Gastric mucosa during treatment with lansoprazole: Helicobacter pylori is a risk factor for argyrophil cell hyperplasia

Background & Aims: The mechanisms causing progression of fundic gastritis and changes in argyrophil cell morphology in patients undergoing long-term treatment with proton pump inhibitors are unknown. The hypothesis of this study was that Helicobacter pylori is a risk factor for both gastritis and argyrophil cell hyperplasia. Methods: Forty-two patients with peptic disorders resistant to H-2-blockers were treated with 30-90 mg lansoprazole daily for up to 5 years. Serum gastrin levels, antral gastrin cells, fundic argyrophil cells, parameters of gastritis, and H. pylori infection were evaluated regularly. Results: In nonantrectomized patients, serum gastrin levels increased from a median of 76 pg/mL to 163 pg/mL within 3 months. Antral gastrin cell density increased from 175 to 267 cells/mm(2) (P < 0.001), and fundic argyrophil cell density increased from 83 to 149 cells/mm(2) (P < 0.001). Chronic inflammation, activity, and atrophy of the oxyntic mucosa worsened exclusively in patients with H. pylori infection. Linear and/or micronodular argyrophil cell hyperplasia was diagnosed in 2.6% of patients before lansoprazole and in 29.2% after 5 years treatment. These changes were significantly related to serum gastrin levels, H. pylori infection, chronic inflammation, and atrophy of the oxyntic mucosa. Conclusions: H. pylori represents an important factor for the progression of fundic gastritis and the development of argyrophil cell hyperplasia during long-term treatment with lansoprazole.