Nitric oxide is a potential mediator of hepatic inflammation and fibrogenesis in autoimmune hepatitis

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dc.contributor.authorBeyazıt, Yavuz
dc.contributor.authorEfe, Cumali
dc.contributor.authorTanoğlu, Alpaslan
dc.contributor.authorPurnak, Tuğrul
dc.contributor.authorSayılır, Abdurrahim
dc.contributor.authorTaşkıran, İsmail
dc.contributor.authorKekilli, Murat
dc.contributor.authorTurhan, Turan
dc.contributor.authorÖzaslan, Ersan
dc.contributor.authorWahlin, Staffan
dc.date.accessioned2019-05-10T09:39:17Z
dc.date.available2019-05-10T09:39:17Z
dc.date.issued2015
dc.departmentHitit Üniversitesi, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü
dc.description.abstractBackground. Despite advances in the understanding of the pathophysiological basis of autoimmune hepatitis (AIH), it is still difficult to delineate the mechanisms involved in progression from hepatic inflammation toward fibrosis. Our aim was to study serum concentrations of NO in AIH of different histological severity and possible effects of immunosuppressive therapy on NO production. Materials and methods. We studied serum NO metabolites (NOx) in 47 consecutive patients with AIH and in 28 age- and sex-matched controls. Results. Serum NOx concentrations were higher in AIH patients than in controls (10.3 (4.5-27.3 µmol/L) vs. 4.3 (1.6-14.3 µmol/L), p < 0.001). According to liver histology, median NOx concentrations were significantly higher in patients with severe interface hepatitis compared to patients with mild-moderate interface hepatitis (12.3 (4.5-27.3 µmol/L) vs. 9.3 (4.6-20.3 µmol/L), p = 0.029). Similarly, serum NOx concentrations were significantly higher in patients with advanced fibrosis than in those with early fibrosis (12.2 (4.6-27.3 µmol/L) vs. 9.3 (6.6-12.8 µmol/L), p = 0.018). NOx concentrations decreased in 16 AIH patients who were tested also after biochemical remission was achieved (12.6 (4.5-22.8 µmol/L) at baseline and 5.9 (2.8-10.5 µmol/L) after remission, p = 0.001). Conclusion. This study shows that serum NOx levels are associated with the histological severity of AIH. Hepatocyte inflammation and injury may activate hepatic stellate cells and kupffer cells, and the consequences may include release of NO, which ultimately promotes hepatic fibrosis. Immunosuppressive therapy inhibits this process and the production of NO. © 2015 Informa Healthcare.
dc.identifier.citationBeyazit, Y., Efe, C., Tanoglu, A., Purnak, T., Sayilir, A., Taskıran, I., ... & Wahlin, S. (2015). Nitric oxide is a potential mediator of hepatic inflammation and fibrogenesis in autoimmune hepatitis. Scandinavian journal of gastroenterology, 50(2), 204-210.
dc.identifier.doi10.3109/00365521.2014.974203
dc.identifier.endpage210en_US
dc.identifier.issn0036-5521
dc.identifier.issue2en_US
dc.identifier.scopusqualityQ3
dc.identifier.startpage204en_US
dc.identifier.urihttps://doi.org/10.3109/00365521.2014.974203
dc.identifier.urihttps://hdl.handle.net/11491/656
dc.identifier.volume50en_US
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherInforma Healthcare
dc.relation.ispartofScandinavian Journal of Gastroenterology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAutoimmune Hepatitisen_US
dc.subjectFibrosisen_US
dc.subjectNitric Oxideen_US
dc.subjectOxidative Stressen_US
dc.titleNitric oxide is a potential mediator of hepatic inflammation and fibrogenesis in autoimmune hepatitis
dc.typeArticle

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