Variants of intestinal metaplasia in the evolution of chronic atrophic gastritis and gastric ulcer. A follow up study.

Silva, S; Filipe, M. I.; Pinho, André

doi:10.1136/gut.31.10.1097

Cited by 76 publications

(45 citation statements)

References 16 publications

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“…[15][16][17] The prediction of the progression of these lesions according to the severity at baseline has been referred to by others. [21][22][23] In addition, Lahner and colleagues 24 suggested that the follow up of patients with body predominant atrophic gastritis need not to be earlier than four years after diagnosis, stating that this interval is satisfactory for the detection of potential neoplastic lesions. More than 10 years ago, type III IM 21 25-27 was stated as a lesion with an increased risk for dysplasia and cancer, and it was suggested that its follow up should be intensive.…”

Section: Discussionmentioning

confidence: 99%

A follow up model for patients with atrophic chronic gastritis and intestinal metaplasia

Dinis-Ribeiro

Lopes²,

Costa‐Pereira³

et al. 2004

J Clin Pathol

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Aim: To devise a follow up model for patients with gastric cancer associated lesions, such as atrophic chronic gastritis (ACG) and intestinal metaplasia (IM). Methods: Cohort study of 144 patients, followed for a minimum of one year, in whom at least two upper gastrointestinal endoscopic biopsies in flat gastric mucosa provided a diagnosis of ACG, IM, or low grade dysplasia (LGD). Results: Of those diagnosed with ACG at first endoscopic biopsy (entry biopsy), 12% progressed to LGD in outcome biopsy, as did 8% of those with type I IM, 38% with type II or III IM, and 32% with LGD. Type of IM at entry independently predicted progression to LGD and cancer. Type II and III IM had a higher rate of progression to LGD than type I IM, which showed an indolent behaviour similar to ACG. Patients with type II or III IM were at higher risk for development of dysplasia, and 7% of patients with type III IM at first biopsy progressed to high grade dysplasia (HGD), whereas no cases of ACG or type I/II IM progressed to HGD during the first three years. Conclusion: Patients with ACG or IM could possibly be allocated to different management schedules, based on differences in rate and proportion of progression to LGD or HGD. Less intensive follow up (two/ three yearly with ''serological evaluation'' (pepsinogen)) may suit those with ACG or type I IM. Patients with type III IM may benefit from six to 12 monthly improved endoscopic examination (magnification chromoendoscopy).

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Section: Discussionmentioning

confidence: 99%

A follow up model for patients with atrophic chronic gastritis and intestinal metaplasia

Dinis-Ribeiro

Lopes²,

Costa‐Pereira³

et al. 2004

J Clin Pathol

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show abstract

“…One small study following seven patients with type III metaplasia for 6 years observed development of gastric cancer in one of them. 63 In the large Slovenian study of 1281 subjects with intestinal metaplasia followed for a mean 11 years, gastric cancer developed in 34 (2.7%), 15 of whom were previously diagnosed with type III metaplasia. 34 Gastric cancer was the most commonly occurring malignancy in this population.…”

Section: Atrophy Metaplasia and Gastric Cancer: Prospective Studiesmentioning

confidence: 99%

Relationship between Helicobacter pylori, atrophic gastritis and gastric cancer

Kuipers

1998

Aliment Pharmacol Ther

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“…The pathological indices above described: highly suspected gastric cancer was considered as gastric ulcer with few atypia cells and perishing morphogenesis under endoscope; moderate dysplasia was not included in mild to moderate dysplasia; moderate and severe dysplasia were included in moderate to severe dysplasia. We speculated that gastric ulcer, type III intestinal metaplasia and AG are at risk for cancer, and the effect of having two or three of these factors significantly increase the risk for gastric cancer (9). There is a possible mechanism that molecular biology changes including gp130, MMP, Reg, IL-11 and IGF-1, etc., may be contributed to excessive hyperplasia of mucosal epithelial cells during the occurrence, development and outcome of diseases of gastric ulcer.…”

Section: Discussionmentioning

confidence: 99%

Analysis of alarming signals for the progression of atrophic gastritis to dysplasia

Qiang

Zhou

Wang

et al. 2012

Rev. esp. enferm. dig.

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Background and aims: atrophic gastritis (AG) and dysplasia are precancerous lesions, with which early surveillance of disease progression is particularly important for patients. The present study aimed to explore potential alarming signals for atrophic gastritis progression towards dysplasia.Methods: clinical data for patients with AG in the Digestive Endoscopy Center of Guangzhou Nanfang Hospital between 2001 and 2011 were retrospectively reviewed. Survival analysis, dichotomous logistic regression analysis and rank correlation analysis were carried out.Results: in 234 patients with atrophic gastritis, after follow up of 0.5, 1, 2, 5 and 10 years, the occurrence rates of dysplasia were respectively 2. 3, 4.4, 9.6, 19.3, and 42.4%. Patients with AG combined with antral ulcer or gastric angle ulcer, had a higher risk for dysplasia than patients with simple AG (OR = 2.427, 95%Cl 1.069 5.511, p = 0.034; OR = 2.961, 95%Cl 1.336 ~ 6.564, p = 0.008). The constituent ratios of moderate to severe dysplasia were respectively 8.6, 2.7 and 1.2% (p = 0.000) in three patient groups: AG combined with antral ulcer/gastric angle ulcer (n = 255), antral ulcer/gastric angle ulcer alone (n = 1,389), and AG alone (n = 3,106). The Spearman correlation coefficients between a) Hp infection; and b) atrophy, intestinal metaplasia and dysplasia were -0.114 (p = 0.078), -0.169 (p = 0.009) and 0.064 (p > 0.05), respectively.Conclusions: long follow-up interval and gastric ulcer may be alarming signals for the progression of AG to dysplasia. But in patients with atrophy, intestinal metaplasia or dysplasia, Hp infection may not be a risk factor for these lesions aggravated, further studies are required to confirm it.Key words: Atrophic gastritis. Dysplasia. Helicobacter pylori. Gastric ulcer. Follow-up. INTRODUCTIONAtrophic gastritis (AG) is a recognized precancerous lesion. AG-related lesions (such as intestinal metaplasia and dysplasia) are risk factors for gastric cancer (GC). Studies reported that during 5-year follow-up, the annual incidence rates of GC, intestinal metaplasia, mild to moderate dysplasia and severe dysplasia were, respectively, 0.1, 0.25, 0.6 and 6% in patients with AG in Western countries (1). With the wide application of endoscopy and the improvement of health awareness, the rate of detection of AG in clinical practice is increasing. This means that an increasing number of patients with AG will bear the psychological pressure to have follow-up exams and their financial burden. Currently, no effective preventative strategies have been developed; there is only symptomatic therapy and Helicobacter pylori (Hp) eradication. During follow-up, timely and accurate assessment of disease condition and monitoring of risk factors for dysplasia are critically important for these patients. In the present study, clinical data for patients with AG treated at the Digestive Endoscopy Center of the Guangzhou Nanfang Hospital in the past 11 years were retrospectively analyzed and some valuable characteristics were identified. Our ...

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Variants of intestinal metaplasia in the evolution of chronic atrophic gastritis and gastric ulcer. A follow up study.

Cited by 76 publications

References 16 publications

A follow up model for patients with atrophic chronic gastritis and intestinal metaplasia

A follow up model for patients with atrophic chronic gastritis and intestinal metaplasia

Relationship between Helicobacter pylori, atrophic gastritis and gastric cancer

Analysis of alarming signals for the progression of atrophic gastritis to dysplasia

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