Nitric oxide is a potential mediator of hepatic inflammation and fibrogenesis in autoimmune hepatitis. (February 2014)
- Record Type:
- Journal Article
- Title:
- Nitric oxide is a potential mediator of hepatic inflammation and fibrogenesis in autoimmune hepatitis. (February 2014)
- Main Title:
- Nitric oxide is a potential mediator of hepatic inflammation and fibrogenesis in autoimmune hepatitis
- Authors:
- Beyazit, Yavuz
Efe, Cumali
Tanoglu, Alpaslan
Purnak, Tugrul
Sayilir, Abdurrahim
Taskıran, Ismail
Kekilli, Murat
Turhan, Turan
Ozaslan, Ersan
Wahlin, Staffan - Abstract:
- <abstract> <title>Abstract</title> <p> <bold> <italic>Background.</italic> </bold> 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. <bold><italic>Materials and methods.</italic></bold> We studied serum NO metabolites (NOx) in 47 consecutive patients with AIH and in 28 age- and sex-matched controls. <bold><italic>Results.</italic></bold> 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), <italic>p</italic> &lt; 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), <italic>p</italic> = 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), <italic>p</italic> = 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,<abstract> <title>Abstract</title> <p> <bold> <italic>Background.</italic> </bold> 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. <bold><italic>Materials and methods.</italic></bold> We studied serum NO metabolites (NOx) in 47 consecutive patients with AIH and in 28 age- and sex-matched controls. <bold><italic>Results.</italic></bold> 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), <italic>p</italic> &lt; 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), <italic>p</italic> = 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), <italic>p</italic> = 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, <italic>p</italic> = 0.001). <bold><italic>Conclusion.</italic></bold> 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.</p> </abstract> … (more)
- Is Part Of:
- Scandinavian journal of gastroenterology. Volume 50:Number 2(2015)
- Journal:
- Scandinavian journal of gastroenterology
- Issue:
- Volume 50:Number 2(2015)
- Issue Display:
- Volume 50, Issue 2 (2015)
- Year:
- 2015
- Volume:
- 50
- Issue:
- 2
- Issue Sort Value:
- 2015-0050-0002-0000
- Page Start:
- 204
- Page End:
- 210
- Publication Date:
- 2014-02
- Subjects:
- Gastroenterology -- Periodicals
Digestive organs -- Diseases -- Periodicals
616.33 - Journal URLs:
- http://informahealthcare.com/loi/gas ↗
http://informahealthcare.com ↗ - DOI:
- 10.3109/00365521.2014.974203 ↗
- Languages:
- English
- ISSNs:
- 0036-5521
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 8087.507000
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 4306.xml