eMedicine Specialties > Gastroenterology > Stomach

Peptic Ulcer Disease

Author: Tri H Le, MD, Assistant Professor of Medicine, Division of Gastroenterology and Hepatology, Penn State Milton S Hershey Medical Center
Coauthor(s): George T Fantry, MD, Director of Clinical Gastroenterology, Department of Internal Medicine, Division of Gastroenterology, Associate Professor, University of Maryland School of Medicine
Contributor Information and Disclosures

Updated: Jul 17, 2008

Introduction

Background

Peptic ulcer disease (PUD) is a common disorder that affects millions of individuals in the United States each year. PUD has a major impact on our health care system by accounting for roughly 10% of medical costs for digestive diseases. In the last two decades, major advances have been made in the understanding of the pathophysiology of PUD, particularly regarding the role of Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs). This has led to important changes in diagnostic and treatment strategies, with the potential for improving the clinical outcome and for decreasing health care costs.

Pathophysiology

Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. H pylori infection and NSAID use are the most common etiologic factors. Other less common causes are hypersecretory states, such as Zollinger-Ellison syndrome, G-cell hyperplasia, mastocytosis, and basophilic leukemias.

Under normal conditions, a physiologic balance exists between peptic acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as NSAIDs, H pylori, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive mechanisms include tight intercellular junctions, mucus, mucosal blood flow, cellular restitution, and epithelial renewal.

Frequency

United States

  • One-year point prevalence is 1.8%. Lifetime prevalence is approximately 10%. PUD affects approximately 4.5 million people annually.

International

The frequency of PUD in other countries is variable and determined primarily by association with the major causes of PUD: H pylori and NSAIDs.

Mortality/Morbidity

Medical office visits and hospitalizations for PUD have decreased in the last few decades. The mortality rate has decreased modestly in the last few decades and is approximately 1 death per 100,000 cases. The hospitalization rate is approximately 30 patients per 100,000 cases.

Sex

  • Prevalence has shifted from predominance in males to similar occurrences for both sexes.
  • Lifetime prevalence is approximately 11-14% for men and 8-11% for women.

Age

  • Age trends for ulcer occurrence reveal declining rates in younger men, particularly for duodenal ulcer, and increasing rates in older women.
  • Trends reflect complex changes in risk factors for PUD, including age-cohort phenomena with the prevalence of H pylori infection and the use of NSAIDs in older populations.

Clinical

History

  • Epigastric pain (the most common symptom)
    • Gnawing or burning sensation
    • Occurs 2-3 hours after meals
    • Relieved by food or antacids
    • Patient awakens with pain at night.
    • May radiate to the back (consider penetration)
  • Nausea
  • Vomiting, which might be related to partial or complete gastric outlet obstruction
  • Dyspepsia, including belching, bloating, distention, and fatty food intolerance
  • Heartburn
  • Chest discomfort
  • Anorexia, weight loss
  • Hematemesis or melena resulting from gastrointestinal bleeding
  • Dyspeptic symptoms that might suggest PUD are not specific because only 20-25% of patients with symptoms suggestive of peptic ulceration are found on investigation to have a peptic ulcer.

Physical

  • In uncomplicated PUD, clinical findings are few and nonspecific.
    • Epigastric tenderness
    • Guaiac-positive stool resulting from occult blood loss
    • Melena resulting from acute or subacute gastrointestinal bleeding
    • Succussion splash resulting from partial or complete gastric outlet obstruction

Causes

  •  H pylori infection
    • H pylori infection and NSAID use account for most cases of PUD.
    • The rate of H pylori infection for duodenal ulcers in the United States is less than 75% for patients who do not use NSAIDs. Excluding patients who use NSAIDs, 61% of duodenal ulcers and 63% of gastric ulcers are positive for H pylori in one study. This rate also depends on the demographic, which appears to be less frequent in whites as compared to nonwhites.
    • Prevalence in complicated ulcers (ie, bleeding, perforation) is significantly lower than that found in uncomplicated ulcer disease.
  • Nonsteroidal anti-inflammatory drugs
    • Similar to H pylori infection, NSAID use is a common cause for PUD.
    • Corticosteroids alone do not increase the risk for PUD; however, they can potentiate the ulcer risk in patients who use NSAIDs concurrently.
  • Severe physiologic stress
    • Burns
    • CNS trauma
    • Surgery
    • Severe medical illness
  • Hypersecretory states (uncommon)
    • Gastrinoma (Zollinger-Ellison syndrome) or multiple endocrine neoplasia (MEN-I)
    • Antral G cell hyperplasia
    • Systemic mastocytosis
    • Basophilic leukemias
  • Diseases associated with an increased risk of PUD include cirrhosis, chronic obstructive pulmonary disease, renal failure, and organ transplantation.
  • Additional rare, miscellaneous causes include radiation-induced or chemotherapy-induced ulcers, vascular insufficiency (crack cocaine), and duodenal obstruction.

More on Peptic Ulcer Disease

Overview: Peptic Ulcer Disease
Differential Diagnoses & Workup: Peptic Ulcer Disease
Treatment & Medication: Peptic Ulcer Disease
Follow-up: Peptic Ulcer Disease
References
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References

  1. Chan FK, Graham DY. Review article: prevention of non-steroidal anti-inflammatory drug gastrointestinal complications--review and recommendations based on risk assessment. Aliment Pharmacol Ther. May 15 2004;19(10):1051-61. [Medline].

  2. Conn HO, Poynard T. Corticosteroids and peptic ulcer: Meta-analysis of adverse events during steroid therapy. J Intern Med. 1994;236:619. [Medline].

  3. Ford AC, Delaney BC, Forman D, Moayyedi P. Eradication therapy in Helicobacter pylori positive peptic ulcer disease: systematic review and economic analysis. Am J Gastroenterol. Sep 2004;99(9):1833-55. [Medline].

  4. Gisbert JP, Khorrami S, Carballo F, et al. Meta-analysis: Helicobacter pylori eradication therapy vs. antisecretory non-eradication therapy for the prevention of recurrent bleeding from peptic ulcer. Aliment Pharmacol Ther. Mar 15 2004;19(6):617-29. [Medline].

  5. Hawkey CJ, Karrasch JA, Szczepanski L, et al. Omeprazole compared with misoprostol for ulcers associated with nonsteroidal anti-inflammatory drugs. Omeprazole versus Misoprostol for NSAID-induced Ulcer Management (OMNIUM) Study Group. N Engl J Med. 338(11):727-34. [Medline].

  6. Jyotheeswaran S, Shah AN, Jin HO, et al. Prevalence of Helicobacter pylori in peptic ulcer patients in greater Rochester, NY: is empirical triple therapy justified?. Am J Gastroenterol. Apr 1998;93(4):574-8. [Medline].

  7. Piper JM, Ray WA, Daugherty JR, Griffin MR. Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs. Ann Intern Med. May 1 1991;114(9):735-40. [Medline].

  8. Quan C, Talley NJ. Management of peptic ulcer disease not related to Helicobacter pylori or NSAIDs. Am J Gastroenterol. Dec 2002;97(12):2950-61. [Medline].

  9. Rautelin H, Lehours P, Megraud F. Diagnosis of Helicobacter pylori infection. Helicobacter. 2003;8 Suppl 1:13-20. [Medline].

  10. Salcedo JA, Al-Kawas F. Treatment of Helicobacter pylori infection. Arch Intern Med. Apr 27 1998;158(8):842-51. [Medline].

  11. Silverstein FE, Graham DY, Senior JR, et al. Misoprostol reduces serious gastrointestinal complications in patients with rheumatoid arthritis receiving nonsteroidal anti-inflammatory drugs. A randomized, double-blind, placebo-controlled trial. Ann Intern Med. 123(4):241-9. [Medline].

  12. 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].

  13. Wolfe MM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs. N Engl J Med. Jun 17 1999;340(24):1888-99. [Medline].

  14. Yeomans ND, Tulassay Z, Juhasz L, et al. A comparison of omeprazole with ranitidine for ulcers associated with nonsteroidal anti-inflammatory drugs. Acid Suppression Trial: Ranitidine versus Omeprazole for NSAID-associated Ulcer Treatment (ASTRONAUT) Study Group. N Engl J Med. 338(11):719-26. [Medline].

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Further Reading

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Keywords

PUD, Helicobacter pylori infection, H pylori infection, nonsteroidal anti-inflammatory drugs, NSAIDs, mucosal break, dyspepsia, heartburn, smoking, stress, epigastric pain, belching, bloating, distention, fatty food intolerance, hematemesis, melena, gastrointestinal bleeding, Guaiac-positive stool, occult blood loss, succussion splash, gastric outlet obstruction, duodenal ulcers, perforation, gastrinoma, Zollinger-Ellison syndrome, multiple endocrine neoplasia syndrome, MEN-I, antral G cell hyperplasia, systemic mastocytosis, basophilic leukemias, cirrhosis, chronic pulmonary disease, renal failure, renal transplantation, radiation-induced ulcers, chemotherapy-induced ulcers, vascular insufficiency, crack cocaine, duodenal obstruction

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Contributor Information and Disclosures

Author

Tri H Le, MD, Assistant Professor of Medicine, Division of Gastroenterology and Hepatology, Penn State Milton S Hershey Medical Center
Tri H Le, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society of Gastrointestinal Endoscopy, and Crohns and Colitis Foundation of America
Disclosure: Nothing to disclose.

Coauthor(s)

George T Fantry, MD, Director of Clinical Gastroenterology, Department of Internal Medicine, Division of Gastroenterology, Associate Professor, University of Maryland School of Medicine
George T Fantry, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Medical Editor

Terence David Lewis, MBBS, FRACP, FRCPC, FACP, Program Director, Internal Medicine Residency, & Assistant Chairman, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, Loma Linda University Medical Center
Terence David Lewis, MBBS, FRACP, FRCPC, FACP is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, California Medical Association, Royal College of Physicians and Surgeons of Canada, and Sigma Xi
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Noel Williams, MD, Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada
Noel Williams, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal 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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