eMedicine Specialties > Gastroenterology > Stomach

Gastric Ulcers: Differential Diagnoses & Workup

Author: Sanjeeb Shrestha, MD, Consulting Staff, Division of Gastroenterology, North West Arkansas Gastroenterology Clinic
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
Contributor Information and Disclosures

Updated: Aug 24, 2009

Differential Diagnoses

Cholecystitis
Crohn Disease
Duodenal Ulcers
Gastric Cancer
Pancreatitis, Chronic
Zollinger-Ellison Syndrome

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

Laboratory 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.

More on Gastric Ulcers

Overview: Gastric Ulcers
Differential Diagnoses & Workup: Gastric Ulcers
Treatment & Medication: Gastric Ulcers
Follow-up: Gastric Ulcers
Multimedia: Gastric Ulcers
References
Further Reading

References

  1. Musumba C, Pritchard DM, Pirmohamed M. Review article: Cellular and molecular mechanisms of NSAID-induced peptic ulceration. Aliment Pharmacol Ther. Jul 3 2009;[Medline].

  2. Sadic J, Borgström A, Manjer J, Toth E, Lindell G. Bleeding peptic ulcer - time trends in incidence, treatment and mortality in Sweden. Aliment Pharmacol Ther. Aug 15 2009;30(4):392-8. [Medline].

  3. Taha AS, McCloskey C, Prasad R, Bezlyak V. Famotidine for the prevention of peptic ulcers and oesophagitis in patients taking low-dose aspirin (FAMOUS): a phase III, randomised, double-blind, placebo-controlled trial. Lancet. Jul 11 2009;374(9684):119-25. [Medline].

  4. Baldwin CM, Keam SJ. Rabeprazole: a review of its use in the management of gastric acid-related diseases in adults. Drugs. 2009;69(10):1373-401. [Medline].

  5. 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].

  6. 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].

  7. Wang HM, Hsu PI, Lo GH, Chen TA, Cheng LC, Chen WC, et al. Comparison of Hemostatic Efficacy for Argon Plasma Coagulation and Distilled Water Injection in Treating High-risk Bleeding Ulcers. J Clin Gastroenterol. May 14 2009;[Medline].

  8. [Best Evidence] 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].

  9. 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].

  10. Jensen DM. Management of severe ulcer rebleeding. N Engl J Med. Mar 11 1999;340(10):799-801. [Medline].

  11. 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].

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  13. 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].

  14. 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].

  15. 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].

  16. 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].

  17. Sonnenberg A, Everhart JE. Health impact of peptic ulcer in the United States. Am J Gastroenterol. Apr 1997;92(4):614-20. [Medline].

  18. 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].

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  20. 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].

  21. Wallace JL. Recent advances in gastric ulcer therapeutics. Curr Opin Pharmacol. Dec 2005;5(6):573-7. [Medline].

  22. Yang YX, Lewis JD, Epstein S, Metz DC. Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA. Dec 27 2006;296(24):2947-53. [Medline].

  23. [Best Evidence] van Rensburg C, Barkun AN, Racz I, et al. Clinical trial: intravenous pantoprazole vs. ranitidine for the prevention of peptic ulcer rebleeding: a multicentre, multinational, randomized trial. Aliment Pharmacol Ther. Mar 1 2009;29(5):497-507. [Medline].

Further Reading

Related eMedicine Topics

Clinical trials

National Guideline Clearinghouse

Keywords

gastric ulcers, ulcers, peptic ulcer disease, PUD, peptic ulcer, Helicobacter pylori infection, H pylori infection, NSAID toxicity, nonsteroidal anti-inflammatory drug toxicity, Zollinger-Ellison syndrome, ZES, gastrinoma, gastric cancer, stomach ulcer, GI ulcer, gastrointestinal ulcer, gastric ulcer, duodenal ulcer, cigarette smoking, gastroduodenal ulcer, hypersecretion of gastric acid, chronic renal insufficiency, diabetes, ulcer pain, epigastric pain, hematemesis, melena, presyncope, peritonitis, gastric perforation

Contributor Information and Disclosures

Author

Sanjeeb Shrestha, MD, Consulting Staff, Division of Gastroenterology, North West Arkansas Gastroenterology Clinic
Sanjeeb Shrestha, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and American Society of Gastrointestinal Endoscopy
Disclosure: 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
Daryl Lau, MD, MPH, FRCP(C) is a member of the following medical societies: American Association for the Study of Liver Diseases and American Gastroenterological Association
Disclosure: Nothing to disclose.

Medical Editor

David Greenwald, MD, Fellowship Program Director, Associate Professor, Department of Medicine, Division of Gastroenterology, Montefiore Medical Center, Albert Einstein College of Medicine
David Greenwald, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: 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
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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