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J Med Life ; 14(2): 176-180, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34104240

RESUMO

The study of the pathogenetic treatment and prevention of Helicobacter pylori (Hp)-associated gastroduodenopathies (GDP) induced by nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with osteoarthritis (OA) is one of the most serious problems in modern clinical medicine. Sixty patients with OA and concomitant Hp-associated GDP induced by NSAIDs were examined. The levels of epidermal growth factor (EDF), sAPO-1/Fas and tumor necrosis factor-α (TNF-α) were determined. Group I included 30 patients who received triple anti-Helicobacter (AHT) therapy, and group II included 30 patients who received rebamipide. Long-term effects were assessed 6 months and 1 year after treatment. All subjects showed a significant increase in TNF-α (4.7 times), EDF (2.2 times) and a decrease in sAPO-1/Fas (3.6 times) levels compared to healthy individuals. After 1 month of treatment, a significantly more significant decrease in TNF-α and an increase in sAPO-1/Fas and EDF was found in group II. In the long-term treatment, a further decrease in TNF-α and an increase in the content of sAPO-1/Fas levels were observed in all groups. However, these changes were significantly more significant in group I compared to group I. The long-term follow-up showed a declining trend of EDF in all groups. The data obtained indicate the effectiveness of rebamipide in the complex pathogenetic treatment and prevention of Hp-associated GDP induced by NSAIDs in patients with OA.


Assuntos
Anti-Inflamatórios não Esteroides/efeitos adversos , Anti-Inflamatórios não Esteroides/uso terapêutico , Duodeno/patologia , Infecções por Helicobacter/microbiologia , Helicobacter pylori/fisiologia , Osteoartrite/tratamento farmacológico , Gastropatias/induzido quimicamente , Gastropatias/microbiologia , Fator de Crescimento Epidérmico/sangue , Infecções por Helicobacter/sangue , Humanos , Osteoartrite/sangue , Osteoartrite/complicações , Gastropatias/sangue , Fator de Necrose Tumoral alfa/sangue , Receptor fas/sangue
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