Systemic endothelial dysfunction in patients with cerebrovascular diseases

Relevance of the work. Chronic gastritis remains one of the most common pathologies in the clinic of internal diseases. Existing staging systems (OLGA/OLGIM) allow for effective stratification of cancer risk, but they do not take into account the vascular component and are primarily focused on neoplastic transformation, leaving open the questions of predicting non-oncological complications (erosions, bleeding, anemia), especially in comorbid patients. A special group includes patients with severe cerebrovascular diseases (CVD). In addition to the classic factors of aggression (Helicobacter pylori, antiplatelet agents), this category of patients has a systemic pathophysiological background, such as endothelial dysfunction and microangiopathy, which can modify the structure and function of the gastric mucosa. Systemic endothelial dysfunction in CVD is characterized by an imbalance of vasoactive substances, overexpression of adhesion molecules, and pro-inflammatory cytokines, leading to to the violation of local angiogenesis and microcirculation. A key role in the pathogenesis of ischemic damage is played by thromboinflammation (thromboinflammation), which is directly related to the state of microcirculation in various organs. The concept of the brain-gut axis opens up new prospects for understanding gastroduodenal pathology in neurological patients. In CVD, neurohumoral dysregulation factors are added, which can further affect motility, secretion, and microcirculation in the gastroduodenal zone. Materials and methods. In accordance with the set goal, the analysis of the world literature was performed using the TripDataBase search system, which allowed to study and structure the main pathophysiological mechanisms of chronic gastritis in patients with CVD. Results. According to the data of the world literature. despite the presence of theoretical prerequisites for secondary damage to the gastric mucosa in patients with CVD, a systematic analysis of the state of the microcirculatory bed (CD34) and its relationship with the mucin profile (MUC5AC, MUC2) has not been previously studied in this patient population. There are no predictive models for the risk of gastrointestinal complications that take into account the morphological characteristics of the mucous membrane in addition to standard clinical factors. Conclusion. The need to identify a “vascular-modified” phenotype of gastritis in patients with cerebrovascular diseases has been substantiated. Integration of clinical, endoscopic (in white light and narrow-spectrum imaging modes), and immunohistochemical parameters (CD34, MUC5AC, MUC2) will allow the development of a prognostic model for the risk of gastrointestinal complications, which is in line with the principles of personalized medicine and has high clinical significance for the management of comorbid patients at high risk of both vascular events and hemorrhagic complications.