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Peptic Ulcer DiseaseEdit

Peptic ulcer disease (PUD) refers to ulcers that develop in the lining of the stomach or the first part of the small intestine, the duodenum. These ulcers arise when the mucosal defenses of the gastrointestinal tract are overwhelmed by aggressive factors such as acid, pepsin, or bile, or when protective mechanisms are impaired. For much of the 20th century, lifestyle factors like stress and spicy foods were widely blamed for ulcers. The modern understanding centers on two primary etiologies: infection with Helicobacter pylori and the use of nonsteroidal anti-inflammatory drugs (NSAIDs), with other contributors including age, smoking, and certain chronic diseases. The discovery of H. pylori and its role in most duodenal and many gastric ulcers transformed diagnosis and treatment, shifting management toward targeted antibiotic therapy in addition to acid suppression and risk reduction. Helicobacter pylori gastric ulcer duodenal ulcer

In current practice, PUD is a disease of medical management and prudent prevention. Most ulcers heal with appropriate therapy, and the risk of serious complications such as bleeding or perforation is now lower in many parts of the world thanks to widespread use of proton-pump inhibitors (PPIs) and more effective strategies for eradicating H. pylori. Yet PUD remains a concern because it can cause significant bleeding, require urgent intervention, and serve as a marker of NSAID exposure or other health risks. The balance between aggressive treatment of infection, careful management of medications, and sensible lifestyle changes is central to contemporary care. Proton-pump inhibitors Nonsteroidal anti-inflammatory drug Gastrointestinal bleeding

Pathophysiology

Peptic ulcers form where the stomach or duodenal mucosa is exposed to damaging factors beyond its protective barriers. The two most common pathways are:

  • H. pylori infection: The bacterium colonizes the stomach lining, causing chronic gastritis and disruption of mucosal defenses, which can progress to ulceration in the stomach or duodenum. Helicobacter pylori The infection also increases the risk of recurrent ulcers if not treated.

  • NSAID-related injury: NSAIDs inhibit cyclooxygenase enzymes, reducing prostaglandin synthesis. Prostaglandins help maintain the protective mucus and blood flow of the gastric mucosa; when their production falls, the mucosa becomes more vulnerable to acid injury. This mechanism explains why NSAID use is a major, modifiable risk factor for PUD. Nonsteroidal anti-inflammatory drug Prostaglandin Cyclooxygenase

Other factors—such as smoking, older age, genetic predisposition, and certain systemic illnesses—can amplify risk or hinder healing. Inflammation, mucosal blood flow, and acid secretion interact in a dynamic balance, and treatment aims to restore that balance while addressing the underlying cause. Dyspepsia Gastric acid

Epidemiology and risk factors

PUD occurs worldwide, with regional variation in prevalence tied to H. pylori infection rates and NSAID exposure. In high-income countries, the decline of H. pylori prevalence and the widespread adoption of safer NSAID practices have reduced ulcer rates and lowered the incidence of severe complications, though NSAID-related ulcers remain a substantial issue, particularly among older adults and those with complex medical regimens. Key risk factors include chronic NSAID use (often with concurrent risk factors such as age and smoking), active H. pylori infection, prior ulcer disease, and significant comorbidity that necessitates NSAID therapy. H. pylori Nonsteroidal anti-inflammatory drug Stomach Duodenal ulcer

Signs and symptoms

Typical manifestations of peptic ulcers include:

  • Epigastric pain: a burning or gnawing sensation that may be worsened by fasting and relieved by meals in duodenal ulcers, or worsened by meals in gastric ulcers. Dyspepsia
  • Nausea or vomiting
  • Bloating, burping, and loss of appetite
  • Weight loss in some cases

Alarm features requiring urgent evaluation include progressive dysphagia, persistent vomiting, weight loss, anemia, and signs of gastrointestinal bleeding (e.g., black tarry stools or vomiting blood). These red flags prompt prompt diagnostic testing and possible endoscopic assessment. Gastrointestinal bleeding Endoscopy

Diagnosis

Diagnosis combines clinical assessment with targeted testing:

  • Noninvasive tests for H. pylori: urea breath test and stool antigen test are preferred for active infection, especially in symptomatic patients. Serology may indicate exposure but is less reliable for active infection. Urea breath test Stool antigen test

  • Endoscopy with biopsy: Indicated in older patients or those with alarm features, persistent symptoms, or suspected complications. Biopsies allow histology and rapid testing for H. pylori (rapid urease test) and help exclude other pathology. Esophagogastroduodenoscopy Rapid urease test

  • Imaging and laboratory studies: In complicated cases, imaging to assess perforation or obstruction and laboratory tests to evaluate anemia or ongoing bleeding may be used. Gastrointestinal bleeding

Treatment

Management focuses on eradicating infection when present, protecting and healing mucosa, and addressing causative medications.

H. pylori eradication

For patients with confirmed H. pylori infection, first-line therapy typically includes a proton-pump inhibitor-based regimen plus two antibiotics (commonly amoxicillin and clarithromycin or metronidazole, depending on local resistance patterns). Alternative regimens include bismuth-based quadruple therapy. After completion, confirm eradication with a noninvasive test at least four weeks later. Helicobacter pylori Proton-pump inhibitors

NSAID-related ulcers and protection in high-risk patients

  • Reduce or discontinue NSAIDs where possible; switch to alternative analgesics or ensure the lowest effective dose for the shortest duration. In patients who must continue NSAIDs, co-therapy with a PPI or misoprostol can reduce ulcer risk, and some may benefit from using COX-2 selective inhibitors when clinically appropriate. Nonsteroidal anti-inflammatory drug Misoprostol COX-2 inhibitor

  • When ulcers are NSAID-induced, management emphasizes symptom relief, mucosal protection, and re-evaluation of NSAID necessity. Gastric ulcer Duodenal ulcer

Acid suppression

  • Proton-pump inhibitors are the mainstay for healing and symptom control, often combined with eradication therapy if H. pylori is present. In milder cases or where PPIs are contraindicated, H2 receptor antagonists can be used. Proton-pump inhibitors H2 receptor antagonists

Management of complications

  • Bleeding ulcers may require endoscopic hemostasis, transfusion, and, occasionally, angiographic or surgical intervention. Perforated ulcers are surgical emergencies. Obstructive complications may necessitate endoscopic or surgical relief. Gastrointestinal bleeding Endoscopy

Follow-up

  • Reassessment ensures healing has occurred and that any ongoing risk factors, such as NSAID use or persistent infection, are addressed. Post-treatment testing for H. pylori is recommended where appropriate. Endoscopy

Prevention

Prevention centers on minimizing exposure to modifiable risk factors and optimizing treatment choices:

  • Use NSAIDs judiciously: lowest effective dose, shortest duration, with protective strategies when needed. Nonsteroidal anti-inflammatory drug
  • Screen for and treat H. pylori in high-risk circumstances to reduce ulcer recurrence and related complications. Helicobacter pylori
  • Lifestyle measures such as smoking cessation and moderation of alcohol intake can support mucosal health, though they are not sole preventive measures. Dyspepsia

Controversies and debates

  • Primary drivers and public health strategies: In many settings, H. pylori infection is a dominant cause, while NSAID exposure remains a major, preventable risk. The debate centers on how aggressively to pursue population-wide H. pylori screening versus targeted testing and treatment, balancing antibiotic stewardship with ulcer prevention. Critics of broad campaigns argue for cost-effective, risk-based approaches and patient-centered decision making. Antibiotic stewardship Cost-effectiveness

  • Diet, stress, and symptom attribution: The old notion that spicy foods or stress alone cause ulcers has largely been discredited. A right-of-center perspective tends to emphasize evidence-based guidance and personal responsibility, avoiding broad lifestyle prescriptions that lack solid causal support, while recognizing that certain foods or stressors may aggravate symptoms in susceptible individuals. Dyspepsia

  • Long-term acid suppression and safety: Long-term PPI use raises questions about potential adverse effects and costs. Proponents emphasize symptom control and mucosal healing, while critics urge careful monitoring and periodic reassessment to minimize unnecessary exposure and ensure appropriate indications. Proton-pump inhibitors

  • Access and health-system design: From a policy angle, improving access to affordable diagnostics, generic medications, and efficient endoscopic services is crucial. Advocates stress market-based competition and prudent regulation to lower costs without compromising safety. Disparities in care can affect ulcer outcomes, underscoring the need for targeted improvements in accessibility and quality of care. Health care costs Health economics

See also