Lien Van Landeghem
Katholieke Universiteit Leuven
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Featured researches published by Lien Van Landeghem.
Liver International | 2005
Wim Laleman; Lien Van Landeghem; Alexander Wilmer; Johan Fevery; Frederik Nevens
Abstract: Portal hypertension (PHT) is responsible for the more severe and often lethal complications of cirrhosis such as bleeding oesophageal varices, ascites, renal dysfunction and hepatic encephalopathy. Because of the combined impact of these complications, PHT remains the most important cause of morbidity and mortality in patients with cirrhosis. Over the years, it has become clear that a decrease in portal pressure is not only protective against the risk of variceal (re)bleeding but is also associated with a lower long‐term risk of developing complications and an improved long‐term survival. A milestone in therapy was the introduction of non‐selective β‐blockers for the prevention of bleeding and rebleeding of gastro‐esophageal varices. However, in practice, less than half the patients under β‐blockade are protected from these risks, supporting the overall demand for innovation and expansion of our therapeutic armamentarium. Recent advances in the knowledge of the pathophysiology of cirrhotic PHT have directed future therapy towards the increased intrahepatic vascular resistance, which, in part, is determined by an increased hepatic vascular tone. This increased vasculogenic component provides the rationale for the potential use of therapies aimed at increasing intrahepatic vasorelaxing capacity via gene therapy, liver‐selective nitric oxide donors and statines on the one hand, and at antagonizing excessive intrahepatic vasoconstrictor force through the use of endothelin antagonists, angiotensin blockers, α1 adrenergic antagonists or combined α1‐ and non‐selective β‐blockers or somatostatin analogues on the other. The focus of this review is to give an update on the pathophysiology of PHT in order to elucidate these potential novel strategies subsequently.
Hepatology | 2005
Wim Laleman; Anita K. Omasta; Marc Van de Casteele; Marcel Zeegers; Ingrid Vander Elst; Lien Van Landeghem; Tamara Severi; Jos van Pelt; Tania Roskams; Johan Fevery; Frederik Nevens
Reduced intrahepatic endothelial nitric oxide synthase (eNOS) activity contributes to the pathogenesis of portal hypertension (PHT) associated with cirrhosis. We evaluated whether asymmetric dimethylarginine (ADMA), a putative endogenous NOS inhibitor, may be involved in PHT associated with cirrhosis. Two rat models of cirrhosis (thioacetamide [TAA]‐induced and bile duct excision [BDE]‐induced, n = 10 each), one rat model of PHT without cirrhosis (partial portal vein–ligated [PPVL], n = 10), and sham‐operated control rats (n = 10) were studied. We assessed hepatic NOS activity, eNOS protein expression, plasma ADMA levels, and intrahepatic endothelial function. To evaluate intrahepatic endothelial function, concentration–effect curves of acetylcholine were determined in situ in perfused normal rat livers and livers of rats with TAA‐ or BDE‐induced cirrhosis (n = 10) that had been preincubated with either vehicle or ADMA; in addition, measurements of nitrite/nitrate (NOx) and ADMA were made in perfusates. Both models of cirrhosis exhibited decreased hepatic NOS activity. In rats with TAA‐induced cirrhosis, this decrease was associated with reduced hepatic eNOS protein levels and immunoreactivity. Rats with BDE‐induced cirrhosis had eNOS protein levels comparable to those in control rats but exhibited significantly higher plasma ADMA levels than those in all other groups. In normal perfused liver, ADMA induced impaired endothelium‐dependent vasorelaxation and reduced NOx perfusate levels, phenomena that were mimicked by NG‐nitro‐L‐arginine‐methyl ester. In contrast to perfused livers with cirrhosis induced by TAA, impaired endothelial cell‐mediated relaxation in perfused livers with cirrhosis induced by BDE was exacerbated by ADMA and was associated with a decreased rate of removal of ADMA (34.3% ± 6.0% vs. 70.9% ± 3.2%). In conclusion, in rats with TAA‐induced cirrhosis, decreased eNOS enzyme levels seem to be responsible for impaired NOS activity; in rats with biliary cirrhosis, an endogenous NOS inhibitor, ADMA, may mediate decreased NOS activity. (HEPATOLOGY 2005;42:1382–1390.)
Liver International | 2009
Lien Van Landeghem; Wim Laleman; Ingrid Vander Elst; Marcel Zeegers; Jos van Pelt; David Cassiman; Frederik Nevens
Background/Objective: Carbon monoxide (CO) produced by haem‐oxygenase isoforms (HO‐1 & HO‐2) is involved in the regulation of systemic vascular tone. We aimed to elucidate the vasoregulatory role of CO in the microcirculation in normal and thioacetamide cirrhotic rat livers.
American Journal of Physiology-gastrointestinal and Liver Physiology | 2007
Wim Laleman; Lien Van Landeghem; Tamara Severi; Ingrid Vander Elst; Marcel Zeegers; Raf Bisschops; Jos van Pelt; Tania Roskams; David Cassiman; Johan Fevery; Frederik Nevens
Gastroenterology | 2007
Wim Laleman; Lien Van Landeghem; Ingrid Vander Elst; Marcel Zeegers; Johan Fevery; Frederik Nevens
Journal of Hepatology | 2005
Wim Laleman; Tamara Severi; Lien Van Landeghem; I. Vander Elst; Tania Roskams; Johan Fevery; Frederik Nevens
Hepatology | 2008
Jonel Trebicka; Martin Hennenberg; Andrea Schulze Proebsting; Frank Lammert; Wim Laleman; Lien Van Landeghem; Frederik Nevens; Joerg Heller; Tilman Sauerbruch
Hepatology | 2008
Lien Van Landeghem; Wim Laleman; Ingrid Vander Elst; Joseph Van Pelt; David Cassiman; Frederik Nevens
Hepatology | 2007
Lien Van Landeghem; Wim Laleman; Marcel Zeegers; Ingrid Vander Elst; Jos van Pelt; David Cassiman; Frederik Nevens
Hepatology | 2006
Wim Laleman; Lien Van Landeghem; Tamara Severi; Ingrid Vander Elst; Marcel Zeegers; Johan Fevery; Frederik Nevens