INTRODUCTION

Section 2 of 11  

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Background

Peptic ulcer disease (PUD) is one of the most common diseases affecting the 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.

Pathophysiology

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. 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.

Frequency

United States

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.

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.

CLINICAL

Section 3 of 11  

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History

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.

Physical

Physical examination usually is not helpful.

• Epigastric tenderness may or may not be present.
• 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.

Causes

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).

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Nonulcer dyspepsia (NUD) or functional dyspepsia: A diagnosis of exclusion, patients with chronic persistent epigastric pain in the absence of any organic disease after thorough evaluation are thought to have functional dyspepsia. Patients may primarily have epigastric pain, which is referred to as ulcerlike dyspepsia, or they may have symptoms of postprandial bloating, which is referred to as motilitylike dyspepsia.

Crohn disease: Crohn ulceration can involve any part of the GI tract from the buccal mucosa to the rectum. Isolated Crohn ulceration of the stomach is rare, although it may cause duodenal or ileal ulcerations.

WORKUP

Section 5 of 11  

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Lab Studies

• 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.

Imaging Studies

• Upper GI radiography
• • 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.

Other Tests

• 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.

Procedures

• Esophagogastroduodenoscopy (EGD)
• • 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.

Histologic Findings

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.

TREATMENT

Section 6 of 11  

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Medical Care

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), 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), 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. 
• 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.¹ This was further confirmed in a double-blind randomized study in 2006 by Lai and colleagues.⁵  
• 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 American College 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. 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.

Surgical Care

• 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.

Consultations

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.

Diet

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.

Activity

Normal activity is encouraged.

MEDICATION

Section 7 of 11  

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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.

Drug Category: Proton pump inhibitors

These agents act by irreversibly binding the H⁺/K⁺-ATPase pump and effectively suppressing acid secretion.

Drug Category: Histamine H2 antagonists

These drugs inhibit histamine stimulation of H2 receptor in gastric parietal cells.

Drug Category: Helicobacter pylori eradication agents

Antibiotics and other agents are used as adjuvants to treat duodenal ulcer disease associated with H pylori.

Drug Category: Gastrointestinal agents

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.

Drug Category: Nonsteroidal anti-inflammatory agents

These agents are the most commonly used medications to control mild to moderate pain and to decrease inflammation.

FOLLOW-UP

Section 8 of 11  

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Further Inpatient Care

• 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.

Further Outpatient Care

• 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.

In/Out Patient Meds

• 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.

Deterrence/Prevention

• 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

• 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.

Prognosis

• 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.

Patient Education

• Instruct patients to avoid NSAIDs.
• Discourage alcohol consumption and cigarette smoking because these activities impair gastric mucosal protection.
• For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education article Peptic Ulcers.

MISCELLANEOUS

Section 9 of 11  

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Medical/Legal Pitfalls

• Failure to be vigilant about gastric cancer in patients with nonhealing ulcers or any alarm signs, such as anemia or weight loss
• Failure to document the eradication of H pylori with UBT, fecal stool antigen, or repeat upper endoscopy with biopsy in a patient with bleeding PUD.

MULTIMEDIA

Section 10 of 11  

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Media file 1:  Gastric ulcer with punched-out ulcer base with whitish fibrinoid exudates.
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Media file 2:  Gastric ulcer (lesser curvature) with punched-out ulcer base with whitish exudate.
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Media type:  Image

Media file 3:  Gastric cancer. Note the irregular heaped up overhanging margins.
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Media file 4:  Gastric cancer with ulcerated mass.
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Media type:  Image

REFERENCES

Section 11 of 11

• Authors and Editors
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• Miscellaneous
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• References

1. Chan KL, Ching YL, Hung CY. Clopidogrel versus aspirin and esomeprazole to prevent ulcer bleeding. N Eng J Med. 2005;352:238-44. [Full Text].
2. Ford AC, Delaney BC, Forman D, Moayyedi P. Eradication therapy for peptic ulcer disease in Helicobacter pylori positive patients. Cochrane Database Syst Rev. 2006;(2):CD003840. [Medline].
3. Graham DY, Klein PD. Accurate diagnosis of Helicobacter pylori. 13C-urea breath test. Gastroenterol Clin North Am. Dec 2000;29(4):885-93, x. [Medline].
4. Jensen DM. Management of severe ulcer rebleeding. N Engl J Med. Mar 11 1999;340(10):799-801. [Medline].
5. Lai KC, Chu KM, Hui WM, et al. Esomeprazole with aspirin versus clopidogrel for prevention of recurrent gastrointestinal ulcer complications. Clin Gastroenterol Hepatol. Jul 2006;4(7):860-5. [Medline].
6. Lai KC, Lam SK, Chu KM, Wong BC, Hui WM, Hu WH. Lansoprazole for the prevention of recurrences of ulcer complications from long-term low-dose aspirin use. N Engl J Med. Jun 27 2002;346(26):2033-8. [Medline].
7. Lau JY, Chung SC. Surgery in the acute management of bleeding peptic ulcer. Baillieres Best Pract Res Clin Gastroenterol. Jun 2000;14(3):505-18. [Medline].
8. 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. [Full Text].
9. Lo CC, Hsu PI, Lo GH, et al. Comparison of hemostatic efficacy for epinephrine injection alone and injection combined with hemoclip therapy in treating high-risk bleeding ulcers. Gastrointest Endosc. May 2006;63(6):767-73. [Medline].
10. Silverstein FE, Faich G, Goldstein JL, et al. Gastrointestinal toxicity with celecoxib vs nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: A randomized controlled trial. Celecoxib Long-term Arthritis Safety Study. JAMA. 284(10):1247-55. [Medline].
11. Soll AH. Consensus conference. Medical treatment of peptic ulcer disease. Practice guidelines. Practice Parameters Committee of the American College of Gastroenterology. JAMA. Feb 28 1996;275(8):622-9. [Medline].
12. Sonnenberg A, Everhart JE. Health impact of peptic ulcer in the United States. Am J Gastroenterol. Apr 1997;92(4):614-20. [Medline].
13. Steinbach G, Ford R, Glober G, et al. Antibiotic treatment of gastric lymphoma of mucosa-associated lymphoid tissue. An uncontrolled trial. Ann Intern Med. Jul 20 1999;131(2):88-95. [Medline].
14. Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med. Oct 10 2002;347(15):1175-86. [Medline].
15. Vaira D, Gatta L, Ricci C, et al. Peptic ulcer and Helicobacter pylori: update on testing and treatment. Postgrad Med. Jun 2005;117(6):17-22, 46. [Medline].
16. Wallace JL. Recent advances in gastric ulcer therapeutics. Curr Opin Pharmacol. Dec 2005;5(6):573-7. [Medline].
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Article Last Updated: May 2, 2007