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Revista Española de Enfermedades Digestivas

versión impresa ISSN 1130-0108

Resumen

QIANG, Zhang et al. Analysis of alarming signals for the progression of atrophic gastritis to dysplasia. Rev. esp. enferm. dig. [online]. 2012, vol.104, n.8, pp.399-404. ISSN 1130-0108.  https://dx.doi.org/10.4321/S1130-01082012000800002.

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.

Palabras clave : Atrophic gastritis; Dysplasia; Helicobacter pylori; Gastric ulcer; Follow-up.

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