TY - JOUR
T1 - Gastric mucosa during treatment with lansoprazole
T2 - Helicobacter pylori is a risk factor for argyrophil cell hyperplasia
AU - Eissele, R.
AU - Brunner, G.
AU - Simon, B.
AU - Solcia, E.
AU - Arnold, R.
PY - 1997
Y1 - 1997
N2 - Background and 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 iansoprazole and in 29.2% after 5 years treatment. These changes were significantly related to serum gastrin levels, H. pylori infection, chronic inflammation, and atrephy of the oxyntic mucosa. Conclusions: H. pylori represents an important factor for the progression of gastritis and the development of argyrophil cell hyperplasia during long- term treatment with lansoprazole.
AB - Background and 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 iansoprazole and in 29.2% after 5 years treatment. These changes were significantly related to serum gastrin levels, H. pylori infection, chronic inflammation, and atrephy of the oxyntic mucosa. Conclusions: H. pylori represents an important factor for the progression of gastritis and the development of argyrophil cell hyperplasia during long- term treatment with lansoprazole.
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U2 - 10.1053/gast.1997.v112.pm9041231
DO - 10.1053/gast.1997.v112.pm9041231
M3 - Article
C2 - 9041231
AN - SCOPUS:0031056626
VL - 112
SP - 707
EP - 717
JO - Gastroenterology
JF - Gastroenterology
SN - 0016-5085
IS - 3
ER -