This study presents a comparative characterization of morphological alterations in the gastric mucosa under various experimental models of liver injury, including toxic (carbon tetrachloride-induced), ischemic-reperfusion, and cholestatic (bile duct ligation) damage. Histological (H&E, PAS, Van Gieson), immunohistochemical (TNF-α, IL-6, VEGF, CD31), and electron-microscopic techniques were used to examine changes in the gastric epithelium, glandular apparatus, vascular bed, inflammatory infiltrate, and microcirculation. Liver injury was shown to significantly exacerbate the severity of epithelial dystrophy, erosive-ulcerative lesions, hemorrhages, and microcirculatory disturbances in the gastric mucosa. The most severe pathological changes were observed in the ischemia-reperfusion and toxic hepatitis models. These findings confirm the pathogenetic relationship along the liver–stomach axis (gut–liver axis) and underscore its clinical relevance for early diagnosis and prevention of gastric complications in patients with liver diseases, particularly in Uzbekistan, where chronic liver pathology remains highly prevalent.
Davronov et al. (Wed,) studied this question.