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  • Title: [Clinico-morphological variants of gastric mucosa atrophic lesions].
    Author: Naumova LA, Pal'tsev AI, Beliaeva IaIu.
    Journal: Ter Arkh; 2009; 81(2):17-23. PubMed ID: 19334483.
    Abstract:
    AIM: To characterize clinicomorphological manifestations of atrophic process (AP) in gastric mucosa (GM) in chronic atrophic gastritis (CAG) associated and not associated with Helicobacter pylori infection. MATERIAL AND METHODS: Clinicoendoscopic and pathomorphological (light microscopy of gastric biopsies, 6 point scale assessment of dysregeneratory alterations) investigations were made in 98 patients aged 16 to 68 years. H. pylori-negative CAG was diagnosed in 52 of them, H. pylori-positive one in 46 patients (groups 1 and 2, respectively). RESULTS: A comparative clinicomorphological analysis has identified 2 variants of AP morphogenesis in GM. Variant 1 is not associated with H. pylori but associated with a combined action of several endogenic risk factors of chronic gastritis or failure of regeneration, with diffuse or diffuse-focal changes with initial prevalence of dysregeneratory changes in a fundal stomach manifesting as a trend to atrophy of the glands. Clinically, this variant is characterized by longer disease, frequent systemic atrophic lesions of gastrointestinal mucosa, prevalent complaints of dyspeptic pain. Variant 2 is associated with a combined action of endo- and exogenic factors, H. pylori infection in particular, pathogenetic components of "chemical" gastritis (duodenogastric reflux, malnutrition), prevalence of dysregeneratory and sclerotic alterations in the antral stomach. CONCLUSION: GM atrophy is characterized by a significant frequency of concomitant endocrinopathies, undifferentiated connective tissue dysplasia, systemic lesions, structurally--by multidirectional disorders of proliferation and differentiation. First of all, it is the result of impaired regulation of regenerative processes. AP polyetiology and different morphogenetic variants in GM suggest necessity of both individual diagnostic algorithm and pathogenetically sound therapy in each individual case.
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