Evidence of an increased nitric oxide production in primary biliary cirrhosis

Battista, Stefania; Bar, Fabrizio; Mengozzi, Giulio; Pollet, Cristina; Torchio, Mauro; Cavalli, G.; Rosina, F.; David, Ezio; Cutrìn, Juan Carlos; Cavalieri, Barbara; Poli, Giuseppe; Molino, Gianpaolo

doi:10.1016/s0002-9270(00)02263-2

Cited by 7 publications

(11 citation statements)

References 18 publications

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“…Serum levels of NOx in all stages of PBC patients were found significantly higher than controls in agreement with a few previous studies. 17,19 Cirrhotic patients in our study were also found to have significantly increased levels of NOx, a fact that has also been described elsewhere. 23,39,40 In this respect, it is possible that the high levels of NOx, found in PBC stages III and IV, are indeed related to the advanced liver injury.…”

Section: Discussionsupporting

confidence: 89%

Ursodeoxycholic acid reduces increased circulating endothelin 2 in primary biliary cirrhosis

Dimoulios

Kolios

Notas

et al. 2005

Aliment Pharmacol Ther

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SUMMARYBackground: Endothelins and nitric oxide regulate sinusoidal blood flow and the perfusion of the peribiliary vascular plexus. Aims: To study the serum and hepatic vein concentration of ET-1, ET-2, ET-3 and nitric oxide in patients with primary biliary cirrhosis and the effect of ursodeoxycholic acid treatment. Methods: Endothelins and nitrites/nitrates were measured in serum and hepatic vein blood in primary biliary cirrhosis and viral cirrhotic patients prior and after ursodeoxycholic acid therapy and in serum in controls. Endothelins were measured with commercial enzymelinked immunosorbent assays and nitrites/nitrates with a modification of Griess reaction. Results: The ET-1 and ET-3 levels were similar in patients and controls. Primary biliary cirrhosis patients

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Section: Discussionsupporting

confidence: 89%

Ursodeoxycholic acid reduces increased circulating endothelin 2 in primary biliary cirrhosis

Dimoulios

Kolios

Notas

et al. 2005

Aliment Pharmacol Ther

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“…However, the physiopathological role of cholangiocytes with apocrine‐like changes, as well as iNOS and/or NT expression in these cholangiocytes in TGH, is unclear. It was proposed that iNOS‐ and/or NT‐expressing cholangiocytes might be highly susceptible to the development of biliary cirrhosis and/or cholangiocarcinoma due to the production of NO induced by iNOS in biliary epithelial cells; this has been postulated to contribute to epithelial cell cirrhosis and/or carcinogenesis by causing damage to DNA and proteins (34,35).…”

Section: Discussionmentioning

confidence: 99%

Enhanced inducible nitric oxide synthase expression and nitrotyrosine accumulation in experimental granulomatous hepatitis caused by Toxocara canis in mice

Fan

Lin

Hung

et al. 2004

Parasite Immunology

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The involvement of inducible nitric oxide synthase (iNOS) and nitrotyrosine (NT) in pathogenesis of toxocaral granulomatous hepatitis (TGH) in a murine host was quantitatively determined by biochemical, parasitological, pathological, and immunohistochemical assessments in a 42-week investigation. Mice were sacrificed for serum collection and histological processing as well as acid-pepsin digestion of the liver in a larval recovery study. Significantly increased levels of total serum NO were found in the trial, indirectly suggesting iNOS activation in the liver. iNOS reactivity was predominantly observed in infiltrating leucocytes in lesions and normal and apocrine-like cholangiocytes; in contrast, hepatocytes and multinucleated giant cells showed negative cytoplasmic staining in TGH. Strong iNOS-like reactivity was also detected on the body wall of larvae. The locations of NT reactivity were nearly identical to those of iNOS expression; infiltrating leucocytes or cholangiocytes stained for iNOS were also stained for NT in TGH. Enhanced iNOS expression, but not invading larvae (r = 0.256, P = 0.211), seemed to play a certain role in pathological damage in TGH due to a significant correlation between iNOS expression and serum alanine aminotransferase (ALT) levels (r =0.593, P = 0.021) in the trial. Our present results indicate a potential therapeutic strategy for treatment of GH caused by other nematodes through manipulation of iNOS expression.

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“… 8 Additionally, patients with PBC have increased nitric oxide levels, which may allow for the vasodilation required in early stages of angiogenesis. 5,9 Similar mechanisms of angiogenesis and increased expression of VEGF have been characterized in other biliary tract diseases. 6 The relationship between fibrosis and angiogenesis not only exists in primary biliary cirrhosis, but has been observed in chronic liver diseases such as hepatitis B, hepatitis C, and alcoholic liver disease.…”

Section: Discussionmentioning

confidence: 74%

Intraoperative management of a carbon dioxide embolus in the setting of laparoscopic cholecystectomy for a patient with primary biliary cirrhosis: A case report

Cadis

Velasquez

Brauer

et al. 2014

International Journal of Surgery Case Reports

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HighlightsWe discuss appropriate detection and management of a carbon dioxide embolus.We review the pathologic hepatic changes in patients with primary biliary cirrhosis.We postulate that cirrhosis may increase the risk of a carbon dioxide embolus.We share an understanding that more invasive monitoring may be helpful, but ultimately hypervigilance from the anesthesia team is the number one safeguard.

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Evidence of an increased nitric oxide production in primary biliary cirrhosis

Cited by 7 publications

References 18 publications

Ursodeoxycholic acid reduces increased circulating endothelin 2 in primary biliary cirrhosis

Ursodeoxycholic acid reduces increased circulating endothelin 2 in primary biliary cirrhosis

Enhanced inducible nitric oxide synthase expression and nitrotyrosine accumulation in experimental granulomatous hepatitis caused by Toxocara canis in mice

Intraoperative management of a carbon dioxide embolus in the setting of laparoscopic cholecystectomy for a patient with primary biliary cirrhosis: A case report

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