Recovery of gastric function after Helicobacter pylori eradication in subjects with body atrophic gastritis: prospective 4-year study.
BACKGROUND
The relationship between Helicobacter pylori (H. pylori) eradication and atrophic changes in the gastric mucosa has not yet been fully defined. Although studies report a partial restoration of serum pepsinogen I (sPGI) levels after eradication, it is not clear if this finding reflects gastric mucosal healing on a morphological level.


OBJECTIVE
To assess alterations in gastric function after H. pylori eradication on moderate/severe body atrophic gastritis by determination of sPGI levels.


METHODS
Twenty-three dyspeptic patients, selected from 284 consecutive H. pylori positive patients, with histological features of moderate/severe body atrophic gastritis and sPGI < 25 microg/L (11 men, mean age: 51.8 years, range: 29-79 years), underwent an upper gastrointestinal endoscopy with gastric biopsies and sPGI determination at baseline. All patients underwent eradication therapy. Serum pepsinogen I was measured again after 6 months, and at 1, 2, 3 and 4 years after eradication therapy.


RESULTS
Mean sPGI levels prior to eradication were 11.9 microg/L (range: 4-23 microg/L). Six months after eradication therapy, mean sPGI levels significantly increased to 17.4 microg/L (P = 0.04). At the completion of the study, 4 years after eradication, sPGI levels increased from 17.4 to 32.7 microg/L (P = 0.01). A significant progressive increase in sPGI levels was observed from 6 months to 1 year (17.4 to 23.9 microg/L) and from 1 to 2 years (23.9 to 26.0 microg/L, P = 0.01). Serum pepsinogen I levels higher than the cut-off value of 25 microg/L were observed at various time-points: 6.3% of patients at 6 months (1/16), 33.3% (5/15) at 1 year, 50% (7/14) at 24 months, 66.7% (6/9) at 36 months and 87.5% (7/8) at 4 years.


CONCLUSIONS
After H. pylori eradication, subjects with body atrophic gastritis showed long-term improvement of physiological gastric function, reflected by significantly and continually increasing sPGI levels over a 4-year period.
Di Mario
Francesco
F
Department of Clinical Sciences, University of Parma, Parma, Italy. francesco.dimario@unipr.it
Moussa
Ali M
AM
Dal Bò
Nadia
N
Caruana
Pietro
P
Pilotto
Alberto
A
Cavallaro
Lucas G
LG
Cavestro
Giulia M
GM
Iori
Veronica
V
Merli
Roberta
R
Franzé
Angelo
A
Rugge
Massimo
M
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D005260:Female; D005757:Gastritis, Atrophic / Q000382:microbiology* / Q000503:physiopathology*; D016481:Helicobacter Infections / Q000188:drug therapy*; D016480:Helicobacter pylori; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D020116:Pepsinogen A / Q000097:blood; D011446:Prospective Studies; D013270:Stomach / Q000503:physiopathology*; D013997:Time Factors
D000900:Anti-Bacterial Agents; D020116:Pepsinogen A