J. Stachura et al., GROWTH MARKERS IN THE HUMAN GASTRIC-MUCOSA DURING ADAPTATION TO CONTINUED ASPIRIN ADMINISTRATION, Journal of clinical gastroenterology, 22(4), 1996, pp. 282-287
The mechanism of gastric mucosal adaptation to continued aspirin (ASA)
administration is unknown. We have investigated growth and proliferat
ion markers in healthy subjects under prolonged ASA treatment. In eigh
t healthy volunteers, ASA treatment (2 g/day) was continued for 14 day
s. Endoscopy was performed before medication; at days 3, 7, and 14 of
ASA treatment; and at days 16 and 18 (2 and 4 days, respectively, afte
r medication was ceased). Gastric biopsies from oxyntic and antral muc
osa were studied by histology and by histochemistry for proliferating
cell nuclear antigen (PCNA), epidermal growth factor (EGF), transformi
ng growth factor-alpha (TGF-alpha), and epidermal growth factor recept
or (EGFr). ASA treatment did not change the expression of EGF and EGFr
significantly. The PCNA index showed local inconsistent variations. H
owever, increased TGF-alpha expression after ASA was noted, particular
ly in hyperplastic surface epithelium. Edema and teleangiectases were
common in gastric mucosa after ASA. An increasing incidence of foveola
r hyperplasia was also noted in the antral mucosa. Healthy subjects on
prolonged ASA treatment gradually develop parameters of chronic react
ive gastritis accompanied by increased TGF-alpha expression in gastric
surface epithelial cells, especially in hyperplastic areas.