bicarbonate that neutralizes stomach acid, and blood circulation to the stomach lining that aids in cell renewal and repair. NSAIDs hinder all of these protective mechanisms, and with the stomach’s defenses down, digestive juices can damage the sensitive stomach lining and cause ulcers.

NSAID-induced ulcers usually heal once the person stops taking the medication. To help the healing process and relieve symptoms in the meantime, the doctor may recommend taking antacids to neutralize the acid and drugs called H2-blockers or proton-pump inhibitors to decrease the amount of acid the stomach produces.

Medicines that protect the stomach lining also help with healing. Examples are bismuth subsalicylate, which coats the entire stomach lining, and sucralfate, which sticks to and covers the ulcer.

If a person with an NSAID ulcer also tests positive for H. pylori, he or she will be treated with antibiotics to kill the bacteria. Surgery may be necessary if an ulcer recurs or fails to heal, or if complications like severe bleeding, perforation, or obstruction develop.

Anyone taking NSAIDs who experiences symptoms of peptic ulcer should see a doctor for prompt treatment. Delaying diagnosis and treatment can lead to complications and the need for surgery.

Alcohol

Alcoholic beverages stimulate gastric secretion, the level of stimulation being dependent on the type of beverage and its alcohol concentration. High concentrations of alcohol break the mucosal barrier, lead to back diffusion of hydrogen ions into the mucosal layer, and may promote the development of gastritis in the long run. Studies confined to patients with moderate drinking habits have been unable to show any adverse effects or have even observed beneficial effects of alcohol on ulcer disease. Chronic consumption of large amounts of alcohol leads to liver cirrhosis and, via portal hypertension, to hypertensive gastrophy, which may be less resistant than normal mucosa to the corrosive action of acid. This chain of events is not restricted to alcohol-induced cirrhosis because portal hypertension from any reason appears to promote the development of peptic ulceration. Multiple studies have reported that gastric and duodenal ulcerations coexist with hepatic cirrhosis more frequently than expected from the general distribution of these diseases.

Stress

“Environmental stress” is a vaguely defined term. Situations that are stressful to one group of people may represent no stress at all to another group. Nevertheless, multiple studies related to the social environment of ulcer patients have suggested that mental stress plays a contributory role in the development of mucosal ulceration. The observation that emotion such as anger and anxiety influence gastric secretion provides further evidence for the association between psyche and ulcer.

Social Class and Occupational Energy Expenditure

Peptic ulcer more frequently affects the lower rather than the higher social classes. It is also more common among blue than white collar workers and manual than sedentary workers. The increased prevalence of duodenal ulcer in migrant workers compared with the indigenous population exists because migrant workers are employed predominantly as manual workers. The previously described higher prevalence of duodenal ulcer in urban rather than rural populations might have been secondary to a higher prevalence of physically demanding work in the townships where most heavy industry and factories were located. In general, these kinds of relationships are less obvious for gastric than duodenal ulcer.

Several epidemiologic studies have revealed a relationship between occupational energy expenditure and the prevalence of duodenal ulcer. Preliminary evidence suggests that acute physical exercise leads to increased acid output,with the increase more pronounced in patients with duodenal ulcer than in healthy controls.In the United States, the prevalence of infection with H. pylori is inversely correlated with family income and length of education. Accordingly, the socioeconomic gradients of peptic ulcer disease also might be influenced by similar gradients in sanitation and exposure to H. pylori.