eMedicine Specialties > Gastroenterology > Stomach

Gastric Ulcers

Author: Sanjeeb Shrestha, MD, Consulting Staff, Division of Gastroenterology, North West Arkansas Gastroenterology Clinic
Coauthor(s): Daryl Lau, MD, MPH, FRCPC, Assistant Professor, Department of Medicine, Division of Gastroenterology, University of Texas Medical Branch at Galveston
Contributor Information and Disclosures

Updated: May 2, 2007

Introduction

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

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).

• Search for CME/CE on This Topic »

• Helicobacter Pylori Infection (Gastroenterology)
• Intestinal Perforation (General Surgery)

• Peptic Ulcers Causes
• Peptic Ulcers Treatment
• Peptic Ulcers Overview
• Esophagus, Stomach, and Intestine Center
• Peptic Ulcers Symptoms

• Supplemental Dietary Glutamine Reduces H. Pylori-Related Pathology
• FDA Safety Changes: Zantac, Zithromax, Noxafil
• FDA Safety Changes: Prevacid NapraPAC 500, Prezista, Arixtra

• Asia-Pacific Consensus Guidelines on Gastric Cancer Prevention
• Characteristics of Patients Initiating Raloxifene Compared to Those Initiating Bisphosphonates
• Polymorphisms of Interleukin-1 and Interleukin-2 Genes in Patients With Gastric Cancer in Korea