Metaplasia in the ileal reservoir

firmed these findings in a small group of patients. It appears that destruction of the glandular basement membrane and the immediately surrounding sheath of supporting cells prevents orderly regeneration. When applying a strict definition of atrophy, as proposed by Genta (8), it is highly unlikely that cure of H. pylon infection will result in restitutlo ad integrum i.e., glandular parenchyma regeneration and functional recovery. Few studies have given indications that intestinal metaplasia may reverse. Genta et al. (9) have shown in a small but detailed study that intestinal metaplasia regresses. In conclusion, the mechanisms leading to mutation of the genes in epithelial cells may be triggered very early in the H. pylon gastritis-gastric cancer sequence. Atrophic gastritis and intestinal metaplasia may result from these processes. Moreover, these changes would seem to be the point of no return.