Relationship of Helicobacter pylori eradication with gastric cancer and gastric
mucosal histological changes: a 10-year follow-up study.
Author(s): Zhou L(1), Lin S(2), Ding S(1), Huang X(1), Jin Z(1), Cui R(1), Meng L(1), Li
Y(1), Zhang L(1), Guo C(1), Xue Y(1), Yan X(1), Zhang J(1).
Affiliation(s): Author information:
(1)Department of Gastroenterology, Third Hospital of Peking University, Beijing
100191, China. (2)Department of Gastroenterology, Third Hospital of Peking
University, Beijing 100191, China. Email: linsanren@medmail.com.cn).
Publication date & source: 2014, Chin Med J (Engl). , 127(8):1454-8
BACKGROUND: Helicobacter pylori (Hp) is a common and potentially curable cause of
gastric mucosa lesion. This study investigated the relationship of Hp infection
with histological changes in gastric mucosa and gastric cancer in Hp-positive
patients compared with Hp-eradication patients followed up for ten years.
METHODS: From an initial group of 1 006 adults, 552 Hp-positive subjects were
randomly assigned to a treatment group (T; n = 276) or a placebo group (P; n =
276). In the randomized, double-blind, placebo-controlled, parallel trial, T
group subjects received oral doses of omeprazole, amoxicillin and clarithromycin
for 1 week; those in the P group received a placebo. One month after treatment
ended, a 13C urea breath test was performed, and Hp was undetectable in 88.89% of
the T group. All subjects were followed at 1, 5, 8, and 10 years after treatment,
with endoscopy and biopsies for histological examination.
RESULTS: Gastric mucosa inflammation was significantly milder in the T group than
that in the P group one year after Hp eradication and this persisted for 10
years. Glandular atrophy and intestinal metaplasia (IM) had deteriorated in both
groups during ten years. However, the increased score of glandular atrophy at
both the gastric antrum and corpus, and IM only at the gastric antrum, in the P
group was more obvious than that in the T group. During the 10 years, 9 patients
were diagnosed with gastric cancer (2 in the T group; 7 in the P group; P =
0.176). When mucosal atrophy was absent at the gastric antrum and corpus when
entering the study, the incidence of gastric cancer in the P group (n = 6) was
much higher than that in the T group (n = 0, P = 0.013).
CONCLUSIONS: Hp eradication may significantly diminish and help halt progression
of gastric mucosal inflammation and delay the development of IM and atrophy
gastritis. Hp eradication is helpful for reducing the risk for gastric cancer,
especially in the early stage of Hp infection.
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