TY - JOUR
T1 - Long-term follow-up in atrophic body gastritis patients
T2 - Atrophy and intestinal metaplasia are persistent lesions irrespective of Helicobacter pylori infection
AU - Lahner, E.
AU - Bordi, C.
AU - Cattaruzza, M. S.
AU - Iannoni, C.
AU - Milione, M.
AU - Delle Fave, G.
AU - Annibale, B.
PY - 2005/9/1
Y1 - 2005/9/1
N2 - Background: Long-term outcome of atrophic body gastritis has not yet been defined. Aim: To investigate at long-term follow-up the behaviour of atrophy and intestinal metaplasia and the occurrence of neoplastic lesions in atrophic body gastritis patients. Methods: Overall 106 atrophic body gastritis patients with ≥ 4-year follow-up were studied; 38 were Helicobacter pylori-positive at histology + serology and cured of infection (group A), 36 were positive at serology and not treated (group B) and 32 were H. pylori-negative (group C). Patients underwent gastroscopy with antral (n = 3) and body (n = 3) biopsies for histology accord-ing to the Sydney System. Results: At 6.7-year follow-up body atrophy and intestinal metaplasia remained unchanged in all 106 patients irrespective of H. pylori status. Antral atrophy was significantly increased at follow-up only in group C, whereas antral intestinal metaplasia was unchanged in all three groups. During follow-up eight (8%) patients developed neoplastic lesions (one adenocarcinoma, one adenoma with low-grade dysplasia and six low-grade dysplasia without endoscopic lesions). Antral atrophic gastritis was present at baseline in all but one (88%) of the eight patients with neoplastic lesions, but only in 15 (15%) of the 98 patients without (P <0.0001, RR = 26.7). Conclusions: Atrophy and intestinal metaplasia persist at 6.7-year follow-up and atrophic body gastritis patients with panatrophic gastritis are at increased risk of developing neoplastic lesions.
AB - Background: Long-term outcome of atrophic body gastritis has not yet been defined. Aim: To investigate at long-term follow-up the behaviour of atrophy and intestinal metaplasia and the occurrence of neoplastic lesions in atrophic body gastritis patients. Methods: Overall 106 atrophic body gastritis patients with ≥ 4-year follow-up were studied; 38 were Helicobacter pylori-positive at histology + serology and cured of infection (group A), 36 were positive at serology and not treated (group B) and 32 were H. pylori-negative (group C). Patients underwent gastroscopy with antral (n = 3) and body (n = 3) biopsies for histology accord-ing to the Sydney System. Results: At 6.7-year follow-up body atrophy and intestinal metaplasia remained unchanged in all 106 patients irrespective of H. pylori status. Antral atrophy was significantly increased at follow-up only in group C, whereas antral intestinal metaplasia was unchanged in all three groups. During follow-up eight (8%) patients developed neoplastic lesions (one adenocarcinoma, one adenoma with low-grade dysplasia and six low-grade dysplasia without endoscopic lesions). Antral atrophic gastritis was present at baseline in all but one (88%) of the eight patients with neoplastic lesions, but only in 15 (15%) of the 98 patients without (P <0.0001, RR = 26.7). Conclusions: Atrophy and intestinal metaplasia persist at 6.7-year follow-up and atrophic body gastritis patients with panatrophic gastritis are at increased risk of developing neoplastic lesions.
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U2 - 10.1111/j.1365-2036.2005.02582.x
DO - 10.1111/j.1365-2036.2005.02582.x
M3 - Article
C2 - 16128686
AN - SCOPUS:24344488684
VL - 22
SP - 471
EP - 481
JO - Alimentary Pharmacology and Therapeutics
JF - Alimentary Pharmacology and Therapeutics
SN - 0269-2813
IS - 5
ER -