Peptic Ulcer Disease

Basics

Peptic ulcer disease (PUD) is characterized by defects in the stomach and/or duodenal mucosa, leading to inflammation and erosion of the underlying tissue by gastric acid and pepsin.

Description

  • Esophageal ulcers: located in the distal esophagus; usually secondary to gastroesophageal reflux disease (GERD); also seen with gastrinoma
  • Duodenal ulcer: the most common form of PUD; usually located in the anterior wall of proximal duodenum (duodenal bulb)
  • Gastric ulcer: less common than duodenal ulcer in absence of NSAID use; often located along lesser curvature of the antrum
  • Multiple ulcers/ulcers distal to the second portion of duodenum and/or jejunum raise possibility of gastrinoma (Zollinger-Ellison syndrome [ZES]).
  • Ectopic gastric mucosal ulceration: caused by residual columnar epithelium of the embryonic esophagus; often seen in the upper esophagus; can be seen with Meckel diverticulum (1)

Epidemiology

The global prevalence of PUD has dramatically decreased in the past decade due to improved sanitary conditions, effective treatment of Helicobacter pylori infection, and careful NSAID use (1).

Incidence

  • PUD can affect any age group.
  • Duodenal ulcers typically appear between age 30 and 50 years and are more common in men.
  • Gastric ulcers tend to occur after age 60 years and affect women more than men.
  • Duodenal/gastric ulcer incidence increases with age in both sexes.
  • Peptic ulcer: 500,000 new cases per year
  • Recurrence: 4 million per year
  • Global incidence rate 0.1–0.19%; overall decrease from improved sanitary conditions, effective treatment and careful NSAIDs use.
  • Lifetime risk globally: 5–10%

Prevalence
PUD affects 4 million people worldwide annually and has an estimated lifetime prevalence of 5–10% in the general population. Prevalence increases to 10–20% in H. pylori–positive patients.

Etiology and Pathophysiology

Genetics
Increased incidence in families due to familial clustering of H. pylori infection and inherited genetic factors reflecting response to the bacteria

Risk Factors

  • Most common cause: H. pylori (gram-negative bacteria) infection
  • Second most common cause: NSAIDs use (including aspirin and COX-2 inhibitors)
  • Other medications: corticosteroids (high dose; prolonged therapy), bisphosphonates, potassium chloride, clopidogrel, sirolimus chemotherapeutic agents
  • Hypersecretion syndromes: gastrinoma (ZES), systemic mastocytosis, cystic fibrosis, hyperparathyroidism, carcinoid syndrome, antral G-cell hyperplasia
  • Others factors: tobacco use, alcohol use, stress (e.g., acute illness, ventilator support, extensive burns, head injury), radiation therapy, obesity

General Prevention

  • Educate patients about harmful agents like NSAIDs, aspirin, alcohol, tobacco, caffeine.
  • NSAID ulcers: discontinue use of NSAIDs, use acetaminophen instead when appropriate, or add proton pump inhibitor [PPI] in patients with previous NSAID-related ulcer.
    • If NSAIDs necessary, use the lowest possible dose with a PPI or misoprostol.
    • To reduce ulcer risk, consider testing for and eradicating H. pylori.
  • Maintenance therapy with PPIs or H2 blockers is indicated for history of ulcer complications, recurrences, refractory ulcers, or persistent H. pylori infection.
  • Consider maintenance PPI treatment in patients with H. pylorinegative, non–NSAID-induced ulcers.
  • Strong association between obesity and PUD; counsel patients on weight loss.

Commonly Associated Conditions

Gastrinoma (ZES); multiple endocrine neoplasia type 1; carcinoid syndrome

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