Duodenal Ulcers

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Author

Alan BR Thomson, MD, Professor of Medicine, Division of Gastroenterology, University of Alberta, Canada

Nothing to disclose.

Coauthor(s)

Jon Meddings, MD, Head, Department of Medicine, Professor, Department of Internal Medicine, University of Alberta, Canada

Nothing to disclose.

Shane M Devlin, MD, FRCP(C), Clinical Assistant Professor, Department of Internal Medicine, Peter Lougheed Center, University of Calgary, Canada

Nothing to disclose.

Yvette PY Leung, MD, Fellow in Gastroenterology, Department of Internal Medicine, University of Calgary Medical Clinic

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.

BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

Nothing to disclose.

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

eMedicine Salary Employment

Waqar A Qureshi, MD, Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center

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

When we speak of duodenal ulcers, we often imply that these are part of what is known as peptic ulcer disease; duodenal ulceration may be only rarely due to other conditions. Most duodenal ulcers are associated with a Helicobacter pylori infection, or the use of gastric irritating medications such as aspirin, non-steroidal anti-inflammatory drugs (NSAIDs), or bisphosphonates.

Duodenal ulcers are a common condition characterized by the presence of a well-demarcated break in the mucosa that may extend into the muscularis propria of the duodenum (see images below). More than 95% of duodenal ulcers are found in the first part of the duodenum; most are less than 1 cm in diameter.[1]


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Duodenal ulcer in an elderly patient who presented with melena and hypotension.


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Duodenal ulcer in a 35-year-old woman who presented with tarry stools and a hemoglobin level of 75 g/L.


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Duodenal ulcer in a 65-year-old man with osteoarthritis who presented with hematemesis and melena stools. The patient took naproxen on a daily basis.

Proper diagnosis of duodenal ulcers is important because prompt initiation of treatment can effectively prevent potentially serious complications.

For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education articles Peptic Ulcers, Helicobacter Pylori (H. Pylori), and Gastritis.

Pathophysiology

The duodenal mucosa resists damage from the effect of aggressive factors, such as gastric acid and the proteolytic enzyme pepsin, with the help of several protective factors, such as a mucous layer, bicarbonate secretion, and protective prostaglandins.

The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. A portion of the gastric and duodenal mucus exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer.

In the event of acid and pepsin entering the epithelial cells, additional mechanisms are in place to reduce injury. Within the epithelial cells, ion pumps in the basolateral cell membrane help to regulate intracellular pH by removing excess hydrogen ions. Through the process of restitution, healthy cells migrate to the site of injury. Mucosal blood flow removes acid that diffuses through the injured mucosa and provides bicarbonate to the surface epithelial cells.

A duodenal ulcer occurs when an alteration occurs in the aggressive and/or protective factors such that the balance is in favor of gastric acid and pepsin. Any process that increases gastric acidity (eg, individuals with increased maximal and basal acid output), decreases prostaglandin production (eg, NSAIDs), or interferes with the mucous layer (eg, H pylori infection) can cause such an imbalance and lead to peptic ulcer disease.

Full understanding of the pathophysiology and pathogenesis of duodenal ulcers requires a brief discussion of the 2 major etiologies: NSAID use and H pylori infection. NSAIDs are pathogenic through their inhibition of the cyclooxygenase-1 (COX-1) pathway, which normally produces protective prostaglandins. These prostaglandins are protective because they augment both bicarbonate and mucous production, as mentioned above. However, perhaps more important, prostaglandins augment mucosal blood flow, and their inhibition leads to impairment of blood flow, leaving the mucosa vulnerable to damage.

Infection with H pylori is likely pathogenic by means of a variety of indirect mechanisms as the organism does not generally colonize the duodenum. The mechanisms are described as follows[2] :

Epidemiology

Frequency

United States

The prevalence of duodenal ulcers is estimated to be 6-15% in the general population. Most individuals do not have clinically significant ulcer disease, peptic ulcer disease is decreasing,[17] and ulcers have become a rare cause for hospital admission.[18] The prevalence is linked to the presence of H pylori. Approximately only 10% of young persons have H pylori infection, and the proportion of people with the infection increases steadily with age.

Approximately 10% of the US population has evidence of a duodenal ulcer at some time. Of those infected with H pylori, the lifetime prevalence is approximately 20%. Overall, the incidence of duodenal ulcers has been decreasing over the past 3-4 decades.

International

As in the US, duodenal ulcer disease prevalence is linked to H pylori infection. The prevalence of H pylori infection varies widely among countries and even in regions within countries.

Mortality/Morbidity

Duodenal ulcers cause significant morbidity, which is mainly related to pain, and hospitalization for complications, such as ulcer hemorrhage, perforation, penetration, and obstruction.

Rates of duodenal ulcer complications and mortality are generally increased in elderly patients, perhaps because of the high incidence of comorbid diseases in this group and their increased use of NSAIDs.

Race

No specific relationship between race and the occurrence of duodenal ulcers exists. In general, areas with a high prevalence of H pylori infection have a high prevalence of duodenal ulcers.

Sex

Age

The prevalence of duodenal ulcers increases with age. This is probably related to the increased prevalence of H pylori infection in older age groups, coupled with increased use of NSAIDs.

History

Patients with duodenal ulcers have a variety of clinical presentations, ranging from individuals who are completely asymptomatic to those who develop severe complications, such as gastrointestinal (GI) hemorrhage. Some generalizations can be made with respect to common clinical presentations of duodenal ulcers.

Physical

No characteristic physical findings are associated with duodenal ulcers. In general, most patients have tenderness over the epigastrium, but this finding has a low sensitivity and specificity. Less often, tenderness is present over the right upper quadrant (RUQ), left upper quadrant (LUQ), or supraumbilical region. Most patients with an uncomplicated duodenal ulcer do not have any other physical findings.

Causes

The understanding of the etiology of duodenal ulcers changed dramatically in the latter part of the 20th century. Historically, duodenal ulcers were thought to be a disease related to diet and environmental stress alone. Subsequent studies revealed the importance of pepsin and acid secretion in the pathogenesis of duodenal ulcers. The most revolutionary change in the knowledge of duodenal ulcers was the discovery in 1982 that the bacterium H pylori was present in most affected patients.

Laboratory Studies

Imaging Studies

Other Tests

Procedures

Medical Care

Treatment of duodenal ulcers varies depending on the etiology and clinical presentation. The initial management of a stable patient with dyspepsia differs from the management of an unstable patient with upper GI hemorrhage. In the latter scenario, failure of medical management not uncommonly leads to surgical intervention.

Although the therapeutic principles of these distinct clinical scenarios share some similarities, they differ sufficiently to warrant separate discussions. Age is an independent risk factor for the incidence and mortality from bleeding peptic ulcer, with the risk increasing in persons older than 65 years, and increasing further in those older than age 75 years.[64] In one study, at least 2 risk factors (previous duodenal ulcer, H pylori infection, use of ASA/NSAID, and smoking) were present in two thirds of persons with acute gastroduodenal bleeding.[65]

The principles of management of bleeding peptic ulcers outlined below are equally applicable to both gastric and duodenal ulcers.

Surgical Care

Endoscopic intervention is the primary mode of treating bleeding ulcers. Surgical management of duodenal ulcers is generally reserved for refractory ulcers and bleeding ulcers that fail to respond to medical management.

Consultations

Surgical consultation is recommended for all patients with bleeding ulcers, especially those patients who are at high risk of significant bleeding. Such ulcers include those that are causing hemodynamic instability, those that are actively bleeding, and those that are showing a visible vessel on endoscopy.

Diet

Diet, Alcohol Consumption, and Smoking

A special diet is not indicated in patients with duodenal ulcers. It is common sense to avoid any food or beverages which on a person-by-person basis aggravate symptoms. Although the link between duodenal ulcers and alcohol use and smoking is inconclusive, moderation of alcohol intake and cessation of smoking may be recommended for other health reasons.

Medication Summary

The goals of pharmacotherapy are to eradicate H pylori infection, to reduce morbidity, and to prevent complications in patients with duodenal ulcers.

Class Summary

PPIs are inhibitors of the gastric H+/K+ -ATPase (proton pump) enzyme system, which catalyzes the exchange of H+ and K+.

Omeprazole (Prilosec)

Clinical Context:  Suppresses gastric acid secretion by specifically inhibiting H+/K+ -ATPase system at the secretory surface of gastric parietal cells. Administer 30 min before sucralfate to prevent reduction in bioavailability.

Pantoprazole (Protonix, Pantoloc)

Clinical Context:  Suppresses gastric acid secretion by specifically inhibiting H+/K+ -ATPase system at the secretory surface of gastric parietal cells. Indicated for < 8-wk treatment of erosive esophagitis associated with GERD. May consider additional 8-wk course if ulcer does not heal. Safety and efficacy for maintenance therapy (eg, >16 wk) not established.

Lansoprazole (Prevacid)

Clinical Context:  Suppresses gastric acid secretion by specifically inhibiting H+/K+ -ATPase system at the secretory surface of gastric parietal cells. Used for < 4 wk to treat and relieve the symptoms of an active duodenal ulcer.

Esomeprazole magnesium (Nexium)

Clinical Context:  Inhibits gastric acid secretion by inhibiting H+/K+ -ATPase system at the secretory surface of gastric parietal cells.

Class Summary

H2 blocker antihistamine agents are used in the short-term treatment of an active duodenal ulcer and as prophylaxis in the long term.

Cimetidine (Tagamet)

Clinical Context:  Inhibits histamine at H2 receptors of gastric parietal cells, reducing gastric acid secretion, gastric secretory volume, and hydrogen concentration.

Famotidine (Pepcid AC, Pepcid)

Clinical Context:  Competitively inhibits histamine at H2 receptors of gastric parietal cells, reducing gastric acid secretion, gastric secretory volume, and hydrogen concentration.

Nizatidine (Axid)

Clinical Context:  Competitively inhibits histamine at H2 receptors of the gastric parietal cells, reducing gastric acid secretion, gastric secretory volume, and hydrogen concentration.

Ranitidine (Zantac)

Clinical Context:  Inhibits histamine stimulation of H2 receptors in gastric parietal cells, reducing gastric acid secretion, gastric secretory volume, and hydrogen concentration.

Administer 30 min before sucralfate to prevent decrease in bioavailability.

Ranitidine bismuth citrate (Tritec, Pylorid)

Clinical Context:  Combination of ranitidine and bismuth citrate, compound with bactericidal effects against H pylori. Used in with clarithromycin, because drugs act synergistically against H pylori.

Class Summary

Antimicrobial agents exert an antibacterial effect on H pylori.

Amoxicillin (Amoxil, Trimox)

Clinical Context:  Semisynthetic penicillin antibiotic; interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Metronidazole (Flagyl)

Clinical Context:  Imidazole ring-based antibiotic active against anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents.

Tetracycline (Sumycin)

Clinical Context:  Semisynthetic antibacterial agent derived from Streptomyces cultures. Effective against gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and, possibly, 50S ribosomal subunit(s).

Clarithromycin (Biaxin)

Clinical Context:  Macrolide antibiotic that inhibits bacterial growth, possibly by blocking the dissociation of peptidyl tRNA from ribosomes, arresting RNA-dependent protein synthesis.

Class Summary

Antidiarrheal agents may have antisecretory and antimicrobial action.

Bismuth subsalicylate (Pepto-Bismol, Pink Bismuth, Bismatrol, Devrom)

Clinical Context:  Used in combination with antibiotics and H2RAs or PPIs to treat active duodenal ulcers associated with H pylori.

Further Inpatient Care

Further Outpatient Care

Inpatient & Outpatient Medications

Deterrence/Prevention

Complications

Prognosis

References

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Duodenal ulcer in an elderly patient who presented with melena and hypotension.

Duodenal ulcer in a 35-year-old woman who presented with tarry stools and a hemoglobin level of 75 g/L.

Duodenal ulcer in a 65-year-old man with osteoarthritis who presented with hematemesis and melena stools. The patient took naproxen on a daily basis.

Deformity of duodenal cap caused by recurrent ulceration. Single-contrast view.

Double-contrast upper gastrointestinal series. Posterior wall duodenal ulcer (same patient in Images 5 and 6).

Lateral view of a posterior wall ulcer (same patient in Images 5 and 6).

An antral gland of the stomach with a large Giemsa-stained colony of Helicobacter pylori in the lumen (arrow) at 250X power. Courtesy of Pantaleo Bufo, University of Foggia, Italy.

A transverse section of the gastric lamina propria is shown in a patient with Helicobacter pylori infection. In the lower part, an antral gland of the stomach is present with some H pylori in the lumen (red-blue arrow). In the upper part, a mast cell (yellow arrow) is present (Giemsa staining, 250X). Courtesy of Pantaleo Bufo, University of Foggia, Italy.