Abstract:
Rheumatoid arthritis (RA) is a progressive autoimmune disease of unknown etiology with predominant joint damage, characterized by the development of chronic erosive arthritis and frequent systemic inflammation of internal organs [1]. NSAIDs are an important component of the complex therapy of rheumatic diseases. At least 68.5% of patients with rheumatoid arthritis are constantly taking NSAIDs [2].
Therefore, among patients with RA, the highest incidence of NSAID-associated gastropathy, erosive and ulcerative lesions complicated by gastrointestinal bleeding and other complications [3]. Therefore, the use of non-steroidal anti-inflammatory drugs (NSAIDs) is also a factor in ulcerogenesis. However, the influence of pathogenic factors of H. pylori on the likelihood of erosive and ulcerative damage to the gastroduodenal zone induced by NSAID intake has not been sufficiently studied.
