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Peptic Ulcer Disease

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Last Update: December 4, 2018.

Introduction

Peptic ulcer disease is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. It may involve lower esophagus, distal duodenum or jejunum.

Etiology

Peptic ulcer disease (PUD) has various causes however Helicobacter pylori-associated PUD and NSAID-associated PUD account for the majority of the disease etiology.[1]

Causes of Peptic Ulcer Disease

Common

  • H. pylori infection
  • NSAIDs
  • Medications

Rare

  • Zollinger-Ellison syndrome
  • Malignancy (gastric/lung cancer, lymphomas)
  • Stress (Acute illness, burns, head injury)
  • Viral infection
  • Vascular insufficiency
  • Radiation therapy
  • Crohn disease
  • Chemotherapy

Helicobacter Pylori-Associated PUD

H. pylorus is a gram-negative bacillus that is found within the gastric epithelial cells. This bacterium is responsible for 90% of duodenal ulcers and 70% to 90% of gastric ulcers. H. pylori infection is more prevalent among those with a lower socioeconomic status and is commonly acquired during childhood. The organism has a wide spectrum of virulence factors allowing it to adhere to and inflame the gastric mucosa. This results in hypochlorhydria or achlorhydria leading to gastric ulceration.

 Virulence Factors of  Helicobacter pylori

  1. Urease: Secretion of urease breaks down urea into ammonia and protects the organism by neutralizing the acidic gastric environment.
  2. Toxins: CagA/ VacA are associated with stomach mucosal inflammation and host tissue damage.
  3. Flagella: Provides motility and allows movement toward the gastric epithelium.

NSAID-associated PUD

Nonsteroidal anti-inflammatory drugs and aspirin use is the second most common cause of PUD after H. pylori infection.[2][3] The gastric mucosa is normally protected by secretion of prostaglandin. NSAIDs block prostaglandin synthesis by inhibiting COX-1 enzyme resulting in a decrease in gastric mucus and bicarbonate production and a decrease in mucosal blood flow.

Medications

Apart from NSAIDs, bisphosphonates, potassium chloride, steroids, and fluorouracil have been implicated in etiology of PUD.

Epidemiology

PUD is a global problem with a lifetime risk of development ranging from 5% to 10%.[4][5] Overall, there is a decrease in incidence of PUD worldwide due to improved hygienic and sanitary conditions combined with effective treatment and judicious use of NSAIDs.[5] Duodenal ulcers are four times more common than gastric ulcers. Also, duodenal ulcers are more common in men than in the woman.

Pathophysiology

The mechanism of occurrence of PUD results from an imbalance between gastric mucosal protective and destructive factors. Risk factors predisposing to the development of PUD:

  • H. pylori infection
  • NSAID use
  • First-degree relative with PUD
  • Emigrant from a developed nation
  • African American/Hispanic ethnicity

Histopathology

Gastric ulcers are most commonly located on the lesser curvature whereas duodenal ulcers are most common at the duodenal bulb. The ulcer is round to oval with a smooth base. Acute ulcers have regular borders while chronic ulcers have elevated borders with inflammation. An ulcer extends beyond the muscularis mucosa.

History and Physical

Signs and symptoms of peptic ulcer disease may vary depending upon the location of the disease and age. Gastric and duodenal ulcers can be differentiated from the timing of their symptoms in relation to meals. Common signs and symptoms include:

  • Epigastric abdominal pain
  • Bloating
  • Abdominal fullness
  • Nausea and vomiting
  • Weight loss/weight gain
  • Hematemesis
  • Melena

Evaluation

Diagnosis of PUD requires history taking, physical examination, and invasive/noninvasive medical tests.

History

A careful history should be obtained and noted for the presence of any complications. Patient reporting of epigastric abdominal pain, early satiety, and fullness following a meal raise suspicion of PUD. The pain of gastric ulcers increases 2 to 3 hours after a meal and may result in weight loss whereas pain of duodenal ulcers decreases with meal resulting in weight gain. Any patient presenting with anemia, melena, hematemesis or weight loss should be further investigated for complications of PUD predominantly bleeding, perforation or cancer.

Physical Exam

A physical exam may reveal epigastric abdominal tenderness and signs of anemia.

Laboratory Investigations

  1. Esophagogastroduodenoscopy (EGD): Gold standard and most accurate diagnostic test with sensitivity and specificity up to 90% in diagnosing gastric and duodenal ulcers.
  2. Barium swallow: It is indicated when EGD is contraindicated.
  3. Helicobacter pylori testing:
  • Serologic testing
  • Urea breath test: High sensitivity and specificity. It may be used to confirm eradication after 4 to 6 weeks of stopping treatment.
  • Stool antigen test
  • Urine-based ELISA and rapid urine test
  • Endoscopic biopsy: Culture is not generally recommended as it is expensive, time-consuming and invasive. It is indicated if eradication treatment fails or there is suspicion about antibiotic resistance.

Treatment / Management

Medical

Anti-secretory drugs used for PUD include H2-receptor antagonists and the proton pump inhibitor (PPIs). H2 receptor blockers have been largely replaced by PPIs due to their superior healing and efficacy. PPIs block acid production in the stomach providing relief of symptoms and promote healing. Treatment may be incorporated with calcium supplements as long-term use of the PPIs can increase the risk of bone fractures. NSAIDs induced PUD can be treated by stopping the use of NSAIDs or switching to a lower dose. Corticosteroid, bisphosphonates, and anticoagulants should also be discontinued if possible. Prostaglandin analogs (misoprostol) are sometimes used as prophylaxis for NSAID-induced peptic ulcers. First line treatment for H. pylori-induced PUD is a triple regimen comprising two antibiotics and a proton pump inhibitor. Pantoprazole, clarithromycin, and metronidazole or amoxicillin are used for 7 to 14 days.[6] Antibiotics and PPIs work synergistically to eradicate H. pylori.[7] 

Surgical

Surgical treatment is indicated if the patient is unresponsive to medical treatment, noncompliant or at high risk of complications. Surgical options include vagotomy or partial gastrectomy.

Differential Diagnosis

  • Gastritis
  • Pancreatitis
  • Gastroesophageal reflux disease (GERD)
  • Cholecystitis
  • Stomach cancer
  • Biliary colic
  • Myocardial infarction (inferior)
  • Referred pain

Prognosis

The prognosis of PUD is excellent after the underlying cause is successfully treated. Recurrence of the ulcer may be prevented by maintaining good hygiene and avoiding alcohol, smoking, and NSAIDs.

Complications

  • Bleeding
  • Gastric outlet obstruction
  • Perforation
  • Penetration
  • Stomach cancer

Consultations

Once a diagnosis of peptic ulcer disease is made, consult with a gastroenterologist and dietician.

Pearls and Other Issues

Ulcers are differentiated from erosions based on size. Lesions less than 5 mm in diameter are termed erosions, whereas lesions greater than 5 mm in diameter are termed ulcers.

COX-2 selective NSAIDs are less likely to cause PUD as COX-2 is not expressed on the gastric mucosa. Therefore, in patients with a history of PUD, COX-2 selective NSAIDs are preferred.

A gastrin-producing endocrine tumor causes Zollinger-Ellison syndrome. It usually arises from the pancreas or duodenum. It results in multiple ulcers in the duodenum and jejunum. It can be diagnosed by measuring serum gastrin levels.

Enhancing Healthcare Team Outcomes

An evidence-based approach to peptic ulcer disease is recommended.

PUD is a very common disorder that affects millions of people. When left untreated, it has significant morbidity. The majority of patients with PUD present to their primary caregiver but others may present to the emergency department, urgent care clinic or an outpatient clinic. Because the presentation of PUD is often vague, healthcare workers including nurses need to be aware of this diagnosis. The abdominal pain can mimic a number of other pathologies and consequently lead to a delay in treatment. Once the diagnosis is made, the key is to educate the patient on lifestyle changes which include discontinuation of smoking, abstaining from alcohol and avoid consumptions of too many NSAIDs. The pharmacist should educate the patient on medication compliance to obtain symptom relief and a cure. For most patients with PUD who are treated with the triple regimen or PPI, the outcomes are excellent, but recurrence of symptoms is not uncommon.[8][9] (Level II)

Questions

To access free multiple choice questions on this topic, click here.

References

1.
Narayanan M, Reddy KM, Marsicano E. Peptic Ulcer Disease and Helicobacter pylori infection. Mo Med. 2018 May-Jun;115(3):219-224. [PMC free article: PMC6140150] [PubMed: 30228726]
2.
Snowden FM. Emerging and reemerging diseases: a historical perspective. Immunol. Rev. 2008 Oct;225:9-26. [PubMed: 18837773]
3.
Lanas A, Chan FKL. Peptic ulcer disease. Lancet. 2017 Aug 05;390(10094):613-624. [PubMed: 28242110]
4.
Lanas Á, Carrera-Lasfuentes P, Arguedas Y, García S, Bujanda L, Calvet X, Ponce J, Perez-Aísa Á, Castro M, Muñoz M, Sostres C, García-Rodríguez LA. Risk of upper and lower gastrointestinal bleeding in patients taking nonsteroidal anti-inflammatory drugs, antiplatelet agents, or anticoagulants. Clin. Gastroenterol. Hepatol. 2015 May;13(5):906-12.e2. [PubMed: 25460554]
5.
Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis. Lancet. 2002 Jan 05;359(9300):14-22. [PubMed: 11809181]
6.
Malfertheiner P, Megraud F, O'Morain CA, Gisbert JP, Kuipers EJ, Axon AT, Bazzoli F, Gasbarrini A, Atherton J, Graham DY, Hunt R, Moayyedi P, Rokkas T, Rugge M, Selgrad M, Suerbaum S, Sugano K, El-Omar EM., European Helicobacter and Microbiota Study Group and Consensus panel. Management of Helicobacter pylori infection-the Maastricht V/Florence Consensus Report. Gut. 2017 Jan;66(1):6-30. [PubMed: 27707777]
7.
Strand DS, Kim D, Peura DA. 25 Years of Proton Pump Inhibitors: A Comprehensive Review. Gut Liver. 2017 Jan 15;11(1):27-37. [PMC free article: PMC5221858] [PubMed: 27840364]
8.
Young PJ, Bagshaw SM, Forbes A, Nichol A, Wright SE, Bellomo R, Bailey MJ, Beasley RW, Eastwood GM, Festa M, Gattas D, van Haren F, Litton E, Mouncey PR, Navarra L, Pilcher D, Mackle DM, McArthur CJ, McGuinness SP, Saxena MK, Webb S, Rowan KM., Australian and New Zealand Intensive Care Society Clinical Trials Group on behalf of the PEPTIC investigators. A cluster randomised, crossover, registry-embedded clinical trial of proton pump inhibitors versus histamine-2 receptor blockers for ulcer prophylaxis therapy in the intensive care unit (PEPTIC study): study protocol. Crit Care Resusc. 2018 Sep;20(3):182-189. [PubMed: 30153780]
9.
Ayoub F, Khullar V, Banerjee D, Stoner P, Lambrou T, Westerveld DR, Hanayneh W, Kamel AY, Estores D. Once Versus Twice-Daily Oral Proton Pump Inhibitor Therapy for Prevention of Peptic Ulcer Rebleeding: A Propensity Score-Matched Analysis. Gastroenterology Res. 2018 Jun;11(3):200-206. [PMC free article: PMC5997469] [PubMed: 29915630]
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Bookshelf ID: NBK534792PMID: 30521213

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