Premium
The long‐term effects of cure of Helicobacter pylori infection on patients with atrophic body gastritis
Author(s) -
Annibale B.,
Di Giulio E.,
Caruana P.,
Lahner E.,
Capurso G.,
Bordi C.,
Delle Fave G.
Publication year - 2002
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2002.01336.x
Subject(s) - atrophy , atrophic gastritis , gastroenterology , medicine , helicobacter pylori , gastritis , intestinal metaplasia , basal (medicine) , spirillaceae , gastrin , pepsin , secretion , biology , insulin , biochemistry , enzyme
Summary Background : Helicobacter pylori infection induces atrophic body gastritis, but the long‐term effect of its cure on body atrophy is unclear. Aim : To investigate the long‐term effects of H. pylori cure on gastric morpho‐functional parameters in patients with atrophic body gastritis. Methods : Forty patients with atrophic body gastritis were cured of H. pylori infection. Gastroscopy with biopsies, gastrin and pepsinogen I levels and basal and stimulated acid secretion were evaluated before and 6–12 months after treatment. Results : At eradication assessment (6–12 months), in eight of the 40 patients, body atrophy was no longer observed, whereas in 32 of the 40 it remained substantially unchanged (2.03 ± 0.12 vs. 1.83 ± 0.15). In the eight patients with reversed body atrophy, gastrinaemia decreased significantly with respect to pre‐treatment values (265 ± 59.9 pg/mL vs. 51.8. ± 6.04 pg/mL), and basal and stimulated acid secretion increased significantly after cure. In the 32 patients still presenting body atrophy, gastrinaemia was similar topre‐treatment values (457 ± 76.04 pg/mL vs. 335.1 ± 58.8 pg/mL). At follow‐up (21–25 and 32–70 months), the eight patients with reversed body atrophy continued with normal gastrinaemia (35.3 ± 10.1 pg/mL vs. 38.5 ± 8.8 pg/mL), but in the 19 patients with continued atrophy, both corporal atrophy and intestinal metaplasia remained substantially unchanged. Conclusions : Following successful treatment in patients with atrophic body gastritis and H. pylori infection, long‐term histological investigations are crucial in order to detect reversed body damage or to confirm continued body atrophy.