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Thomas Damgaard Sandahl

Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review

Standard

Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS. / Holland-Fischer, Peter; Grønbæk, Henning; Sandahl, Thomas Damgaard; Moestrup, Søren Kragh; Riggio, Oliviero; Ridola, Lorenzo; Aagaard, Niels Kristian; Møller, Holger Jon; Vilstrup, Hendrik.

In: Gut, Vol. 60, No. 10, 10.2011, p. 1389-93.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review

Harvard

Holland-Fischer, P, Grønbæk, H, Sandahl, TD, Moestrup, SK, Riggio, O, Ridola, L, Aagaard, NK, Møller, HJ & Vilstrup, H 2011, 'Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS', Gut, vol. 60, no. 10, pp. 1389-93. https://doi.org/10.1136/gut.2010.234542

APA

Holland-Fischer, P., Grønbæk, H., Sandahl, T. D., Moestrup, S. K., Riggio, O., Ridola, L., Aagaard, N. K., Møller, H. J., & Vilstrup, H. (2011). Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS. Gut, 60(10), 1389-93. https://doi.org/10.1136/gut.2010.234542

CBE

Holland-Fischer P, Grønbæk H, Sandahl TD, Moestrup SK, Riggio O, Ridola L, Aagaard NK, Møller HJ, Vilstrup H. 2011. Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS. Gut. 60(10):1389-93. https://doi.org/10.1136/gut.2010.234542

MLA

Holland-Fischer, Peter et al. "Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS". Gut. 2011, 60(10). 1389-93. https://doi.org/10.1136/gut.2010.234542

Vancouver

Holland-Fischer P, Grønbæk H, Sandahl TD, Moestrup SK, Riggio O, Ridola L et al. Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS. Gut. 2011 Oct;60(10):1389-93. https://doi.org/10.1136/gut.2010.234542

Author

Holland-Fischer, Peter ; Grønbæk, Henning ; Sandahl, Thomas Damgaard ; Moestrup, Søren Kragh ; Riggio, Oliviero ; Ridola, Lorenzo ; Aagaard, Niels Kristian ; Møller, Holger Jon ; Vilstrup, Hendrik. / Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS. In: Gut. 2011 ; Vol. 60, No. 10. pp. 1389-93.

Bibtex

@article{0099af15dfa64457bf3226d7b4d22fcc,
title = "Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS",
abstract = "Introduction Hepatic macrophages (Kupffer cells) undergo inflammatory activation during the development of portal hypertension in experimental cirrhosis; this activation may play a pathogenic role or be an epiphenomenon. Our objective was to study serum soluble CD163 (sCD163), a sensitive marker of macrophage activation, before and after reduction of portal venous pressure gradient by insertion of a transjugular intrahepatic portosystemic shunt (TIPS) in patients with cirrhosis. Methods sCD163 was measured in 11 controls and 36 patients before and 1, 4 and 26 weeks after TIPS. We used lipopolysaccharide binding protein (LBP) levels as a marker of endotoxinaemia. Liver function and clinical status of the patients were assessed by galactose elimination capacity and Model for End Stage Liver Disease score. Results The sCD163 concentration was more than threefold higher in the patients than in the controls (median 5.22 mg/l vs 1.45 mg/l, p",
author = "Peter Holland-Fischer and Henning Gr{\o}nb{\ae}k and Sandahl, {Thomas Damgaard} and Moestrup, {S{\o}ren Kragh} and Oliviero Riggio and Lorenzo Ridola and Aagaard, {Niels Kristian} and M{\o}ller, {Holger Jon} and Hendrik Vilstrup",
year = "2011",
month = oct,
doi = "10.1136/gut.2010.234542",
language = "English",
volume = "60",
pages = "1389--93",
journal = "Gut",
issn = "0017-5749",
publisher = "B M J Group",
number = "10",

}

RIS

TY - JOUR

T1 - Kupffer cells are activated in cirrhotic portal hypertension and not normalised by TIPS

AU - Holland-Fischer, Peter

AU - Grønbæk, Henning

AU - Sandahl, Thomas Damgaard

AU - Moestrup, Søren Kragh

AU - Riggio, Oliviero

AU - Ridola, Lorenzo

AU - Aagaard, Niels Kristian

AU - Møller, Holger Jon

AU - Vilstrup, Hendrik

PY - 2011/10

Y1 - 2011/10

N2 - Introduction Hepatic macrophages (Kupffer cells) undergo inflammatory activation during the development of portal hypertension in experimental cirrhosis; this activation may play a pathogenic role or be an epiphenomenon. Our objective was to study serum soluble CD163 (sCD163), a sensitive marker of macrophage activation, before and after reduction of portal venous pressure gradient by insertion of a transjugular intrahepatic portosystemic shunt (TIPS) in patients with cirrhosis. Methods sCD163 was measured in 11 controls and 36 patients before and 1, 4 and 26 weeks after TIPS. We used lipopolysaccharide binding protein (LBP) levels as a marker of endotoxinaemia. Liver function and clinical status of the patients were assessed by galactose elimination capacity and Model for End Stage Liver Disease score. Results The sCD163 concentration was more than threefold higher in the patients than in the controls (median 5.22 mg/l vs 1.45 mg/l, p

AB - Introduction Hepatic macrophages (Kupffer cells) undergo inflammatory activation during the development of portal hypertension in experimental cirrhosis; this activation may play a pathogenic role or be an epiphenomenon. Our objective was to study serum soluble CD163 (sCD163), a sensitive marker of macrophage activation, before and after reduction of portal venous pressure gradient by insertion of a transjugular intrahepatic portosystemic shunt (TIPS) in patients with cirrhosis. Methods sCD163 was measured in 11 controls and 36 patients before and 1, 4 and 26 weeks after TIPS. We used lipopolysaccharide binding protein (LBP) levels as a marker of endotoxinaemia. Liver function and clinical status of the patients were assessed by galactose elimination capacity and Model for End Stage Liver Disease score. Results The sCD163 concentration was more than threefold higher in the patients than in the controls (median 5.22 mg/l vs 1.45 mg/l, p

U2 - 10.1136/gut.2010.234542

DO - 10.1136/gut.2010.234542

M3 - Journal article

C2 - 21572121

VL - 60

SP - 1389

EP - 1393

JO - Gut

JF - Gut

SN - 0017-5749

IS - 10

ER -