Rj. Cahill et al., EFFECT OF ERADICATION OF HELICOBACTER-PYLORI INFECTION ON GASTRIC EPITHELIAL-CELL PROLIFERATION, Digestive diseases and sciences, 40(8), 1995, pp. 1627-1631
Helicobacter pylori infection has been linked with gastric carcinoma.
Epithielial cell proliferation is an indicator of cancer risk. The aim
of this study was to assess gastric epithelial cell proliferation bef
ore and after eradication therapy and to assess the efficacy of treatm
ent of H. pylori infection using lanzoprazole and clarithromycin. Twen
ty-three patients with H. pylori-associated gastritis were treated wit
h lanzoprazole 30 mg daily for four weeks and clarithromycin 500 mg th
ree times a day for two weeks. Antral mucosal biopsies were taken for
gastric epithelial cell proliferation analysis using the in vitro brom
odeoxyuridine (BrdU) immunohistochemical technique before and four wee
ks after eradication therapy. Labeling index percent (LI%) was calcula
ted as the percent ratio of proliferating cells to the total number of
cells in the gastric pit. Efficacy of treatment was assessed in 16 su
bjects. Eight were negative for H. pylori infection 28 days after ther
apy and in eight patients H. pylori infection was not eradicated. The
eradication rate for the regimen was 50%. Cell kinetics were assessed
in 19 subjects who completed treatment. Patients with H. pylori infect
ion had a significantly higher LI% compared to normal (N = 19, LI%: 5.
01 +/- 0.3 vs 3.2 +/- 0.2, N = 29). Eradication of H. pylori infection
significantly reduced epithelial cell proliferation (N = 9, LI%: 5.2
+/- 0.4 to 3.2 +/- 0.8, P < 0.001), whereas it was unaltered in those
whose infection was not eradicated (N = 10, LI%: 4.8 +/- 0.4 to 5.5 +/
- 0.5, P = 0.18). Eradication of H. pylori reduces gastric epithelial
cell proliferation to normal levels and may reduce the long-term the r
isk of gastric carcinoma.