eMedicine Specialties > Gastroenterology > Intestine

Duodenal Ulcers

Author: Alan BR Thomson, MD, MSc, PhD, Professor, Department of Medicine, Division of Gastroenterology, University of Alberta Faculty of Medicine
Coauthor(s): Yvette PY Leung, MD, Fellow in Gastroenterology, Department of Internal Medicine, University of Calgary Medical Clinic; Shane M Devlin, MD, FRCP(C), Clinical Assistant Professor, Department of Internal Medicine, Peter Lougheed Center, University of Calgary, Canada; Jon Meddings, MD, Head, Department of Medicine, Professor, Department of Internal Medicine, University of Alberta, Canada
Contributor Information and Disclosures

Updated: Jun 3, 2009

Introduction

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

Duodenal ulcer in an elderly patient who presente...

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

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Duodenal ulcer in an elderly patient who presente...

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


Duodenal ulcer in a 35-year-old woman who present...

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 35-year-old woman who present...

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 osteoart...

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.

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Duodenal ulcer in a 65-year-old man with osteoart...

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 follows2 :

  • H pylori infection that follows an antral predominant pattern leads to an inflammatory state in which high levels of tumor necrosis factor-alpha (TNF-alpha) and other cytokines are produced. These stimulate gastric acid production directly by increasing gastrin release from G cells and inhibit somatostatin production by antral D cells. This leads to a net increase in gastric acid secretion, which leads to an increased acid load in the duodenum, overwhelming the mucosal defense.3,4
  • Duodenal acid exposure can lead to gastric metaplasia, whereby the duodenal mucosa can take on characteristics of gastric mucosa. H pylori can then colonize the duodenal mucosa and adhere to cells. This adherence leads to a variety of second-messenger signals, which invoke an immunologic response against those cells causing mucosal damage by host neutrophils and other inflammatory cells.
  • H pylori also affects the gastric and duodenal mucous layer, because this organism produces proteases that degrade the protective mucous layer. Moreover, H pylori infection decreases the production of epidermal growth factor, which normally promotes healing of gastric and duodenal mucosa.
  • H pylori organisms produce urease. Urease hydrolyzes urea to ammonia and carbon dioxide. Hydroxide ions produced by equilibration of ammonia with water may damage the gastric and duodenal mucosa. H pylori produces proteins that may serve as chemotactic factors for neutrophils and monocytes, which act as proinflammatory cells. H pylori also affects the gastric and duodenal mucous layer, because these organisms produce proteases that degrade the protective mucous layer. H pylori does not lead to the development of gastric and duodenal ulcers through alteration of the bacterial flora.
  • H pylori gene cagA and s1 or m1 forms of VacA (especially the intermediate region) are more common in disease-associated strains,5 especially cagPA1 and vacA s1 genotypes.6  CagA may be a risk factor for intestinal metaplasia.7
  • The cellular immune response in the H pylori– infected gastric mucosa is predominantly the T helper cell type 1 (Th1) type. Interleukin (IL)-18 levels are increased in this setting.8  The acidic environment of the gastric lumen induces the gastric mucosal production of IL-8, which is involved in the proinflammatory pathways.9
  • The receptors for bacterial adhesins include the Lewis b structures of the secretory M4C 5AC mucin, and in H pylori –positive duodenal ulcer patients, the initial low level of MUC1 mucin in gastric juice increases with eradication of this organism.10
  • The secretion of soluble triggering receptor is increased in H pylori –positive persons with gastric but not duodenal ulcers,11 suggesting that the host response may determine the site of ulceration. The age of the host may also influence the type of immune mechanism(s) involved in the pathogenesis of the H pylori –associated gastroduodenal disease.12
  • The 3 putative regions of H pylori include strain-specific genes, phase-variable genes, and genes with variable structures/genotype.13  Some strain-specific genes are in the plasticity regions, away from the cag pathogenicity island.14
  • Enhanced expression and release of endothelins (ET-1), an increase in the expression of the immediate early gene EGR-1, and the upregulation of angiogenic growth factors necessarily initiated by hydrochloric acid and proteolytic enzymes are also mechanisms in duodenal ulceration.15
  • There are new controversies emerging in the H pylori story, including investigators that question whether H pylori does cause duodenal ulcers and whether H pylori infection persists until it is pharmacologically eradicated.16

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.

  • With NSAID-related ulcers, the incidence of perforation is approximately 0.3% per patient year and of obstruction, approximately 0.1% per patient year. Combining both duodenal ulcers and gastric ulcers, the rate of any complication in all age groups combined is approximately 1-2% per ulcer per year.
  • Over the last 20 years, the mortality rate in the setting of ulcer hemorrhage has not changed appreciably despite the advent of histamine-2 receptor antagonists (H2RAs) and proton pump inhibitors (PPIs). However, evidence from meta-analyses and other studies has shown a decreased mortality rate from bleeding peptic ulcers when intravenous PPIs are used after successful endoscopic therapy.19,20,21,22 In general, if one considers all patients with duodenal ulcers, the mortality rate due to ulcer hemorrhage is approximately 5%.
  • The mortality rate of patients requiring surgical intervention for complications of duodenal ulcers, such as perforation and obstruction, is significantly higher than the general rate and related to the age of the patient. Most deaths in this setting result from postoperative complications.
  • Giant duodenal ulcers have high rates of morbidity and mortality.23

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

  • Over the last several years, a trend toward an increasing incidence of duodenal ulcers in females and decreasing incidence in males has been observed, especially in younger males, in whom the prevalence of H pylori infection is decreasing.
  • Historically, duodenal ulcers were believed to be more common in men than in women. Today, the prevalence is probably equal in men and women.

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.

Clinical

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.

  • Some common symptoms in patients with duodenal ulcers follow:
    • Epigastric pain can be sharp, dull, burning, or penetrating.
    • Many patients experience a feeling of hunger.
    • The pain may radiate into the back.
    • About 20-40% of patients describe bloating, belching, or symptoms suggestive of gastroesophageal reflux.
    • Ulcer-related pain generally occurs 2-3 hours after meals and often awakens the patient at night. This pattern is believed to be the result of increased gastric acid secretion, which occurs after meals and during the late night and early morning hours when circadian stimulation of gastric acid secretion is the highest.
    • About 50-80% of patients with duodenal ulcers experience nightly pain, as opposed to only 30-40% of patients with gastric ulcers and 20-40% of patients with nonulcer dyspepsia (NUD).
    • Pain is often relieved by food, a finding often cited as being specific for a duodenal ulcer. However, this symptom is present in only 20-60% of patients and is probably not specific for duodenal ulcers.
  • The pain of duodenal ulcers is generally episodic; however, the pain can evolve into a chronic, daily occurrence in some patients.
    • A change in the patient's usual pattern of ulcer pain should be considered serious, because it may herald an imminent complication. When food or antacids fail to relieve the pain or when the pain begins to radiate to new anatomic locations, a high index of suspicion of a complication is warranted.
      • Concern is especially warranted in the setting of new-onset nausea and vomiting, decreased appetite, and weight loss.
  • GI bleeding is a common complication of duodenal ulcers and can have serious consequences.
    • Patients may present with melena, coffee-ground emesis, or hematemesis.
    • The passage of frank blood in the stool or maroon-colored stool in the presence of a bleeding duodenal ulcer suggests precipitous GI bleeding.
  • Patients who develop gastric outlet obstruction as a result of a chronic, untreated duodenal ulcer usually report a history of fullness and bloating associated with nausea and emesis that occurs several hours after food intake. A common misconception is that adults with gastric outlet obstruction present with nausea and emesis immediately after a meal.
  • A few individuals with duodenal ulcers are completely asymptomatic.
    • According to one study, typical epigastric pain was rare in patients older than 65 years with peptic ulcer disease (ie, gastric ulcer and duodenal ulcer).
    • Elderly patients are more likely than younger patients to present in an asymptomatic fashion, which is especially common in the setting of NSAID use.

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.

  • In the presence of a complication, such as gastric outlet obstruction, the physician may note upper abdominal distention and hear a succussion splash on auscultation.
  • Perforation of peptic ulcers is common in older persons using aspirin (ASA)/NSAIDs.24
  • Perforation usually results in classic findings of diffuse peritonitis with abdominal rigidity, guarding, and rebound tenderness. Bowel sounds may initially be hyperactive but, with time, become absent.
  • Risk factors for mortality from peptic ulceration include preoperative metabolic acidosis, renal insufficiency at the time of admission, reduced serum albumin concentrations on admissions or poor postoperative nutrition.25

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.

  • NSAIDs
    • Long before the discovery of H pylori, NSAIDs were known to be associated with GI toxicity, including the formation of gastric ulcers and duodenal ulcers.26  H pylori enhances the damaging effect of NSAIDs on the gastroduodenal mucosa,27  and NSAID GI-complications also occur in children.28
    • As many as 4-10% of patients on daily therapeutic-dose NSAIDs develop a duodenal ulcer within 3 months of initiation of therapy, and up to 1% of these duodenal ulcers are clinically significant.
    • A clear dose-response relationship exists, with high NSAID doses associated with increased risk of duodenal mucosal damage. Clinically, NSAID-induced duodenal ulcers are most likely to bleed. In one study, NSAID use was associated with a relative risk for bleeding of 8.4, as opposed to 1.5 for H pylori –associated duodenal ulcers. Patients taking NSAIDs, especially elderly patients, are most likely to present with an asymptomatic bleeding duodenal ulcer.
    • Factors associated with an increased risk of duodenal ulcers in the setting of NSAID use are a history of previous peptic ulcer disease, advanced age, female sex, high doses or combinations of NSAIDs, long-term NSAID use, concomitant use of anticoagulants, and severe comorbid illnesses. Corticosteroids do not increase the risk of duodenal ulcers by themselves, but the risk of duodenal ulcers is increased when corticosteroids are used in combination with NSAIDs, as compared to NSAID use alone.
    • Aspirin is a significant risk factor for damage to the gastroduodenal mucosa.29,30 ; however, its damaging effect does not depend on an H pylori infection.31
    • Giving a PPI with the episodic use of the naproxen (500 mg bid) reduces gastroduodenal ulcers from 46.9% to 11.8%,32 as well as reduces the risk of ulcers in persons with continuous low dose aspirin.33
    • H pylori eradication in persons on long-term therapy with an NSAID has no beneficial effect on the development of ulcers, erosions, or dyspepsia.34
    • Using the antiplatelet drug clopidrogel rather than aspirin plus a PPI causes fewer GI complications in persons with no pervious history of duodenal or gastric ulcers, but the difference is very small and the number-needed-to-treat (NNT) to prevent 1 episode of bleeding per year is approximately 200.35
    • Acetaminophen given with a PPI is associated with the same increased risk of hospitalization as with a traditional NSAID plus a PPI.36
    • Although initially controversial, most evidence now supports the assertion that H pylori and NSAIDs are synergistic with respect to the development of peptic ulcer disease. Eradication of H pylori in the setting of chronic NSAID use is associated with a decreased risk of ulcer bleeding.37  A meta-analysis found that H pylori eradication in NSAID-naive users before the initiation of NSAIDs was associated with a decrease in peptic ulcers.38
    • The potential for decreased GI mucosal injury with newer COX-2–selective inhibitors, celecoxib and rofecoxib, has been emphasized. On September 30, 2004, Merck & Co, Inc, announced a voluntary withdrawal of rofecoxib (Vioxx) from the US and worldwide markets because of its association with an increased rate of cardiovascular events (including heart attacks and strokes) compared with placebo. The newer NSAIDs do not inhibit COX-1 and, therefore, do not have the disadvantage of reducing the synthesis of protective prostaglandins. Overall, selective COX-2 inhibitors are associated with, at best, a modest decrease in the risk of ulcer bleeding. One study showed that the combination of a traditional NSAID with a daily PPI had the same risk of bleeding as that of a COX-2 inhibitor alone.39
  • H pylori bacteria
    • H pylori bacteria are small, microaerophilic, spiral-shaped, gram-negative rods. The presence of H pylori in the stomach and duodenum is probably the most common bacterial infection in the world. Areas with a high prevalence of H pylori infection have a high incidence of duodenal ulcer.
    • H pylori infection is generally regarded as the most important etiologic factor in the development of duodenal ulcer.40 Most authors regard H pylori as the cause of 85-95% of duodenal ulcers. Even in chronic scarred duodenal ulcers, H pylori may be found in 63% of subjects.41
    • The bacterium can induce duodenal mucosal damage by means of several mechanisms (see Pathophysiology).
    • All evidence supports the assertion that H pylori is the major cause of duodenal ulcers. However, the risk of developing a duodenal ulcer in an individual infected with H pylori is only about 1% per year, and only 10-15% of individuals with H pylori infection develop a duodenal ulcer at any point in life. Therefore, other pathogenic factors must function either independently or in concert with H pylori to produce duodenal ulcers.
    • Factors other than H pylori are likely involved in the pathogenesis of peptic ulcer disease in persons with hepatic cirrhosis42 and chronic renal failure on dialysis.43 The eradication of H pylori does not prevent ulcer formation or complications in persons with cirrhosis.44  Endoscopic lesions of the upper GI tract are less common in those persons as compared with individuals without end-stage renal disease (ESRD).45 Chronic obstructive pulmonary disease (COPD) increases the 30-day mortality in patients with bleeding or perforated peptic ulcers.46
    • Duodenal ulcers that are not associated with H pylori or NSAIDs may include Crohn disease,47 lymphoma or adenocarcinoma, selective internal radiation therapy,48  or localized ischemia from sickle cell disease.49
  • H pylori –negative duodenal ulcer
    • In one study, among 608 patients with duodenal ulcers, 42 (6.9%) were classified as idiopathic, but 3% had isolated duodenal colonization.50  Some studies have shown that the proportion of H pylori –related duodenal ulcers is significantly less than the commonly reported 85-95%. One group examined nearly 2400 cases of endoscopically proven, non–NSAID-related duodenal ulcers and found that only 73% patients were positive for H pylori.51 However, other studies have produced conflicting results, and another study showed that antibiotic use within 1 month of diagnosis may have resulted in false-negative results.
    • Epstein-Barr virus either alone or in combination with H pylori infection may be associated with peptic ulcer disease.52
    • In up to one third of patients with duodenal ulcers, basal acid output (BAO) and maximal acid output (MAO) are increased. In one study, increased BAO was associated with an odds ratios [OR] of up to 3.5, and increased MAO was associated with an OR of up to 7, for the development of duodenal ulcers. People at especially high risk are those with a BAO greater than 15 mEq/h. The increased BAO may reflect the fact that, in a significant proportion of patients with duodenal ulcers, the parietal cell mass is increased to nearly twice that of the reference range.53
    • In addition to the increased gastric and duodenal acidity observed in some patients with duodenal ulcers, accelerated gastric emptying is often present. This acceleration leads to a high acid load delivered to the first part of the duodenum, where 95% of all duodenal ulcers are located. Acidification of the duodenum leads to gastric metaplasia, which indicates replacement of duodenal villous cells with cells that share morphologic and secretory characteristics of gastric epithelium. Gastric metaplasia may create an environment that is well suited to colonization by H pylori.
    • Tramadol also increases a person’s risk of perforation and mortality from peptic ulcers.54
    • Duodenal ulcers occur in 3.6% of dyspeptic persons infected with the human immunodeficiency virus (HIV) and treated with highly active antiretroviral therapy (HAART); gastric ulcers occur in 2.7%.55  H pylori becomes more prevalent as the CD4 cell count rises, and endoscopy becomes more useful for persons with CD4 cell counts less than or equal to 200, when opportunistic infections and malignancies are more common.
  • Lifestyle factors
    • Smoking: Evidence that tobacco use is a risk factor for duodenal ulcers is not conclusive. Evidence supporting a pathogenic role for smoking comes from the finding that smoking may accelerate gastric emptying and decrease pancreatic bicarbonate production. However, studies have produced contradictory findings. In one prospective study of more than 47,000 men with duodenal ulcers, smoking did not emerge as a risk factor.56 However, smoking in the setting of H pylori infection may increase the risk of relapse of PUD.57
    • Smoking is harmful to the gastroduodenal mucosa, and H pylori infiltration is denser in the gastric antrum of smokers.58
    • Alcohol use: Ethanol is known to cause gastric mucosal irritation and nonspecific gastritis. Evidence that consumption of alcohol is a risk factor for duodenal ulcer is inconclusive. A prospective study of more than 47,000 men with duodenal ulcer did not find an association between alcohol intake and duodenal ulcer.56
    • Caffeine intake: Little evidence suggests that caffeine intake is associated with an increased risk of duodenal ulcers.
    • Diet: Historically, diet was considered one of the primary causes of peptic ulcer disease. However, current knowledge indicates that diet probably has little influence on the pathogenesis of duodenal ulcers. Deficiency of certain essential fatty acids necessary for prostaglandin production has been examined as a possible risk factor. Moreover, some physicians hypothesize that regional variability of duodenal ulcer prevalence not directly related to H pylori prevalence may be related to diet. In general, evidence linking diet and duodenal ulcer is weak.
  • Genetics
    • More than 20% of patents have a family history of duodenal ulcers, compared with only 5-10% of control groups. In addition, weak associations have been observed between duodenal ulcers and blood type O. Furthermore, patients who do not secrete ABO antigens in their saliva and gastric juices are known to be at higher risk. The reason for these apparent genetic associations is unclear.
    • A rare genetic association exists between familial hyperpepsinogenemia type I (a genetic phenotype leading to enhanced secretion of pepsin) and duodenal ulcers. However, H pylori can increase pepsin secretion, and a retrospective analysis of the sera of one family studied before the discovery of H pylori revealed that their high pepsin levels were more likely related to H pylori infection.
  • Other causes
    • Acid hypersecretory syndromes
      • Gastrinoma (Zollinger-Ellison syndrome): First described in 1955, Zollinger-Ellison syndrome is caused by a tumor of pancreatic islet cells that produces gastrin. It is associated with gastric acid hypersecretion and development of peptic ulcer disease. From 0.1% to 1% of duodenal ulcers are thought to be secondary to an underlying gastrin-secreting tumor.59  With the shortage of secretion for diagnostic testing in persons suspected of Zollinger-Ellison syndrome, the glucagon provocative test may prove to be a suitable alternative.60
      • Systemic mastocytosis: Systemic mastocytosis is a disease associated with diffuse infiltration of the skin, GI tract, bone marrow, spleen, and liver with mastocytes. Gastric acid hypersecretion occurs in response to histamine production by mastocytes.
      • Basophilia: In the setting of a myeloproliferative disorder, basophilia can be associated with duodenal ulcer secondary to histamine production, as is systemic mastocytosis. This tends to occur more frequently after chemotherapy-induced cell lysis that causes increased release of histamine from cells.
    • Other factors
      • Infection: Some evidence suggests that herpes simplex virus-1 (HSV-1) and cytomegalovirus (CMV) may be associated with duodenal ulcers and gastric ulcers in a minority of patients.
      • Chemotherapy: Chemotherapeutic agents, such as 5-fluorouracil (5-FU), methotrexate (MTX), and cyclophosphamide, have been associated with development of duodenal ulcers.
      • Radiation: Local radiation can result in mucosal damage, which may lead to the development of duodenal ulcers.
      • Crack cocaine: Use of crack cocaine causes localized vasoconstriction, and the reduced blood flow may lead to mucosal damage.
      • The risk of upper GI tract bleeding may be increased in users of the diuretic spirolactone,61  or moderate and high affinity serotonin reuptake inhibitors.62

More on Duodenal Ulcers

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

duodenal ulcers, DU, peptic ulcer disease, PUD, dyspepsia, Helicobacter pylori ulcer, H pylori ulcer, nonsteroidal anti-inflammatory drug ulcer, NSAID ulcer, gastric ulcer, gastric acid, pepsin, histamine2 receptor antagonists, H2RA, proton pump inhibitors, PPI, Zollinger-Ellison syndrome, ZES, peptic ulcer perforation, Curling ulcer, Curling's ulcer

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Contributor Information and Disclosures

Author

Alan BR Thomson, MD, MSc, PhD, Professor, Department of Medicine, Division of Gastroenterology, University of Alberta Faculty of Medicine
Alan BR Thomson, MD, MSc, PhD is a member of the following medical societies: American Federation for Aging Research, American Federation for Clinical Research, American Gastroenterological Association, American Geriatrics Society, American Physiological Society, Canadian Association of Gastroenterology, Gastroenterology Research Group, New York Academy of Sciences, and Royal Society of Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Yvette PY Leung, MD, Fellow in Gastroenterology, Department of Internal Medicine, University of Calgary Medical Clinic
Yvette PY Leung, MD is a member of the following medical societies: Alberta Medical Association, American College of Physicians, American Gastroenterological Association, Canadian Association of Gastroenterology, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Shane M Devlin, MD, FRCP(C), Clinical Assistant Professor, Department of Internal Medicine, Peter Lougheed Center, University of Calgary, Canada
Shane M Devlin, MD, FRCP(C) is a member of the following medical societies: American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Jon Meddings, MD, Head, Department of Medicine, Professor, Department of Internal Medicine, University of Alberta, Canada
Jon Meddings, MD is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

Medical Editor

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
Waqar A Qureshi, MD is a member of the following medical societies: 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

BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
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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