Relationship Between Pathogenetic Mechanisms of NSAID-gastropathy Development in Elderly Patients with Concomitant Ischemic Heart Disease

Abstract

The objective: to study the relationship between risk factors and mechanisms of NSAID gastropathy development with concomitant ischemic heart disease.Materials and methods. The study included 125 patients who underwent general clinical examination, upper endoscopy with biopsy of the gastric mucosa (GM), followed by histological examination of biopsies, assessment of mucosal function of GM (content of N-acetylneuraminic acid (NANA) and fucoproteins in the blood), oxidative stress (concentration of TBA-active products and catalase activity in the blood serum), endothelial dysfunction (nitrite concentration and endothelial NO-synthase (eNOS), inducible NOS (iNOS) activity), severity of erosive-ulcerative lesions according to modified Lanzascore scale with assessment of histological changes.Results. In most patients of both groups, the onset of complaints was provoked by taking ASA and/or NSAIDs and had a direct correlation with the number of anti-inflammatory drugs (r=0.72; r=0.63; p=0.025), and also depended on the duration of NSAIDs treatment (r=0.52; r=0.67; p=0.031). There is a strong direct relationship between the concentration of NANA in the blood serum and the amount of NSAIDs (r=0.69; p=0.03), the duration of drugs (r=0.50; p=0.024), the content of TBA reactants in the blood serum (r=0.59; p=0.015), the severity of erosive-ulcerative lesions according to Lanzascore scale (r=0.71; p=0.017) on the background of inverse correlation with eNOS activity (r=–0,65; р=0,024). Correlation analysis showed a direct relationship between iNOS activity and H. pylori infection (r=0.63; p=0.030), the severity of erosive-ulcerative lesions according to Lanzascore scale (r=0.50; p=0.047), the GM infiltration by polymorphonuclear leukocytes (r=0.72; p=0.027) against the background of inverse correlation with the catalase activity (r=–0.41; р=0.030).Conclusion. The degree of GM injury depends on the amount and duration of NSAIDs and/or ASA, the presence of comorbid pathology, H.pylori infection, oxidative stress activity, endothelial dysfunction.