Helicobacter pylori eradication treatment modulates epithelial cell proliferation and tissue content of hepatocyte growth factor in the gastric mucosa.
BACKGROUND
Although Helicobacter pylori infection is now acknowledged as a major promoter of gastric cancer in humans, the carcinogenetic process of this effect has not been fully elucidated. Precancerous lesions such as intestinal metaplasia, enhanced proliferation of epithelial cells and elevated level of growth factors have been postulated to play a role.


OBJECTIVE
To analyse a relationship between gastric mucosal proliferation, mucosal content of hepatocyte growth factor and prevalence of intestinal metaplasia before and after successful H. pylori eradication therapy.


METHODS
We evaluated 25 H. pylori-eradicated patients. At initial endoscopic examination, two biopsy tissue samples each were obtained from the antrum and great curvature of the corpus. Tissue content of hepatocyte growth factor and neutrophil myeloperoxidase were measured using an ELISA method, and histological assessment of intestinal metaplasia (haematoxylin and eosin) and proliferating cells (Ki-67 immunostaining) was performed. The patients were treated with a 1-week course of triple therapy. At 10 months after successful eradication, biochemical and histological assessments were repeated.


RESULTS
Among all patients (n = 25), no intestinal metaplasia was detected in the corpus mucosa, but was observed in 10 patients (40%) in the antrum. This prevalence ratio was not changed after eradication. A slight decrease in HGF content was demonstrated in both sites, but the level of antral hepatocyte growth factor was significantly decreased in patients with intestinal metaplasia but not in those without. Proliferative index (Ki-67 positive cells/epithelium) was decreased after eradication therapy in both sites. An increase in proliferative index was observed in the antrum with intestinal metaplasia compared with that without, which significantly decreased after eradication therapy.


CONCLUSIONS
H. pylori eradication therapy in the present study afforded an inhibitory effect on epithelial cell proliferation and on the mucosal content of HGF.
Suzuki
M
M
Division of Gastroenterology and Clinical Research Institute, National Hospital Organization Tokyo Medical Center, Tokyo, Japan. msuzuki@ntmc.hosp.go.jp
Suzuki
H
H
Masaoka
T
T
Tanaka
S
S
Suzuki
K
K
Ishii
H
H
D000900:Anti-Bacterial Agents; D002455:Cell Division; D004359:Drug Therapy, Combination / Q000627:therapeutic use; D004847:Epithelial Cells / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism* / Q000473:pathology; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D016480:Helicobacter pylori; D017228:Hepatocyte Growth Factor / Q000378:metabolism*; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism; D008679:Metaplasia / Q000378:metabolism / Q000473:pathology; D009195:Peroxidase / Q000378:metabolism; D054328:Proton Pump Inhibitors; D013274:Stomach Neoplasms / Q000382:microbiology
D000900:Anti-Bacterial Agents; D019394:Ki-67 Antigen; D054328:Proton Pump Inhibitors; D017228:Hepatocyte Growth Factor; D009195:Peroxidase