[No acid, no ulcer: such a simple axiom?]

Area of Science:

• Gastroenterology
• Pharmacology

Background:

• Traditional view posits gastric acid and pepsin are essential for ulcer development.
• However, diverse therapeutic approaches with varying mechanisms achieve similar healing rates, suggesting multifactorial pathogenesis.
• The role of acid suppression in ulcer healing presents complexities, with varying drug efficacies and dosing strategies yielding contradictory results.

Purpose of the Study:

• To explore the complex relationship between gastric acid and ulcer healing.
• To evaluate the efficacy of different ulcer treatment modalities and their impact on pathogenesis.
• To reassess the primary role of gastric acid in ulcer development in light of new therapeutic agents.

Main Methods:

• Review of existing literature on ulcer pathogenesis and treatment.
• Comparison of therapeutic outcomes for drugs with different mechanisms of action (antacids, H2-antagonists, cytoprotective agents, ulcer sealants, proton pump inhibitors).
• Analysis of clinical data regarding the relationship between acid suppression levels and ulcer healing rates.

Main Results:

• Diverse treatments like antacids, H2-blockers, and cytoprotective agents show comparable healing rates, indicating multifactorial ulcer development.
• Ulcer sealants (colloidal bismuth, sucralfate) are as effective as H2-antagonists without affecting acid secretion, challenging acid's primary role.
• Proton pump inhibitors like omeprazole demonstrate high healing rates, re-emphasizing gastric acid's significance in pathogenesis.

Conclusions:

• Ulcer pathogenesis is multifactorial, involving more than just gastric acid and pepsin.
• While gastric acid remains a key factor, especially with potent inhibitors like omeprazole, other mechanisms contribute significantly to ulcer healing.
• Future specific therapies targeting predominant pathogenetic factors are conceivable but currently remain a distant possibility.