Sanjeeb Shrestha, MD,
Consulting Staff, Division of
Gastroenterology, North West Arkansas Gastroenterology
Clinic
Nothing to disclose.
Coauthor(s)
Daryl Lau, MD, MPH, FRCP(C),
Director of Translational Liver Research,
Beth Israel Deaconess Medical Center; Associate Professor of
Medicine, Harvard Medical School
Nothing to disclose.
Specialty Editor(s)
Alex J Mechaber, MD, FACP,
Associate Dean for Undergraduate Medical
Education, Associate Professor of Medicine, University of
Miami Miller School of Medicine
Nothing to disclose.
David Greenwald, MD,
Fellowship Program Director, Associate
Professor, Department of Medicine, Division of
Gastroenterology, Montefiore Medical Center, Albert Einstein
College of Medicine
Nothing to disclose.
Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor,
eMedicine
eMedicine Salary Employment
Simmy Bank, MD,
Chair, Professor, Department of Internal
Medicine, Division of Gastroenterology, Long Island Jewish
Hospital, Albert Einstein College of
Medicine
Nothing to disclose.
Chief Editor
Julian Katz, MD,
Clinical Professor of Medicine, Drexel
University College of Medicine; Consulting Staff, Department
of Medicine, Section of Gastroenterology and Hepatology,
Hospital of the Medical College of
Pennsylvania
Nothing to disclose.
Background
Peptic ulcer disease (PUD) is one of the most common diseases affecting the gastrointestinal (GI) tract. It causes inflammatory injuries in the gastric or duodenal mucosa, with extension beyond the submucosa into the muscularis mucosa. The etiologies of this condition are multifactorial and are rarely related simply to excessive acid secretion. Even though gastric ulcer is a common disease, a diagnosis can be difficult because it has a wide spectrum of clinical presentations, ranging from asymptomatic to vague epigastric pain, nausea, and iron-deficiency anemia to acute life-threatening hemorrhage.
View Image
Gastric ulcer with punched-out ulcer base with whitish fibrinoid exudates.
View Image
Gastric ulcer (lesser curvature) with punched-out ulcer base with whitish exudate.
The normal stomach maintains a balance between protective factors, such as mucus and bicarbonate secretion, and aggressive factors, such as acid secretion and pepsin. Gastric ulcers develop when aggressive factors overcome protective mechanisms.
The two major etiological factors for PUD are Helicobacter pylori infection and nonsteroidal anti-inflammatory drug (NSAID) consumption. Currently, 70% of all gastric ulcers occurring in the United States can be attributed to H pylori infection. In addition to an increase in acid secretion, H pylori infection also predisposes patients to ulcer disease by disrupting mucosal integrity. The bacterium's spiral shape and flagella facilitate its penetration into the mucous layer and its attachment to the epithelial layer. Subsequently, it releases phospholipase and proteases, which cause further mucosal damage. A cytotoxin-associated gene (cag A) has been isolated in approximately 65% of the bacteria. The products of this gene are associated with more severe gastritis, gastric ulcer, gastric cancer, and lymphoma.
Cigarette smoking can affect gastric mucosal defense adversely. Cigarette smoking is believed to play a facultative role in H pylori infection. People who smoke tend to develop more frequent and recurrent ulcers and their ulcers are more resistant to therapy. No evidence indicates that dietary habits or alcohol consumption predisposes individuals to gastric ulcer.
NSAID-induced ulcers account for approximately 26% of gastric ulcers, and they are believed to be secondary to a decrease in prostaglandin production resulting from the inhibition of cyclooxygenase.[1] The topical effects of NSAIDs are superficial gastric erosions and petechial lesions. However, the risk of gastroduodenal ulcer is not diminished with parental or rectal use of NSAIDs indicating injury occurring from the systemic effect of NSAIDs on the gastrointestinal mucosa. The greatest risk of developing an ulcer occurs during the first 3 months of NSAID use; thereafter, the risk decreases but continues to be present. Whether concurrent H pylori infection and NSAID use are synergistic in producing gastric ulcers remains unclear. Recent accumulating evidence indicates that patients with H pylori infection may be twice as likely to get a bleeding peptic ulcer.
Selective COX-2 (cyclooxygenase) inhibitors, like celecoxib (Celebrex), rofecoxib (Vioxx), and valdecoxib (Bextra), have been shown to cause gastroduodenal ulcers at a rate comparable to placebo (4%). In the Celecoxib Long-term Arthritis Safety Study (CLASS), they found a significantly lower incidence of symptomatic ulcers in patients taking celecoxib for the initial 6 months as compared to patients taking ibuprofen or diclofenac. Currently, the only US Food and Drug Administration (FDA)-approved COX-2 inhibitor available is celecoxib, as rofecoxib and valdecoxib were withdrawn from the market by the FDA because of increased cardiovascular risk.
Other medications that predispose patients to gastroduodenal ulcers include potassium chloride, chemotherapeutic agents, and bisphosphonates.
A rare cause of PUD is Zollinger-Ellison syndrome (ie, gastrinoma). The hallmark of Zollinger-Ellison syndrome is the profound hypersecretion of gastric acid. Significant disruption of the mucosal integrity often results in multiple duodenal and gastric ulcers.
The annual incidence of gastric ulcer is largely determined from the statistics of the pre– H pylori era (prior to 1979). It is estimated to affect 0.92% of the population or 1.6 million persons. Epidemiological studies show that from 1970-1985, a marked decrease in the rate of duodenal ulcer occurred, while the rate of gastric ulcer remained stable. People with low socioeconomic status are more likely to acquire H pylori infection. Individuals who are infected are 3 times more likely to develop gastric ulcer compared to those unexposed to the bacteria.
Since 1989, approximately 500,000 people are estimated to be afflicted with gastric ulcer. The decline in gastric ulcer is in some part attributable to the declining prevalence of H pylori. Although the rate of simple gastric ulcer is in decline, the incidence of complicated gastric ulcer and hospitalization has remained stable, partly due to the concomitant use of aspirin in an aging population.
International
In Denmark, lifetime prevalence of gastric cancer is 1.2% for men and 0.6% for women. The annual incidence of gastric ulcers varies from approximately 1 case per 1000 population in Japan to 1.5 cases per 1000 population in Norway to 2.7 cases per 1000 population in Scotland. For trends in Sweden, see Sadic et al.[2]
Mortality/Morbidity
The mortality rate is approximately 1 case per 100,000 persons, based on the 1979 estimates from the United States. The mortality rate is higher in patients older than 75 years, which can be attributable to a high rate of NSAID use in this age group. The other high-risk groups include people with chronic renal insufficiency and diabetes. Gastric ulcers are also associated with considerable morbidity related to chronic epigastric pain, nausea, vomiting, and anemia.
Sex
In the United States, the prevalence of gastric ulcer has shifted in the past 2 decades, from a disease predominantly affecting males to one that is equally present in both sexes. The male-to-female ratio is 1:1 in the United States and 18:1 in India.
Age
The incidence of gastric ulcer increases with age because of a combination of increasing NSAID use and a high prevalence of H pylori infection in persons older than 50 years. The prevalence of H pylori in elderly individuals is the result of a cohort effect of the generally poorer socioeconomic condition in the United States in past decades compared to today.
Patients may present with a wide variety of symptoms, or they may remain completely asymptomatic.
Gastric and duodenal ulcers usually cannot be differentiated based on history alone.
Classic gastric ulcer pain is described as pain occurring shortly after meals, for which antacids provide minimal relief.
The pain from gastric ulcer is typically located in the epigastrium; however, it can also be perceived in the right upper quadrant and elsewhere.
Duodenal ulcer pain often occurs hours after meals and at night. Pain is characteristically relieved with food or antacids.
Pain with radiation to the back is suggestive of a posterior penetrating gastric ulcer complicated by pancreatitis.
Patients with bleeding gastric ulcers may give a history of hematemesis, melena, or episodes of presyncope. Melena can be intermittent over several days or multiple episodes in a single day. Rarely, a briskly bleeding ulcer can present as gross hematochezia.
Right upper quadrant tenderness may suggest a biliary etiology or, less frequently, PUD.
In the presence of gastric outlet obstruction, abdominal distension and succussion splash may be found.
A palpable mass should raise the suggestion of a gastric malignancy.
Involuntary guarding is indicative of peritonitis secondary to gastric perforation.
Patients should be checked for melena, which is indicative of bleeding from a gastroduodenal ulcer. Digital rectal examination can be easily performed in the office to check for melena.
The 2 major etiological factors for PUD are H pylori infection and NSAID consumption.
Currently, 70% of all gastric ulcers in the United States can be attributed to H pylori infection.
NSAID-induced ulcers account for approximately 25% of gastric ulcers, and PUD is believed to develop secondary to the decrease in prostaglandin production resulting from the inhibition of cyclooxygenase.
A rare cause of PUD is Zollinger-Ellison syndrome (ie, gastrinoma).
The diagnosis of gastric ulcer can be made based on a characteristic clinical history; however, a high index of suspicion for gastric ulcer is needed in patients without risk factors for PUD.
Routine laboratory tests, such as complete blood cell count and iron studies, can help detect anemia. Anemia and weight loss are alarm signals and mandate early endoscopy to rule out other sources of chronic GI blood loss.
A double-contrast barium study performed by an expert GI radiologist has equivalent accuracy in diagnosing a typical gastric ulcer. However, diagnostic biopsies cannot be performed with radiological studies, and radiographic evidence of a healing ulcer is not adequate to rule out gastric cancer.
Benign gastric ulcers are normally found on the lesser curvature, although they can occur anywhere in the stomach. These ulcers tend to project beyond the contour of the stomach, with radiating folds extending to the ulcer margin.
In contrast, malignant ulcers usually have irregular heaped-up margins that protrude into the lumen of the stomach.
H pylori testing: A strong relationship exists between PUD and H pylori infection. Therefore, to prevent recurrence of ulcer disease, diagnosing and eradicating H pylori infection is important. H pylori infection can be diagnosed using various invasive or noninvasive methods.
Invasive tests
Biopsy: Identification of the organism in an endoscopically obtained biopsy specimen remains the criterion standard for diagnosis of H pylori infection. Routinely, 2 biopsy samples are obtained from the antrum and the body of the stomach. Gastritis is apparent on routine histological slides stained with hematoxylin and eosin; however, special staining with Giemsa or Warthin-Starry silver stain provides almost 100% accurate results. False-negative results can occur in patients with active gastrointestinal bleeding and in patients taking antisecretory agents.
Culture: This is the most specific method; however, it is not routinely performed in clinical practice because of the fastidious nature of the organism.
Rapid urease test: This test contains urea-impregnated agar and a pH indicator that changes color if urease is present in the biopsy sample. This test is quick and accurate, with a sensitivity and specificity of higher than 90%.
Noninvasive tests
Antibody testing: Serological testing is simple, inexpensive, and widely available. Serology can be used to test and treat people with recurrent epigastric pain and symptoms suggestive of PUD and without any alarming signs for malignancy. Serology is of limited value for determining eradication of H pylori because positive results cannot be used to differentiate between past exposure and active infection.
Urea breath testing (UBT): This test is useful for documenting the eradication of H pylori after treatment. H pylori produces a large amount of urease. Patients ingest carbon-labeled urea (ie, carbon 13 or carbon 14) that is broken down by urease with release of the labeled carbon. A failure to detect exhaled labeled carbon dioxide confirms the eradication of the bacteria. UBT should be performed 4 weeks after H pylori eradication to prevent false-negative results.
Stool antigen: This test, approved by the FDA, helps identify bacterial antigens in stool. The test has been shown to be extremely accurate with a sensitivity of 89-98% and with a specificity of greater than 90% in helping to diagnose infection or to document eradication. To assess for eradication of H pylori, stool antigen should be checked only after 8 weeks of completion of therapy.
Diagnostic EGD is the modality of choice in establishing a diagnosis of gastric ulcers. EGD provides the opportunity to perform multiple mucosal biopsies to check for H pylori and to rule out malignancy.
Endoscopy is a relatively safe procedure in experienced hands. This allows direct visualization to obtain biopsy specimens and also to perform endoscopic therapy for bleeding ulcers.
The ability to directly visualize the mucosa makes endoscopy the preferred modality for the diagnosis of gastric ulcer and gastric cancer.
A repeat endoscopy after 6 weeks of therapy is recommended to confirm healing of a gastric ulcer and to help definitively rule out gastric malignancy.
Upper endoscopy with biopsy is the most sensitive and specific method for diagnosing gastric and esophageal cancer.
A single biopsy offers 70% accuracy in diagnosing gastric cancer, but 7 biopsy samples obtained from the base and ulcer margins increase the sensitivity to 99%.
Brush cytology has been shown to increase the biopsy yield, and this method may be useful particularly when bleeding is a concern in a patient with coagulopathy.
Gross appearance
Gastric ulcer is a discrete mucosal lesion with a punched-out smooth ulcer base, which often is filled with whitish fibrinoid exudates (see Images 1-2). Ulcers tend to be solitary and well circumscribed and usually are 0.5-2.5 cm in diameter.
Most gastric ulcers tend to occur at the junction of the fundus and antrum, along the lesser curvature.
Benign ulcers tend to have a smooth, regular, rounded edge with a flat smooth base and surrounding mucosa that shows radiating folds.
Malignant ulcers usually have irregular heaped-up or overhanging margins (see Images 3-4). The ulcerated mass often protrudes into the lumen, and the folds surrounding the ulcer crater are often nodular and irregular.
The histology of gastric ulcer depends on its chronicity. The surface is covered with slough and inflammatory debris. Beneath this neutrophilic infiltration, active granulation with mononuclear leukocytic infiltration and fibrinoid necrosis may be seen. In chronic superficial gastritis, lymphocytes, monocytes, and plasma cells often infiltrate the mucosa and submucosa.
The medical treatment of gastric ulcers is aimed at restoring the balance between aggressive factors (acid secretion) and mucosal protective factors. In patients infected with H pylori, the most effective treatment is therapy to eradicate the organism and to suppress acid secretion.
In patients with bleeding PUD, volume resuscitation with IV fluid and blood products is the most important initial therapy. An intravenous proton pump inhibitor (PPI) is started. This is followed by checking for acute anemia, thrombocytopenia, or coagulopathy, which needs correction with vitamin K or fresh frozen plasma.
Histamine 2 blockers (H2 blockers)
Therapy can be directed toward histamine release, that is, H2 blockers, such as cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid),[3] and nizatidine (Axid). These agents selectively block the H2 receptors in the parietal cells.
All H2 blockers are comparable in efficacy and, when used in twice-daily doses for a period of 8 weeks, have a healing rate of higher than 70%.
Hydrogen pump antagonists or PPIs
PPIs are drugs that covalently bind and irreversibly inhibit the H+/K+ adenosine triphosphatase (ATPase) pump, effectively inhibiting acid release. Omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex),[4] pantoprazole (Protonix), and esomeprazole (Nexium) given in daily or twice-daily doses for 4 weeks heal 80-100% of gastric ulcers if H pylori infection is not present or has been eradicated.
All PPIs are comparable in efficacy. The PPI should preferentially be taken on an empty stomach to allow maximum inhibition of H+/K+ pumps. Prilosec binds irreversibly with the H+/K+ pumps and suppresses acid secretion. This inhibition is at its maximum in 24-48 hours, and when Prilosec is stopped, the secretory activity gradually returns to normal in the next 2-3 days.
Newer forms of the PPI delivery system include Prevacid SoluTab, which is a chewable version of Prevacid with more rapid action. Zegrid is an oral suspension of esomeprazole, which appears to be rapid acting with prolonged efficacy.
Studies have shown that continuous intravenous infusion of omeprazole in patients with active bleeding from gastric ulcer decreases the following: need for transfusion, mortality, and hospital stay. Although widely available in Europe and Asia, IV omeprazole is currently not available in the United States. Available IV PPIs in the United States are Prevacid and Protonix. Prevacid is given as a bolus of 60 mg IV with infusion at the rate of 6 mg/h, while Protonix is given as a bolus of 60-80 mg IV with a continuous infusion at the rate of 6-8 mg/h.
van Rensburg et al compared IV pantoprazole with IV ranitidine for bleeding ulcers in 1256 patients.[23] After endoscopic hemostasis, patients were randomized to pantoprazole 80 mg plus 8 mg/h or ranitidine 50 mg plus 13 mg/h, both for 72 hours. A second-look endoscopy was performed on day 3 or sooner, if clinically indicated. The investigators found similar outcomes between the 2 groups, including 72-hour clinically detected rebleeding, surgery, or day-3 mortality.[23] However, patients in the pantoprazole group had significantly decreased cumulative frequencies of spurting lesions and gastric ulcers.
Mucosal protectants
Mucosal protectants, such as bismuth and sucralfate, can also be effective in healing gastric ulcers; however, they are not as effective as H2 blockers.
Patients taking NSAIDs should discontinue them if possible. If discontinuing NSAIDs is not possible, omeprazole at 40 mg/d (or another PPI) should be given concurrently. However, only misoprostol (Cytotec) has been shown to be cytoprotective when taken with NSAIDs. However, the use of misoprostol is limited because of its adverse effects, including diarrhea and abdominal pain observed in 14-40% of patients, and because it needs to be taken 4 times a day.
A 2005 study showed that in patients with aspirin-induced ulcer, contrary to popular belief, aspirin plus esomeprazole (Nexium) was superior to clopidogrel (Plavix) in preventing recurrent gastric ulcer bleeding.[5] This was further confirmed in a double-blind randomized study in 2006 by Lai and colleagues.[6]
H pylori eradication
Multiple regimens have been evaluated for the eradication of H pylori infection; however, triple therapy has consistently been shown to eradicate the organism more than 90% of the time.
The 5 different regimens approved by AmericanCollege of Gastroenterology are as follows (all 5 regimens are given for a total of 2 wk):
Bismuth, metronidazole, and tetracycline qid with H2 blockers bid
Bismuth, metronidazole, and tetracycline bid with a PPI (Helidac)
Prevacid, amoxicillin, and clarithromycin bid (PrevPac)
Prilosec, metronidazole, and clarithromycin bid
Ranitidine, bismuth, and clarithromycin with amoxicillin, metronidazole, or tetracycline bid
Endoscopic therapy
Upper GI bleeding secondary to a bleeding peptic ulcer is a common medical condition. Endoscopic evaluation of the bleeding ulcer can decrease the duration of the hospital stay by identifying patients at low risk for rebleeding. Moreover, endoscopic therapy reduces the likelihood of recurrent bleeding and decreases the need for surgery.
Patients can be stratified as high or low risk for rebleeding depending on the presence or absence of stigmata during their initial endoscopic examination. High-risk stigmata are active hemorrhage (90% risk of rebleeding), a visible vessel (50% risk of rebleeding), or a fresh overlying clot (30% risk of rebleeding). In the absence of these stigmata, patients can be discharged home on medical therapy within 48 hours.
Ulcers with stigmata (ie, visible vessel, oozing, overlying blood clot) require endotherapy, while ulcers with a clean base crater need not be treated endoscopically.
Several modalities of endotherapy are available, such as injection therapy, coagulation therapy, hemostatic clips, argon plasma coagulator, and combination therapy.[7] Injection therapy is performed with epinephrine in a 1:10,000 dilution or with absolute alcohol. Thermal endotherapy is performed with a heater probe, bipolar circumactive probe, or gold probe. Pressure is applied to cause coagulation of the underlying artery (coaptive coagulation). Combination therapy with epinephrine injection followed by thermal coagulation appears to be more effective than monotherapy for ulcers with a visible vessel, active hemorrhage, or adherent clot.
Different hemoclips have been used successfully to treat an acutely bleeding ulcer by approximating 2 folds and clipping them together. Several clips may need to be deployed to approximate the gastric ulcer folds. In treating high-risk bleeding ulcers, combined therapy with epinephrine and hemoclips seems to be more efficacious than injection alone. However, it is not clear if hemoclip use or thermal coagulation is more effective in treating an acutely bleeding ulcer; both modalities are used depending on physician experience and equipment availability.
With the advent of aggressive intravenous PPI infusion, effective therapy for H pylori infection, and advanced endotherapy, most ulcers can be managed effectively with medical treatment. However, surgery still has a role in life-threatening hemorrhage that cannot be controlled with medical management alone.
Other indications for surgical therapy are ulcer perforation, gastric outlet obstruction, giant gastric ulcer, and a transfusion requirement of more than 6 units in 24 hours.
Distal gastrectomy with Billroth I (gastroduodenostomy) or Billroth II (gastrojejunostomy) is the preferred procedure for these complications. The surgery involves the removal of both the ulcer (mostly on the lesser curvature) and the diseased antrum.
Medical therapy for gastric ulcer has shifted from antisecretory therapy to antimicrobial therapy; however, surgical therapy relies on acid reduction with vagotomy. Although vagotomy may be unnecessary, truncal or selective vagotomy is performed routinely.
In all patients with acute upper GI hemorrhage, a gastroenterologist should be consulted early. Some institutions have a structured GI bleed team consisting of a gastroenterologist, a surgeon, and an interventional radiologist who are consulted simultaneously for all GI bleeds.
Insufficient data exist to support any special diet for the healing of gastric ulcers. In the event of acute upper GI bleeding, patients should be kept without food for the initial 24 hours so that endoscopic evaluation can be expedited without fear of aspiration.
PPIs given daily or twice daily have an ulcer-healing rate of 80-100% and are the most effective drugs used to treat gastric ulcers. H2 blockers and mucosal protectants (ie, sucralfate, bismuth) are also effective.
Clinical Context:
Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATPase pump. Indicated for gastric ulcers, duodenal ulcers, GERD, erosive esophagitis, and for eradication of H pylori when combined with other medications.
Clinical Context:
Inhibits gastric acid secretion. Indicated for gastric ulcers, duodenal ulcers, GERD, erosive esophagitis, and for eradication of H pylori when combined with other medications.
Clinical Context:
For short-term (4-8 wk) treatment and relief of symptomatic erosive or ulcerative GERD. If not healed after 8 wk, consider additional 8-wk course.
Clinical Context:
Indicated for short-term treatment of GERD associated with erosive esophagitis. Also effective in treating gastric ulcers, including those caused by H pylori.
Clinical Context:
Component of drug combination therapy that effectively treats duodenal ulcer or gastric ulcer associated with H pylori infection. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Clinical Context:
Component of drug combination therapy that effectively treats duodenal ulcer or gastric ulcer associated with H pylori infection. Active against various anaerobic bacteria and protozoa. Appears to be absorbed into cells. Intermediate-metabolized compounds formed bind DNA and inhibit protein synthesis, causing cell death.
Clinical Context:
Component of drug combination therapy that effectively treats duodenal ulcer or gastric ulcer associated with H pylori infection. Antimicrobial and cytoprotective effects produced by bismuth and subsalicylate.
Clinical Context:
Component of drug combination therapy that effectively treats duodenal ulcer or gastric ulcer associated with H pylori infection. Treats gram-positive and gram-negative organisms and mycoplasmal, chlamydial, and rickettsial infections.
Clinical Context:
Component of drug combination therapy that effectively treats duodenal ulcer or gastric ulcer associated with H pylori infection. Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.
These agents protect GI lining. Shown to be effective in treating peptic ulcers and preventing relapse. Mechanism of action not clear. Multiple doses are required, and agents are not as effective as other options.
Clinical Context:
Forms viscous adhesive substance that protects GI lining against pepsin, peptic acid, and bile salts. Use for short-term management of ulcers.
Clinical Context:
Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared to nonselective NSAIDs. Seek lowest dose for each patient.
Neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates pro-inflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; may increase CSF IgG (10%).
Has a sulfonamide chain and is primarily dependent upon cytochrome P450 enzymes (a hepatic enzyme) for metabolism.
Patients who have a rebleeding episode while in the hospital should have a second endoscopy prior to surgical management. Patients should continue taking PPIs for at least 8 weeks.
Patients should be reevaluated in 6-8 weeks with a repeat endoscopy to document complete healing of the gastric ulcer. If the ulcer is not healed, multiple biopsies of the ulcer are indicated to conclusively rule out gastric malignancy.
Maintenance therapy with antisecretory medications (eg, H2 blockers, PPIs) for 1 year is indicated in high-risk patients. High-risk patients include those with recurrent ulcers and those with complicated or giant ulcers. If H pylori eradication is not achieved despite repeat treatment, maintenance antisecretory therapy should be recommended.
Some preliminary evidence suggests that PPIs impair the absorption of calcium in the gut and also independently may inhibit osteoclastic activity. Gastric acid increases insoluble calcium absorption and medicines that decrease gastric acid may thereby decrease calcium absorption. A 2006 study demonstrated that high-dose PPIs when taken over several years may independently increase the risk for hip fracture. Patients on long-term or high-dose PPIs should take calcium supplements.
In patients with gastric ulcers, documenting the eradication of H pylori with UBT, rapid urease test, or histology studies on a biopsy sample is imperative. If H pylori is not eradicated, treatment should be repeated with another regimen.
Complications of gastric ulcers include hemorrhage, perforation, and gastric outlet obstruction.
Patients with gastric ulcers are also at risk of developing gastric malignancy.
The risk is approximately 2% in the initial 3 years.
One of the important risk factors is related to H pylori infection. H pylori is associated with atrophic gastritis, which, in turn, predisposes to gastric cancer.
H pylori infection is associated with gastric lymphoma or mucosa-associated lymphoid tissue (MALT) lymphoma. The normal gastric mucosa is devoid of organized lymphoid tissue. H pylori infection promotes acquisition of lymphocytic infiltration and often forms lymphocytic aggregates and follicles from which MALT lymphoma develops. Eradication of H pylori is very important in this group of patients because eradication of H pylori has been shown to cause a remission of MALT lymphoma.
The prognosis of patients with benign gastric ulcers is excellent, especially if H pylori is completely eradicated and NSAIDs are avoided.
Patients with recurrent gastric ulcers should be questioned in detail about NSAID use (particularly over-the-counter varieties), and endoscopy with biopsies should be repeated to help rule out malignancy and to check for the persistence of H pylori.
Malignancy should be strongly considered in the case of a persistent nonhealing gastric ulcer. Endoscopic ultrasound examination may be helpful for assessing mucosal invasion or detecting associated adenopathy in such patients. Surgical resection should be considered if evidence of cancerous transformation is present.
Lau YW, Sung JY, Lee KC. Effect of intravenous omeprazole on recurrent bleeding after endoscopic treatment of bleeding peptic ulcers. N Eng J Med. 2000;343:310-6.
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