A patient takes a proton pump inhibitor (PPI) and develops hypergastrinaemia. The elevated gastrin is due to:

• A Direct stimulation of G cells by the PPI drug
• B Gastrin being released by G cells in response to elevated antral pH when acid secretion is blocked ✓
• C Somatostatin inhibition of gastrin breakdown
• D Cholecystokinin (CCK) cross-reacting with gastrin receptors

Explanation

Normally, acid in the gastric antrum stimulates D cells to secrete somatostatin, which inhibits G cells (suppressing gastrin release). When a PPI blocks parietal cell H+/K+-ATPase, intraluminal pH rises. The elevated antral pH removes the somatostatin feedback, allowing G cells to secrete gastrin uninhibited — resulting in hypergastrinaemia. This is physiological secondary hypergastrinaemia (not gastrinoma). Long-term PPIs can cause parietal cell hyperplasia due to the trophic effect of chronically elevated gastrin.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.