Systemic and hepatic vein galectin-3 are increased in patients with alcoholic liver cirrhosis and negatively correlate with liver function

Wanninger, Josef; Weigert, Johanna; Wiest, Reiner; Bauer, Sabrina; Karrasch, Thomas; Farkas, S.; Scherer, Marcus N.; Walter, Roland; Weiss, Thomas S.; Hellerbrand, Claus; Neumeier, Markus; Schäffler, Andréas; Buechler, Christa

doi:10.1016/j.cyto.2011.06.001

Cited by 46 publications

(44 citation statements)

References 33 publications

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“…During TIPS implantation, samples were obtained simultaneously of one of the hepatic veins (HVS) which was not drained by the TIPS-stent, of the portal vein (PVS) and of a peripheral vein such as the superior caval vein (SVS). Patient samples analyzed herein have been used in previous studies [23][24][25][26]. …”

Section: Transjugular Intrahepatic Portosystemic Shunt (Tips)mentioning

confidence: 99%

Circulating lipocalin 2 is neither related to liver steatosis in patients with non-alcoholic fatty liver disease nor to residual liver function in cirrhosis

et al. 2016

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Section: Transjugular Intrahepatic Portosystemic Shunt (Tips)mentioning

confidence: 99%

Circulating lipocalin 2 is neither related to liver steatosis in patients with non-alcoholic fatty liver disease nor to residual liver function in cirrhosis

et al. 2016

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“…Median age of the cohort was 56 (26-82) years. Part of the blood samples used has been recently described [22][23][24]26].…”

Section: Pvs Hvs and Svs Of Liver-healthy Donorsmentioning

confidence: 99%

Portal vein omentin is increased in patients with liver cirrhosis but is not associated with complications of portal hypertension

Eisinger

Krautbauer

Wiest

et al. 2013

Eur J Clin Investigation

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“…Recently, a novel plasma biomarker, the galectin-3 has been shown to mediate myocardial fibrosis and to be expressed in cirrhosis. Furthermore, galectin-3 binding protein concentrations have also been found to be increased in patients with cirrhosis [60].…”

Section: Laboratory Markersmentioning

confidence: 99%

Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

Páll¹,

Czifra²,

Vitális³

et al. 2014

JGLD

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Hyperdynamic circulation, systolic and diastolic left ventricular dysfunction and certain electrophysiological abnormalities have been associated with cirrhosis and known for a long time. These clinical features have been introduced as cirrhotic cardiomyopathy (CCM), which is characterized by blunted myocardial contractile responsiveness to physical, physiological and pharmacological stress. Importantly, cardiac dysfunction can be reversible and can improve due to effective medical treatment and also after liver transplantation. Echocardiography and electrocardiography are essential tools for recognizing the characteristic changes in the myocardial function and also the alterations in the electrophysiological properties of the heart. Laboratory markers are auxiliary modalities further aiding the establishment of the correct diagnosis. In this review, we aimed to collect the pathophysiological background and clinical characteristics of CCM with the intention of summarizing the current possibilities for the diagnosis establishment and treatment of this cardio-hepatic disorder.Abbreviations: A: late diastolic transmitral peak flow velocity; ACE: angiotensin converting enzyme; ANP: atrial natriuretic peptide; ARB: angiotensin receptor blocker; BNP: brain natriuretic peptide; cAMP: cyclic adenosine monophosphate; CCM: cirrhotic cardiomyopathy; CGRP: calcitonin gene-related peptide; CO: carbon monoxide; DD: diastolic dysfunction; DT: deceleration time; E: early diastolic transmitral peak flow velocity; Ea: early diastolic velocity of the septal mitral annulus; EF: ejection fraction; MUGA: Multi Gated Acquisition Scan; NO: nitric oxide; NSBB: non-selective beta-blocker; pro-BNP: pro-brain natriuretic peptide; QTc: corrected QT interval; RAAS: renin-angiotensin aldosterone system; RALES: Randomized Aldactone Evaluation Study; suPAR: urokinase-type plasminogen activator receptor; TDI: Tissue Doppler Imaging; TIPS: transjugular intrahepatic portosystemic shunt; TNF-alpha: tumor necrosis factor-alpha.

show abstract

Systemic and hepatic vein galectin-3 are increased in patients with alcoholic liver cirrhosis and negatively correlate with liver function

Cited by 46 publications

References 33 publications

Circulating lipocalin 2 is neither related to liver steatosis in patients with non-alcoholic fatty liver disease nor to residual liver function in cirrhosis

Circulating lipocalin 2 is neither related to liver steatosis in patients with non-alcoholic fatty liver disease nor to residual liver function in cirrhosis

Portal vein omentin is increased in patients with liver cirrhosis but is not associated with complications of portal hypertension

Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

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