Abstract
Background/Aims. To assess the effect of Helicobacter pylori eradication on gastric histology and physiology in patients with multifocal atrophic gastritis over 1-year period. Patients. Fourteen consecutive patients with histological evidence of chronic gastritis and Helicobacter pylori infection diagnosed by histology and serology entered this study. Patients with pernicious anaemia, gastric ulcer or carcinoma, duodenal ulcer, reflux oesophagitis and regular intake of nonsteroidal anti-inflammatory drugs were excluded. Methods. Patients underwent triple anti-Helicobacter treatment for one week, which resulted successful in all subjects on the basis of negative CLO test and histology as well as 50% decrease in IgG antibodies after 4 weeks and 6 months of treatment, respectively. Histological and functional investigations were performed at baseline, 6 and 12 months after Helicobacter pylori eradication. Histological assessment of inflammatory cell infiltrates was performed on multiple biopsy specimens of the corpus and fundus. Functional tests were 24-hour continuous gastric pH-metry, fasting serum gastrin assay and pepsinogen I levels. Results. There was a progressive significant improvement (p <0.01-0.001) in acute and chronic inflammatory cell infiltrates in the gastric mucosa throughout the 12-month period. Functional recovery with increase in gastric acidity (p <0.01) and decrease in gastrin and pepsinogen I levels (p <0.001) was more evident at the 6-month than at the 12-month checkpoint after Helicobacter pylori eradication (p = NS for gastric pH and p <0.02 for the other two variables) between 6 and 12 months. Conclusions. Eradication of Helicobacter pylori infection significantly improves the inflammatory status of oxyntic mucosa and this promotes an almost complete functional recovery. However, the non-parallel behaviour of gastric acidity, which was maximal at 6-month checkpoint, and histological parameters which continued to improve throughout the entire 12-month observation period, seems to indicate that removal of acid-inhibitory substances induced by Helicobacter pylori infection was also responsible for the more rapid recovery of gastric secretory function.
| Original language | English |
|---|---|
| Pages (from-to) | 4-8 |
| Number of pages | 5 |
| Journal | Italian Journal of Gastroenterology and Hepatology |
| Volume | 31 |
| Issue number | 1 |
| Publication status | Published - 1999 |
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Keywords
- Gastric pH
- Helicobacter pylori
- Multifocal atrophic gastritis
- Pepsinogen I levels
- Serum gastrin
ASJC Scopus subject areas
- Gastroenterology
Cite this
Histological and functional recovery in patients with multifocal atrophic gastritis after eradication of Helicobacter pylori infection. / Savarino, V.; Mela, G. S.; Zentilin, P.; Lapertosa, G.; Bisso, G.; Mele, M. R.; Pivari, M.; Mansi, C.; Vigneri, S.; Celle, G.
In: Italian Journal of Gastroenterology and Hepatology, Vol. 31, No. 1, 1999, p. 4-8.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Histological and functional recovery in patients with multifocal atrophic gastritis after eradication of Helicobacter pylori infection
AU - Savarino, V.
AU - Mela, G. S.
AU - Zentilin, P.
AU - Lapertosa, G.
AU - Bisso, G.
AU - Mele, M. R.
AU - Pivari, M.
AU - Mansi, C.
AU - Vigneri, S.
AU - Celle, G.
PY - 1999
Y1 - 1999
N2 - Background/Aims. To assess the effect of Helicobacter pylori eradication on gastric histology and physiology in patients with multifocal atrophic gastritis over 1-year period. Patients. Fourteen consecutive patients with histological evidence of chronic gastritis and Helicobacter pylori infection diagnosed by histology and serology entered this study. Patients with pernicious anaemia, gastric ulcer or carcinoma, duodenal ulcer, reflux oesophagitis and regular intake of nonsteroidal anti-inflammatory drugs were excluded. Methods. Patients underwent triple anti-Helicobacter treatment for one week, which resulted successful in all subjects on the basis of negative CLO test and histology as well as 50% decrease in IgG antibodies after 4 weeks and 6 months of treatment, respectively. Histological and functional investigations were performed at baseline, 6 and 12 months after Helicobacter pylori eradication. Histological assessment of inflammatory cell infiltrates was performed on multiple biopsy specimens of the corpus and fundus. Functional tests were 24-hour continuous gastric pH-metry, fasting serum gastrin assay and pepsinogen I levels. Results. There was a progressive significant improvement (p <0.01-0.001) in acute and chronic inflammatory cell infiltrates in the gastric mucosa throughout the 12-month period. Functional recovery with increase in gastric acidity (p <0.01) and decrease in gastrin and pepsinogen I levels (p <0.001) was more evident at the 6-month than at the 12-month checkpoint after Helicobacter pylori eradication (p = NS for gastric pH and p <0.02 for the other two variables) between 6 and 12 months. Conclusions. Eradication of Helicobacter pylori infection significantly improves the inflammatory status of oxyntic mucosa and this promotes an almost complete functional recovery. However, the non-parallel behaviour of gastric acidity, which was maximal at 6-month checkpoint, and histological parameters which continued to improve throughout the entire 12-month observation period, seems to indicate that removal of acid-inhibitory substances induced by Helicobacter pylori infection was also responsible for the more rapid recovery of gastric secretory function.
AB - Background/Aims. To assess the effect of Helicobacter pylori eradication on gastric histology and physiology in patients with multifocal atrophic gastritis over 1-year period. Patients. Fourteen consecutive patients with histological evidence of chronic gastritis and Helicobacter pylori infection diagnosed by histology and serology entered this study. Patients with pernicious anaemia, gastric ulcer or carcinoma, duodenal ulcer, reflux oesophagitis and regular intake of nonsteroidal anti-inflammatory drugs were excluded. Methods. Patients underwent triple anti-Helicobacter treatment for one week, which resulted successful in all subjects on the basis of negative CLO test and histology as well as 50% decrease in IgG antibodies after 4 weeks and 6 months of treatment, respectively. Histological and functional investigations were performed at baseline, 6 and 12 months after Helicobacter pylori eradication. Histological assessment of inflammatory cell infiltrates was performed on multiple biopsy specimens of the corpus and fundus. Functional tests were 24-hour continuous gastric pH-metry, fasting serum gastrin assay and pepsinogen I levels. Results. There was a progressive significant improvement (p <0.01-0.001) in acute and chronic inflammatory cell infiltrates in the gastric mucosa throughout the 12-month period. Functional recovery with increase in gastric acidity (p <0.01) and decrease in gastrin and pepsinogen I levels (p <0.001) was more evident at the 6-month than at the 12-month checkpoint after Helicobacter pylori eradication (p = NS for gastric pH and p <0.02 for the other two variables) between 6 and 12 months. Conclusions. Eradication of Helicobacter pylori infection significantly improves the inflammatory status of oxyntic mucosa and this promotes an almost complete functional recovery. However, the non-parallel behaviour of gastric acidity, which was maximal at 6-month checkpoint, and histological parameters which continued to improve throughout the entire 12-month observation period, seems to indicate that removal of acid-inhibitory substances induced by Helicobacter pylori infection was also responsible for the more rapid recovery of gastric secretory function.
KW - Gastric pH
KW - Helicobacter pylori
KW - Multifocal atrophic gastritis
KW - Pepsinogen I levels
KW - Serum gastrin
UR - http://www.scopus.com/inward/record.url?scp=0032955262&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032955262&partnerID=8YFLogxK
M3 - Article
VL - 31
SP - 4
EP - 8
JO - Digestive and Liver Disease
JF - Digestive and Liver Disease
SN - 1590-8658
IS - 1
ER -