Binge drinking induces an acute burst of markers of hepatic fibrogenesis (PRO-C3)
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Binge drinking induces an acute burst of markers of hepatic fibrogenesis (PRO-C3). / Torp, Nikolaj; Israelsen, Mads; Nielsen, Mette J.; Åstrand, Claus P.; Juhl, Pernille; Johansen, Stine; Hansen, Camilla D.; Madsen, Bjørn; Villesen, Ida F.; Leeming, Diana J.; Thiele, Maja; Hansen, Torben; Karsdal, Morten; Krag, Aleksander.
In: Liver International, Vol. 42, No. 1, 2022, p. 92-101.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Binge drinking induces an acute burst of markers of hepatic fibrogenesis (PRO-C3)
AU - Torp, Nikolaj
AU - Israelsen, Mads
AU - Nielsen, Mette J.
AU - Åstrand, Claus P.
AU - Juhl, Pernille
AU - Johansen, Stine
AU - Hansen, Camilla D.
AU - Madsen, Bjørn
AU - Villesen, Ida F.
AU - Leeming, Diana J.
AU - Thiele, Maja
AU - Hansen, Torben
AU - Karsdal, Morten
AU - Krag, Aleksander
N1 - Publisher Copyright: © 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
PY - 2022
Y1 - 2022
N2 - Background & Aims: Binge drinking is associated with an increased risk of liver disease. Morbidity and mortality of alcohol-related liver disease (ALD) is associated with collagen deposition in the hepatic extracellular matrix (ECM). However, the acute effects of binge drinking on ECM turnover are unknown. We aimed to investigate the effects on hepatic ECM turnover following a binge drinking episode. Methods: We performed a pathophysiological intervention study with 15 non-alcoholic fatty liver disease (NAFLD) patients, 15 ALD patients and 10 healthy controls. We used 40% ethanol in 9 mg/mL NaCl administered through a nasogastric tube to simulate binge drinking. Hepatic vein catheterisation allowed simultaneous hepatic- and systemic vein sampling. Markers of ECM formation and degradation were measured with competitive ELISA. Results: The interstitial matrix formation marker PRO-C3 increased by 1.2 ng/mL (10%, P <.001) 24 hours after binge drinking. In participants with existing liver fibrosis determined by elevated baseline PRO-C3, hepatic levels increased by 0.09 ng/mL (95% CI: 0.03-0.15, P =.005) while systemic PRO-C3 decreased 0.11 ng/mL (95% CI: −0.15 to −0.06, P <.001) in 3 hours. PRO-C8 increased by 30% (+0.9 ng/mL, P =.014) in liver-diseased patients with F0-F1 but not in any other group. Twenty-four-hour changes in systemic C3M and PRO-C3 were not associated (P =.911). Conclusions: Binge drinking induced an acute burst of PRO-C3 in healthy individuals and patients with liver disease. Markers of ECM degradation were not correlated to markers of ECM formation, suggesting that even a single episode of binge drinking promotes excessive hepatic fibrogenesis.
AB - Background & Aims: Binge drinking is associated with an increased risk of liver disease. Morbidity and mortality of alcohol-related liver disease (ALD) is associated with collagen deposition in the hepatic extracellular matrix (ECM). However, the acute effects of binge drinking on ECM turnover are unknown. We aimed to investigate the effects on hepatic ECM turnover following a binge drinking episode. Methods: We performed a pathophysiological intervention study with 15 non-alcoholic fatty liver disease (NAFLD) patients, 15 ALD patients and 10 healthy controls. We used 40% ethanol in 9 mg/mL NaCl administered through a nasogastric tube to simulate binge drinking. Hepatic vein catheterisation allowed simultaneous hepatic- and systemic vein sampling. Markers of ECM formation and degradation were measured with competitive ELISA. Results: The interstitial matrix formation marker PRO-C3 increased by 1.2 ng/mL (10%, P <.001) 24 hours after binge drinking. In participants with existing liver fibrosis determined by elevated baseline PRO-C3, hepatic levels increased by 0.09 ng/mL (95% CI: 0.03-0.15, P =.005) while systemic PRO-C3 decreased 0.11 ng/mL (95% CI: −0.15 to −0.06, P <.001) in 3 hours. PRO-C8 increased by 30% (+0.9 ng/mL, P =.014) in liver-diseased patients with F0-F1 but not in any other group. Twenty-four-hour changes in systemic C3M and PRO-C3 were not associated (P =.911). Conclusions: Binge drinking induced an acute burst of PRO-C3 in healthy individuals and patients with liver disease. Markers of ECM degradation were not correlated to markers of ECM formation, suggesting that even a single episode of binge drinking promotes excessive hepatic fibrogenesis.
KW - acute intoxication
KW - biomarker
KW - cirrhosis
KW - extracellular matrix
KW - fibrosis
U2 - 10.1111/liv.15120
DO - 10.1111/liv.15120
M3 - Journal article
C2 - 34845832
AN - SCOPUS:85120905858
VL - 42
SP - 92
EP - 101
JO - Liver International
JF - Liver International
SN - 1478-3223
IS - 1
ER -
ID: 287115984