Letter to the Editor
Copyright ©The Author(s) 2021.
World J Gastroenterol. Dec 14, 2021; 27(46): 8033-8039
Published online Dec 14, 2021. doi: 10.3748/wjg.v27.i46.8033
Table 1 Characteristics of patients included in the eleven selected studies applying endoscopic surveillance shorter than two years for the evaluation of precancerous gastric conditions following Helicobacter pylori eradication

van der Hulst RW et al[2], 1997
Tucci A et al[3], 1998
Sung JJ et al[4], 2000
Annibale B et al[5], 2000
Ohkusa T et al[6], 2001
Oda Y et al[7], 2004
Annibale B et al[8], 2002
Yamada T et al[9], 2003
Iacopini F et al[10], 2003
Wambura C et al[11], 2004
Panarese et al[12], 2020
StudyProspectiveRetrospectiveProspective, randomized, placebo controlled trialObservational, prospective studySingle-blind, uncontrolled prospective trialRetrospectiveRetrospectiveRetrospectiveObservational, prospective studyObservational, prospective studyObservational, prospective study
CountryNetherlandsItalyChinaItalyJapanJapanItalyJapanItalyJapanItaly
Mean age, yr49.25051 (Median)48.7545146 (Median)52.65551.256.1
Male, %545049.514.37389.822.564.47574.737.6
Overlap AAGNA0NA48.6NANA55NANANA26.3
Mean follow-up, mo1212126-1212-151-26-122212126
Total, n10610226251155940874010785
Resolution of gastric acute/chronic inflammation in the antrum n (%)S10/10 (100)S25/25 (100)NASSSSS81/85 (95.3)
Resolution of gastric acute/chronic inflammation in the corpus, n (%)SNAS25/25 (100)NASSSSS81/85 (85.3)
Resolution of gastric acute/chronic inflammation in the fundus n (%)NA10/10 (100)NANANANANANANANANA
Improvement of AG in the antrum, n (%)NSNSNSNS34/38 (89)NSNSNSNSSNS
Improvement of AG in the corpus, n (%)NSNANSNS34/38 (89)NS8/40 (20) AG reversedSNASNS
Improvement of AG in the fundus, n (%)NASNANANANANASNANANA
Improvement of IM in the antrum, n (%)NSSSNS28/46 (61)NSNSNSNSNSNS
Improvement of IM in the corpus, n (%)NSNANSNS28/46 (61)NSNSNSNASNS
Improvement of IM in the fundus, n (%)NANSNANANANANANANASNA
ECL pattern regression, n (%)NANANA8/15 (53.3) patients with AG in the body (12 mo after curing H. pylori)NANANANANANA36/39 (92.3)
LGD regression (or progression), n (%)NANANA1/1 (100) regression in a patient with AG in the body (12 mo after curing H. pylori)NANANANANANAThe proportion of patients with histological diagnosis of LGD on random biopsies did not significantly change after H. pylori eradication [15 (17.6) vs 9 (10.6)]; the detection of LGD on visible lesions significantly increased after H. pylori eradication [0 (0) vs 19 (22.3)]
ConclusionsThe usefulness of H. pylori eradication to regress precancerous lesions following 12 mo follow-up is uncertainThe natural history of AG can be modified by the eradication of H.pyloriAt 12 mo, H. pylori eradication can block the histological progression of gastric mucosa alterationsH. pylori infection may be cured in patients with AG in the body with a partial reversing of its adverse outcomes on acid secretion and body ECL cell hyperplasiaAfter successful H. pylori eradication, precancerous lesions improved in most patientsAfter H. pylori eradication, neutrophil infiltration in the gastric mucosa improved relatively soon, while AG and IM did not display such tendencyIn patients with AG of the body and H. pylori infection, the assessment of histological data after eradication is essential. In patients with maintaining body atrophy after H. pylori elimination, there is no association with the reversal of body atrophy, even at long-term surveillanceAG in the corpus can be improved after 12 mo following H. pylori eradicationH. pylori positive patients with AG, the overall oxidative damage of the gastric mucosa is more severe than that in H. pylori positive patients with nonatrophic gastritisEradication of H. pylori may decrease the risk of GC, due to the importance of H. pylori infection in the contributory role of gastritis in COX-2 expression and the dissociation between the processes of regression in gastritis and the reduction in COX-2HR-WLE with NBI can be more reliable in diagnosing LGD on visible lesions after H. pylori elimination, presumably due to the removal of the underlying confounding effects of inflammatory and mucosal lymphoproliferative changes induced by H. pylori chronically active infection. Aged patients and those with autoimmune diseases (especially AAG) could be at higher risk for H. pylori persistent infection