Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 707-717 |
| Number of pages | 11 |
| Journal | Gastroenterology |
| Volume | 112 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 1997 |
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ASJC Scopus subject areas
- Gastroenterology
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Gastric mucosa during treatment with lansoprazole : Helicobacter pylori is a risk factor for argyrophil cell hyperplasia. / Eissele, R.; Brunner, G.; Simon, B.; Solcia, E.; Arnold, R.
In: Gastroenterology, Vol. 112, No. 3, 1997, p. 707-717.Research output: Contribution to journal › Article
}
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.
UR - http://www.scopus.com/inward/record.url?scp=0031056626&partnerID=8YFLogxK
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U2 - 10.1053/gast.1997.v112.pm9041231
DO - 10.1053/gast.1997.v112.pm9041231
M3 - Article
VL - 112
SP - 707
EP - 717
JO - Gastroenterology
JF - Gastroenterology
SN - 0016-5085
IS - 3
ER -