Dr Tim Phan( left) Gastroenterology registrar, department of gastroenterology, St Vincent’ s Hospital Melbourne, Victoria.

Dr Andrew Tsoi( right) Gastroenterology registrar, department of gastroenterology, St Vincent’ s Hospital Melbourne, Victoria.

Dr Eshwar Yogakanthi( left) Gastroenterology registrar, department of gastroenterology, St Vincent’ s Hospital Melbourne, Victoria.

Dr Chamara Basnayake( right) Gastroenterologist and head of functional gastrointestinal disorders at St Vincent’ s Hospital Melbourne and senior lecturer at The University of Melbourne, Victoria.

First published online on 17 May 2024

BACKGROUND

PEPTIC ulcer disease remains an

important cause of morbidity and a significant contributor to healthcare costs worldwide. Peptic ulcers are mucosal breaks of the alimentary tract that extend through to the submucosa, as a result of exposure to acid. 1 They are usually located in the stomach or proximal duodenum. 2 Traditionally, a hypersecretory acidic environment in conjunction with dietary factors or stress have been accepted as the primary drivers of peptic ulcer disease. However, the discovery of Helicobacter pylori infection and the widespread use of NSAIDs has shifted this paradigm.

The management of peptic ulcer disease remains challenging, particularly with the threat of increasing antimicrobial resistance, increasing NSAID use and the widespread use of complex anticoagulants in a rapidly ageing population.

This How to Treat covers the causes, pathophysiology, diagnosis and treatment of peptic ulcer disease with a particular focus on H. pylori and NSAID-associated peptic ulcer disease. It aims to ensure GPs feel empowered to effectively manage this condition independently and provide guidance when a specialist referral is warranted.

PATHOPHYSIOLOGY / AETIOLOGY

THE integrity of the gastric and

Department of pathology, Calicut Medical College / CC BY-SA 4.0 / bit. ly / 48H6Wd6

duodenal mucosa is tightly regulated by multiple interacting mechanisms that govern mucosal function and repair. Disruption to any of these protective elements leads to peptic ulcer disease( see figure 1).

As a final common endpoint, multiple aetiological factors contribute to

peptic ulcer disease. NSAID or aspirin use and H. pylori infection represent independent and also synergistic contributors to both gastric( see figure 2) and duodenal ulcers( see figures 3 and 4). 3 Notably, only a small proportion of people with H. pylori infection or NSAID exposure develop peptic

Figure 1. Acute stress ulcer of the stomach in erosive gastritis.

ulcer disease, suggesting that there are likely genetic and environmental cofactors that are essential for the initiation of mucosal damage. 2

H. pylori( see figure 5) is a Gram-negative bacterium that colonises the gastric mucosa, and can proceed to cause gastritis and