New development in the mechanistic understanding of peptic ulcer diseases

Peptic ulcers result from in imbalance of aggressive (e.g., acid-pepsin) and protective factors (e.g., mucosal blood flow, bicarbonate secretion). Most ulcers are etiologically related to infection with Helicobacter pylori or use of nonsteroidal anti-inflammatory drugs (NSAIDs). Mechanisms resulting in improved anti-H. pylori therapy include better delivery of antimicrobials to the sites of infection (e.g., changing dose, formulation, duration or the use of adjuvants), enhancing local immunity or by reducing the mucus barrier to topical therapy. Mechanisms to prevent NSAID ulcers include less damaging NSAIDs (e.g., COX-2 selective NSAIDs, nitric oxide-donating NSAIDs), reduction in acid secretion or replacement of mucosal prostaglandins.

Section editor:Yu-Xiao Yang – Unviversity of Pennsylvania, Philadelphia, PA, USA