Helicobacter pylori (H. pylori) represents an important factor in the
development of atrophic gastritis, intestinal metaplasia (IM), and gastric cancer.
Eradication of H. pylori has been reported to prevent gastric cancer only in
cases without atrophy or IM. However, histological changes with eradication
have yet to be fully clarified. We evaluated 38 H. pylori-positive cases before
and after eradication at the gland level; pyloric glands were classified as
showing gastric proper (G) and IM gland types, with the latter including
gastric-and-intestinal mixed IM (GI-IM) and solely intestinal IM (I-IM),
depending on the remaining gastric phenotypes. On eradication, acute and
chronic inflammation attenuated rapidly and gradually, respectively, whereas
levels of MUC5AC and MUC6 expression were not markedly altered. Gland width,
size of nuclei and cytoplasm and their ratio in surface foveolar epithelium,
the number of Ki-67-positive cells and the length of the proliferating zone in
each gland were significantly decreased in G glands after eradication compared
with those in GI-IM and I-IM. The number of mitotic phase cells, positive for
phosphorylated histone H3 at serine 28, was increased in both types of IM
compared to that in G glands in the H. pylori-infected state, but unexpectedly
remained unchanged with eradication. These results suggest that GI-IM, as the
beginning of IM, could represent a histological irreversible point with
eradication and be considered as a “histological point of no return”.
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