ENDOTHELIAL DYSFUNCTION AND GASTROESOPHAGEAL REFLUX DISEASE: STUDY OF COMMON PATHOGENETIC MECHANISMS AND WAYS OF CORRECTION

Abstract

The aim. To determine the role and place of endothelial dysfunction in the pathogenesis of comorbid gastroesophageal reflux disease (GERD) and obesity by studying the levels of nitric oxide (NO) metabolites in blood and urine. To evaluate the efficacy and benefits of the prescribed therapy, which included the additional inclusion of a peptide compound analogous to leu-enkephalin tyrosine-2-alanine-glycine-phenylalanine-leucyl-arginine diacetate (Dalargin).
 Materials and methods. Clinical manifestations were assessed using the GERD-HRQL questionnaire, levels of stable nitric oxide metabolites NO2 and total metabolites NO2 + NO3 were determined by spectrophotometric method, leptin levels were determined by enzyme-linked immunosorbent assay, pH-metry and motor function was studied by ultrasound. 130 patients were examined, including 70 patients with GERD with comorbid obesity of the first degree, 40 patients with GERD without concomitant pathology and 20 healthy individuals. The study was divided into 3 groups.
 Results. It was determined that the levels of stable metabolites NO2, NO2 + NO3 in blood and urine in the group of GERD with obesity are significantly lower than in the group of isolated GERD (p<0.001). A direct correlation between the level of nitric oxide metabolites in blood and urine and acidity in the stomach and oesophagus was established; an inverse relationship between NO metabolites and the degree of gastrointestinal motor and functional disorders, the severity of clinical manifestations, and the level of hormonal secretion by adipocytes. The supplemental inclusion of Dalargin improved the effectiveness and quality of pathogenetic therapy and achieved a more positive disease dynamics and is recommended for prescription in practice.
 Conclusions. Obesity is a predictor of a more severe course of GERD and more severe endothelial dysfunction. There is a correlation between the severity of endothelial dysfunction and the degree of functional, motor and secretory disorders of the stomach and oesophagus.