Most peptic ulcers heal if gastric acid production is adequately suppressed, or, if the cause is an H. pylori infection, when the infection is eradicated. Otherwise, peptic ulcers will regularly recur.
The strategy for treating peptic ulcer disease is two-pronged: to reduce levels of hostile factors such as stomach acid and H. pylori while augmenting protective factors in the digestive tract. The goals of treatment are relieving symptoms, healing craters, preventing recurrences, and preventing—or dealing with—complications. A change to a bland or other special diet is not required for the treatment of peptic ulcer disease.
This section contains more information on:
- Acid-reducing drugs
- Drugs that protect the GI tract
- Treating H. pylori infection
- Treating nonhealing ulcers
- Treating complications
Several types of medication lower exposure to ulcer-causing stomach acids:
Antacids neutralize gastric acid and are more effective than a placebo in healing gastric and duodenal ulcers. However, antacids must be taken in relatively large doses one and three hours after meals and at bedtime, and they may cause side effects. The major side effect of magnesium-containing antacids (Maalox, Mylanta) is diarrhea.
H2 receptor blockers: Histamine-receptor blockers reduce gastric acid production by blocking the H2 receptor on the parietal cells, or acid-secreting cells, located in the lining of the stomach. The histamine molecule fits into the H2 receptor like a key in a lock. These drugs block the keyhole, shutting off a significant amount of acid production. H2 blockers used to treat gastric and duodenal ulcers include cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid), and nizatidine (Axid). H2 receptor blockers are relatively safe. The choice of drug should be dictated by cost, dosing schedule, convenience, and possible drug interactions.
Proton-pump inhibitors (PPIs): These drugs block the action of cells in the stomach lining that pump hydrogen needed to produce stomach acid, thus completely shutting off acid production and allowing ulcers to heal. PPIs are also used in combination with antibiotics to eradicate H. pylori bacteria and to prevent gastroduodenal ulcers associated with nonsteroidal anti-inflammatory drugs. PPIs generally are well tolerated by most patients, but some people may develop side effects: headache, diarrhea, constipation, abdominal pain, nausea, and rash.
All PPIs are very similar in action, and there is no convincing evidence that one is significantly more effective than another. PPIs available by prescription include omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex), pantoprazole (Protonix), and esomeprazole (Nexium). They differ in how they are broken down by the liver and their drug interactions. The absorption into the body of some drugs is affected by the presence of acid in the stomach, and because PPIs so effectively reduce acid in the stomach, they may affect how well these other medications work.
The following drugs promote improved mucosal integrity and enhance regeneration of the tissue lining the GI tract.
Sucralfate, a drug made up of a sugar combined with sulfate and aluminum, acts by binding to the surface of ulcers, coating and protecting the surface from further injury by acid or pepsin. The drug also stimulates the body's production of prostaglandins, which, among other functions, foster regeneration of the tissue lining of the GI tract.
When patients strictly follow a sucralfate regimen—which requires taking the drug four times per day—the therapy has been shown to be effective in healing both duodenal and gastric ulcers. Sucralfate taken twice a day has been used to relieve or prevent ulcers in people using nonsteroidal anti-inflammatory medications (NSAIDs). Sucralfate can lead to constipation and may reduce the absorption of other drugs, including some H2 blockers and the fluoroquinolone antibiotics, such as Ciprofloxacin.
Misoprostol is a synthetic prostaglandin that stimulates secretion of mucus in the gastrointestinal tract, increasing its resistance to acid. In short-term studies, misoprostol has been shown to reduce the frequency of stomach ulcers caused by NSAIDs. However, the drug is not usually prescribed because of its significant side effects, including mild to moderate diarrhea and abdominal pain. In addition, it is too costly to be used by most patients on long-term NSAID therapy for arthritis. The U.S. Food and Drug Administration has required a printed warning on misoprostol-containing drugs because the substance has been shown to induce abortion, miscarriages, premature labor, birth defects, and uterine rupture in pregnant women.
All ulcers associated with H. pylori should be treated with the aim of eradicating the infection, which restores normal mucosal resistance. Unlike with other treatment options, maintenance therapy to prevent ulcer recurrence is not required.
Although H. pylori is sensitive to a variety of antibiotics in the lab, its habitat beneath the mucous lining makes it difficult to treat. The gold standard has been two weeks of triple therapy, using a proton pump inhibitor to suppress acid and protect the lining of the stomach along with two antibiotics, amoxicillin and clarithromycin. When the treatment is vigilantly followed, the cure rate is at least 90 to 95 percent. But many patients have trouble with this treatment because it may require taking up to eight pills a day. And about 20 percent of people undergoing triple therapy develop such side effects as nausea, vomiting, diarrhea, headache, and yeast infections. Newer, simpler regimens are being developed. For example, a combination pill (Prevpac) containing lansoprazole, amoxicillin, and clarithromycin in one pill requires patients to only take two pills a day.
Gastric ulcers that have not healed after eight weeks of conventional medical therapy should be re-evaluated by multiple endoscopic biopsies to rule out gastric carcinoma. If no malignancy is seen in the biopsies, aggressive treatment should be instituted for six more weeks to eradicate H. pylori and to suppress acid with full doses of a proton pump inhibitor medication. A gastric ulcer that does not heal after this second aggressive course of medical therapy may suggest underlying malignancy, even with negative repeat biopsies. At this point, nonhealing gastric ulcers should undergo further evaluation with endoscopic ultrasound and deeper biopsies.
Over the past few decades, the use of surgery to treat peptic ulcer disease has declined thanks to the widespread use of H2 receptor blockers and proton pump inhibitors, drugs that inhibit acid production in the stomach. Now, the main reason surgery is performed is to treat complications of peptic ulcer disease such as gastrointestinal hemorrhage, perforation, or gastric outlet obstruction.
In the absence of complications, surgical intervention for gastric ulcers may be considered if there is failure of an ulcer to completely heal after other treatments have been tried and further evaluation is inconclusive. Patients are usually given a six-month trial of drugs to stop acid secretion and eradicate H. pylori prior to surgical consultation. The major concern regarding nonhealed ulcers is the high risk of underlying malignancies.
Because of the benign nature of duodenal ulcers, physicians can monitor the patients' response to medications by following their symptoms. When patients with duodenal ulcers require surgery, it is usually one of three procedures: vagotomy (cutting of the vagus nerve to reduce acid production), vagotomy with antrectomy (removal of the narrow portion of the stomach leading to the duodenum), or subtotal gastrectomy (removal of a portion of the stomach).
Despite the availability of effective ulcer medications, some patients still suffer complications related to their ulcers. Hemorrhage, perforation of the lining of the stomach or intestine (and, in some cases, penetration of other organs), and obstruction of the narrow channel where the stomach meets the duodenum, or small intestine, (gastric outlet obstruction) are the major complications associated with peptic ulcer disease.
These complications can be very serious, and their symptoms require immediate attention. They include black, tarry stools; vomit that is bloody or looks as if it has coffee grounds in it; extreme abdominal pain; vomiting of undigested or partially digested food; diminished appetite, and weight loss.
This section contains more information on:
- Perforation of the stomach or duodenal lining
- Penetration of other organs
- Gastric outlet obstruction
Gastrointestinal hemorrhage or bleeding affects 5 to 20 percent of ulcer patients and is more common in people with duodenal ulcers, or ulcers of the small intestine. Bleeding is the most common complication of peptic ulcer disease and occurs more often in men than in women. Hemorrhage from ulcers stops spontaneously in approximately 75 to 80 percent of cases. Approximately one fourth of all bleeding ulcers require an interventional procedure, however.
Endoscopy, in which a flexible tube is inserted through the mouth or nasal passage, is the preferred way to diagnose and treat an upper gastrointestinal hemorrhage because of its accuracy and low complication rate. Endoscopy is able to accurately identify the bleeding source in more than 95 percent of patients with significant upper GI hemorrhage. The goal of endoscopic therapy is to "seal" the blood vessel involved and stop the bleeding. This may be accomplished in a variety of ways.
Several endoscopic methods of treatment rely on heat:
- Laser: A laser light can be focused on a bleeding point to induce rapid tissue heating, which leads to coagulation. Clinical trials of ulcer hemorrhage have confirmed that photocoagulation with a laser effectively seals bleeding and nonbleeding visible vessels at risk of future hemorrhage. Important considerations that limit emergency laser treatment include portability of the lasers and cost; the need for specific expertise by the endoscopist and technician as well as special electrical outlets and eye protection; and technical considerations such as the difficulty in aiming the laser beam.
- Electrocoagulation: Heat generated from high-frequency electrical current is capable of coagulating or cutting tissue. Thermal electrocoagulation is the classic treatment for bleeding during surgery and is now being used endoscopically to treat GI bleeding.
- Heater probe: The heater probe is a hollow aluminum cylinder with an inner coil that transfers heat to tissue when positioned. This probe may be passed through larger endoscopes and positioned on bleeding lesions to compress and heat them. Studies have shown the heater probe to be safe and effective for the treatment of ulcer bleeding and successful at significantly improving clinical outcomes.
Another endoscopic treatment uses chemical agents to seal ulcers:
Injection therapy, an alternative to heat therapy, is inexpensive, simple, and widely used. A catheter with a small retractable needle is passed through the endoscope, and vessels are treated with one or more of several different chemical agents.
A combination of injection and thermal treatment has theoretical advantages in the treatment of bleeding ulcers. Injection with the drug epinephrine constricts the blood vessels and activates platelet coagulation, reducing blood flow and facilitating thermal therapy. Recent studies have shown combination therapy (epinephrine injection and heater probe) to be more effective than either individual therapy alone.
Surgery may be necessary if other methods fail to stop the bleeding or if bleeding recurs, or to rule out cancer.
Approximately 5 to 10 percent of patients with peptic ulcers suffer a perforation of the stomach or duodenum, and about 15 percent of them die from the condition. This rate is higher in men than in women.
Two types of perforation have been observed. Free perforation occurs when duodenal or gastric contents spill into the abdominal cavity and contaminate the peritoneum (the membrane lining the abdominal cavity and organs). Contained perforation occurs when the ulcer produces a hole in the duodenum or stomach, but the folds in the peritoneum or other adjacent organs prevent digestive juices from leaking out.
Perforations are most likely in elderly patients on chronic therapy with nonsteroidal anti-inflammatory drugs and they are more common in stomach than in duodenal ulcers. Initial symptoms of perforated duodenal or gastric ulcers include severe abdominal pain, worse in the upper middle portion of the abdomen, often accompanied by nausea and vomiting. Typically, the patient is acutely and severely ill. The finding of free air on an X-ray taken from an upright position or with the patient lying on one side is noted in approximately 70 percent of cases.
Perforation is a contraindication for endoscopy, because the procedure may worsen spillage of gastric contents or disrupt a sealed perforation. Urgent surgical therapy is recommended in patients with uncontained, free perforated ulcers, because spontaneous sealing is rare. Aggressive surgical intervention helps to decrease the high mortality associated with perforating gastric ulcers.
Five to 10 percent of perforating ulcers may result in erosion into adjacent abdominal organs. Such penetration can involve the pancreas, bile ducts, liver, and the small or large intestine. The pancreas is the most common site of penetration.
The acute onset of associated complications, such as pancreatitis (inflammation of the pancreas), cholangitis (infection of the biliary tract), or diarrhea of undigested food, may indicate penetration. The diagnosis of penetration is more difficult than that of perforation and is based on a combination of severe ulcer symptoms, atypical pain distribution, and diminished response to the usual therapy. Surgery is usually not recommended in the management of penetration unless complications relating to the bile ducts are present or the underlying peptic disease is severe.
Fewer than 5 percent of patients develop gastric outlet obstruction, a blockage that usually occurs at or near the narrow part of the stomach (pyloric canal) as it joins the upper part of the small intestine (duodenum).
Duodenal ulcers give rise to this complication more often than gastric ulcers. Varying degrees of obstruction may be caused by inflammatory swelling of the pyloric channel or chronic scarring.
Patients with gastric outlet obstruction usually have a history of nausea, vomiting, and pain or fullness in the upper middle part of the abdomen. Laboratory findings may show anemia and potassium abnormalities, and an X-ray typically shows a large gastric shadow with an air/fluid level. An upper GI series would show a marked delay in gastric emptying and a large stomach. Endoscopy is the best test for evaluating gastric outlet obstruction.
Endoscopic dilation of the gastric outlet is a reasonable course for treating this complication after medical therapy has failed. Balloon dilation can usually improve the acute problem. A lubricated balloon is passed through the endoscope and is inflated with water or air.
The goal of surgery for gastric outlet obstruction is twofold: 1) improvement of the obstruction, 2) treatment of the predisposing ulcer with an acid-reducing procedure. Vagotomy, in which the vagus nerve is cut to reduce stomach acid, and antrectomy, the removal of the pyloric portion of the stomach, are recommended surgical procedures.
Last reviewed on 7/28/09
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