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Noninvasive evaluation of portal hypertension: emerging tools and techniques.

Snowdon VK, Guha N, Fallowfield JA - Int J Hepatol (2012)

Bottom Line: However, evaluating the development and progression of portal hypertension represents a challenge for clinicians.The pathogenesis of portal hypertension is increasingly understood and emerging knowledge of the vascular processes that underpin portal hypertension has paved the way for exploring novel biomarkers of vascular injury, angiogenesis, and endothelial dysfunction.In this paper we focus on the pathogenesis of portal hypertension and potential non-invasive biomarkers with particular emphasis on serum analytes.

View Article: PubMed Central - PubMed

Affiliation: MRC/Centre for Inflammation Research, QMRI, University of Edinburgh, Edinburgh EH16 4TJ, UK.

ABSTRACT
Portal hypertension is the main cause of complications in patients with cirrhosis. However, evaluating the development and progression of portal hypertension represents a challenge for clinicians. There has been considerable focus on the potential role of noninvasive markers of portal hypertension that could be used to stratify patients with respect to the stage of portal hypertension and to monitor disease progression or treatment response in a longitudinal manner without having to undertake repeated invasive assessment. The pathogenesis of portal hypertension is increasingly understood and emerging knowledge of the vascular processes that underpin portal hypertension has paved the way for exploring novel biomarkers of vascular injury, angiogenesis, and endothelial dysfunction. In this paper we focus on the pathogenesis of portal hypertension and potential non-invasive biomarkers with particular emphasis on serum analytes.

No MeSH data available.


Related in: MedlinePlus

Schematic representation of the pathophysiology of portal hypertension with corresponding potential noninvasive markers. TE: transient elastography; MRI(E): magnetic resonance imaging (elastography); US: ultrasound; CECs: circulating endothelial cells; ADMA: asymmetric dimethylarginine; vWF: von Willebrand factor; ET-1: endothelin-1; MELD: Model for End-Stage Liver Disease.
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fig2: Schematic representation of the pathophysiology of portal hypertension with corresponding potential noninvasive markers. TE: transient elastography; MRI(E): magnetic resonance imaging (elastography); US: ultrasound; CECs: circulating endothelial cells; ADMA: asymmetric dimethylarginine; vWF: von Willebrand factor; ET-1: endothelin-1; MELD: Model for End-Stage Liver Disease.

Mentions: In cirrhosis, PHT is initiated by an increase in intrahepatic vascular resistance (IHVR) and then exacerbated by changes in the systemic and splanchnic circulation that increase the portal inflow. Increased IHVR is caused not only by mechanical factors (e.g., fibrotic scars and regenerative nodules that distort the hepatic vascular architecture), but also by a reversible dynamic component mediated by an increase in vascular tone due to the active contraction of myofibroblasts around the hepatic sinusoids and in fibrous septa (Figure 2). This dynamic component (which accounts for ~30% of increased IHVR) reflects a functional disturbance of the liver circulation, secondary to increased production of vasoconstrictors (e.g., endothelin-1) and reduced release of endogenous vasodilators (mainly nitric oxide, NO) [6–9]. Decreased expression of endothelial NO synthase (eNOS) protein, decreased phosphorylation of eNOS by the serine-threonine kinase AKT, the presence of inhibitory substances (e.g., asymmetric dimethylarginine, ADMA), and hyporesponsiveness to NO underlie this endothelial dysfunction [10–12]. In contrast, extrahepatic endothelial cells have the opposite phenotype producing excessive NO which contributes to increased portal blood flow and an increase in PHT.


Noninvasive evaluation of portal hypertension: emerging tools and techniques.

Snowdon VK, Guha N, Fallowfield JA - Int J Hepatol (2012)

Schematic representation of the pathophysiology of portal hypertension with corresponding potential noninvasive markers. TE: transient elastography; MRI(E): magnetic resonance imaging (elastography); US: ultrasound; CECs: circulating endothelial cells; ADMA: asymmetric dimethylarginine; vWF: von Willebrand factor; ET-1: endothelin-1; MELD: Model for End-Stage Liver Disease.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3376538&req=5

fig2: Schematic representation of the pathophysiology of portal hypertension with corresponding potential noninvasive markers. TE: transient elastography; MRI(E): magnetic resonance imaging (elastography); US: ultrasound; CECs: circulating endothelial cells; ADMA: asymmetric dimethylarginine; vWF: von Willebrand factor; ET-1: endothelin-1; MELD: Model for End-Stage Liver Disease.
Mentions: In cirrhosis, PHT is initiated by an increase in intrahepatic vascular resistance (IHVR) and then exacerbated by changes in the systemic and splanchnic circulation that increase the portal inflow. Increased IHVR is caused not only by mechanical factors (e.g., fibrotic scars and regenerative nodules that distort the hepatic vascular architecture), but also by a reversible dynamic component mediated by an increase in vascular tone due to the active contraction of myofibroblasts around the hepatic sinusoids and in fibrous septa (Figure 2). This dynamic component (which accounts for ~30% of increased IHVR) reflects a functional disturbance of the liver circulation, secondary to increased production of vasoconstrictors (e.g., endothelin-1) and reduced release of endogenous vasodilators (mainly nitric oxide, NO) [6–9]. Decreased expression of endothelial NO synthase (eNOS) protein, decreased phosphorylation of eNOS by the serine-threonine kinase AKT, the presence of inhibitory substances (e.g., asymmetric dimethylarginine, ADMA), and hyporesponsiveness to NO underlie this endothelial dysfunction [10–12]. In contrast, extrahepatic endothelial cells have the opposite phenotype producing excessive NO which contributes to increased portal blood flow and an increase in PHT.

Bottom Line: However, evaluating the development and progression of portal hypertension represents a challenge for clinicians.The pathogenesis of portal hypertension is increasingly understood and emerging knowledge of the vascular processes that underpin portal hypertension has paved the way for exploring novel biomarkers of vascular injury, angiogenesis, and endothelial dysfunction.In this paper we focus on the pathogenesis of portal hypertension and potential non-invasive biomarkers with particular emphasis on serum analytes.

View Article: PubMed Central - PubMed

Affiliation: MRC/Centre for Inflammation Research, QMRI, University of Edinburgh, Edinburgh EH16 4TJ, UK.

ABSTRACT
Portal hypertension is the main cause of complications in patients with cirrhosis. However, evaluating the development and progression of portal hypertension represents a challenge for clinicians. There has been considerable focus on the potential role of noninvasive markers of portal hypertension that could be used to stratify patients with respect to the stage of portal hypertension and to monitor disease progression or treatment response in a longitudinal manner without having to undertake repeated invasive assessment. The pathogenesis of portal hypertension is increasingly understood and emerging knowledge of the vascular processes that underpin portal hypertension has paved the way for exploring novel biomarkers of vascular injury, angiogenesis, and endothelial dysfunction. In this paper we focus on the pathogenesis of portal hypertension and potential non-invasive biomarkers with particular emphasis on serum analytes.

No MeSH data available.


Related in: MedlinePlus