Portal Angiogenesis in Chronic Liver Disease Patients Correlates with Portal Pressure and Collateral Formation

2019 ◽  
Vol 37 (6) ◽  
pp. 498-508 ◽  
Author(s):  
Carolina A. Serrano ◽  
Simon C. Ling ◽  
Sofia Verdaguer ◽  
Miguel León ◽  
Nicolás Jarufe ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Peripheral Circulation ◽  
Chronic Liver ◽  
Noninvasive Markers ◽  
Collateral Formation

Background/Aims: One hallmark of chronic liver disease in patients with portal hypertension is the formation of portal-systemic collaterals in which angiogenesis has a fundamental role. We studied patients with chronic liver disease undergoing liver transplantation to correlate levels of circulating angiogenic factors in portal and peripheral circulation with portal pressure and portal-systemic collaterals. Methods: Sixteen patients who underwent liver transplantation were enrolled. During transplant surgery, we determined portal venous pressure and portal-systemic collateral formation. We determined angiogenics mediator levels in systemic and portal plasma. Peripheral plasma from healthy donors was measured as controls. Results: Vascular endothelial growth factor (VEGF)-R1 and 2, Ang-1 and 2, Tie2, FGF- 1 and 2, CD163, PDGFR-β, PDGFsRα, PDGF-AB and BB, CD163, TGF-β VASH-1 levels were significantly different in the controls in comparison to cases. Significantly decreased portal venous levels of Ang-1, FGF-1, PDGF-AB/BB, and CC were observed in patients with higher portal pressure. Peripheral VEGF, Ang-1, pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation. While peripheral VEGF-R1 was higher in patients with severe collateral formation. For portal circulation, VEGF, Ang-1, ­pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation Conclusions: Angiogenesis factors correlated with portal pressure and collateral formation and different patterns of circulating angiogenesis mediators were found in peripheral and portal blood of patients with chronic liver disease. These results support the importance of angiogenic pathways in cirrhosis and portal hypertension and highlight areas for further study to identify clinically useful noninvasive markers of portal pressure and collateral formation.

scholarly journals Thromboelastometry in patients with advanced chronic liver disease stratified by severity of portal hypertension

2020 ◽  
Author(s):  
Pierre Raeven ◽  
Joanna Baron-Stefaniak ◽  
Benedikt Simbrunner ◽  
Alexander Stadlmann ◽  
Philipp Schwabl ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Cross Sectional Study ◽  
Chronic Liver ◽  
Cross Sectional ◽  
Reactive Protein ◽  
The Impact

Abstract Background Rotational thromboelastometry (ROTEM) has been studied in patients with advanced chronic liver disease (ACLD) without considering the impact of portal hypertension. We evaluated the influence of the hepatic venous pressure gradient (HVPG) on ROTEM results in patients with ACLD. Methods Cross-sectional study; ACLD patients undergoing HVPG measurement within the prospective Vienna Cirrhosis Study (NCT03267615) underwent concomitant ROTEM testing. Results Among 159 patients (68% male; Child–Pugh-A: 53%, Child–Pugh-B: 34%, Child–Pugh-C: 13%), 21 patients (13%) had a HVPG between 6 and 10 mmHg, 84 patients (53%) between 10 and 19 mmHg, and 54 patients (34%) ≥ 20 mmHg. Child–Pugh-C patients (vs. Child–Pugh-A and vs. Child–Pugh-B patients, respectively) showed longer clot formation time (CFT: median 187 s vs. 122 s vs. 122 s, p = 0.007) and lower maximum clot firmness (MCF: median: 45 mm vs. 56 mm vs. 56 mm, p = 0.002) in extrinsic thromboelastometry (EXTEM), while platelet counts were similar across Child–Pugh stages. In the overall cohort, ROTEM parameters did not differ by severity of portal hypertension. However, among compensated Child–Pugh-A patients, MCF decreased with increasing portal pressure, i.e. in higher HVPG strata (HVPG 9–10 mmHg: median MCF: 59 mm vs. HVPG 10–19 mmHg: 56 mm vs HVPG ≥ 20 mmHg: 54 mm, p = 0.023). Furthermore, patients with short CFT and high MCF in EXTEM had higher levels of lipopolysaccharide-binding protein, C-reactive protein, and procalcitonin, as well as higher leukocyte counts (all p < 0.05). Conclusions Portal hypertension seems to impact ROTEM results only in compensated Child–Pugh-A patients. Bacterial translocation and systemic inflammation may trigger a procoagulant state in patients with ACLD.

Measurement of Portal Pressure and its Application in the Clinical Setting

2017 ◽  
Vol 01 (04) ◽  
pp. 241-247
Author(s):  
Anthony Esparaz ◽  
Raza Malik ◽  
Jonathan Pierce
Keyword(s):  
Hepatocellular Carcinoma ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Preoperative Evaluation ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Standard Technique ◽  
Response To Therapy ◽  
Chronic Liver

AbstractPortal hypertension is a severe, yet common sequela of patients with chronic liver disease and is responsible for many of the complications seen in this population. Measurement of the hepatic venous pressure gradient (HVPG) is the current gold standard technique for identifying and evaluating the severity of portal hypertension. Any increase in HVPG to ≥10 mm Hg is considered clinically significant portal hypertension. Above this threshold, complications of portal hypertension begin to manifest. In addition to assessing portal hypertension, various HVPG thresholds have been shown to have strong prognostic value for risk of complications and therapeutic failure, as well as survival in patients with chronic liver disease. These clinical applications include quantification of disease progression and regression in chronic viral hepatitis, acute alcoholic hepatitis, and hepatocellular carcinoma. Other applications include preoperative evaluation of liver resection and transplantation in patients with cirrhosis and hepatocellular carcinoma, assessment of response to therapy for portal hypertension, and identification of the need for transjugular intrahepatic portosystemic shunt (TIPS) revision.

scholarly journals Noninvasive Markers of Portal Hypertension Detect Decompensation in Overweight or Obese Patients With Compensated Advanced Chronic Liver Disease

2020 ◽  
Vol 18 (13) ◽  
pp. 3017-3025.e6 ◽  
Author(s):  
Yuly Mendoza ◽  
Sila Cocciolillo ◽  
Giuseppe Murgia ◽  
Tianyan Chen ◽  
Cristina Margini ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Chronic Liver ◽  
Obese Patients ◽  
Noninvasive Markers

scholarly journals Noninvasive Assessment of Portal Hypertension in Advanced Chronic Liver Disease: An Update

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Federico Ravaioli ◽  
Marco Montagnani ◽  
Andrea Lisotti ◽  
Davide Festi ◽  
Giuseppe Mazzella ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Minimally Invasive ◽  
Chronic Liver Disease ◽  
Venous Pressure ◽  
Chronic Liver ◽  
Minimally Invasive Techniques ◽  
Newly Diagnosed ◽  
Invasive Techniques ◽  
Invasive Evaluation

The assessment of portal hypertension is a relevant step in the evaluation of newly diagnosed advanced chronic liver disease (ACLD). The current gold standard includes the invasive evaluation of hepatic venous pressure gradient (HVPG) and endoscopy. However, noninvasive or minimally invasive techniques to assess portal hypertension have been proposed and well established. In the present manuscript, we review clinical studies on the use of noninvasive or minimally invasive techniques to assess portal hypertension in ACLD patients.

scholarly journals Influence of Genetic Variants on Disease Regression and Outcomes in HCV-Related Advanced Chronic Liver Disease after SVR

2021 ◽  
Vol 11 (4) ◽  
pp. 281
Author(s):  
Georg Semmler ◽  
Teresa Binter ◽  
Karin Kozbial ◽  
Philipp Schwabl ◽  
David Chromy ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Clinical Outcomes ◽  
Genetic Variants ◽  
Antiviral Treatment ◽  
Venous Pressure ◽  
Chronic Liver ◽  
Non Invasive ◽  
Pre Treatment

Genetic variants including PNPLA3-rs738409 C>G, TM6SF2-rs58542926 C>T, MBOAT7-rs641738 C>T, and HSD17B13-rs72613567 T>TA have been shown to influence progression to advanced chronic liver disease (ACLD) in patients with chronic hepatitis C (CHC). We aimed to investigate their impact on disease regression (i.e., changes in hepatic venous pressure gradient [HVPG] and non-invasive surrogates [liver stiffness measurement (LSM), von Willebrand factor (VWF), and VWF/platelet count ratio (VITRO)]) and clinical outcomes after CHC cure in 346 patients with pre-treatment ACLD. Patients carrying the PNPLA3 minor allele had more advanced liver disease prior to antiviral therapy, confirming its impact on liver disease progression. In a subgroup of 88 patients who underwent paired HVPG-measurements and were genotyped for all SNP/indels, PNPLA3/TM6SF2/MBOAT7/HSD17B13 genotypes were not associated with changes in HVPG. In line, changes in non-invasive surrogates of portal hypertension (LSM/VWF/VITRO) were comparable between carriers and non-carriers of the PNPLA3 G-allele in the overall cohort. Finally, carriage of PNPLA3 G-allele was not associated with the development of hepatic decompensation, de-novo hepatocellular carcinoma, or transplant-free mortality during a median follow-up of 42 months after the end of antiviral treatment. Therefore, genetic variants in PNPLA3/TM6SF2/MBOAT7/HSD17B13 do not impact the regression of portal hypertension and clinical outcomes in patients with pre-treatment ACLD after CHC cure.

The Natural History Of Chronic Liver Disease

2018 ◽  
Author(s):  
Esperance A K Schaefer
Keyword(s):  
Hepatocellular Carcinoma ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Natural History ◽  
Chronic Liver Disease ◽  
Venous Pressure ◽  
Chronic Liver ◽  
Medical Attention ◽  
Number Of Patients ◽  
History Of

The natural history of chronic liver disease is that of a slowly progressive course, in most cases evolving over the course of years to decades. The rate of progression varies by disease state and comorbid conditions, but fibrosis advances on average by one stage every 7 to 10 years. While the development of fibrosis is reversible when the underlying etiology is successfully treated, a large number of patients present to medical attention once advanced fibrosis has already developed. The ultimate clinical and pathological manifestation of chronic liver disease is cirrhosis. Cirrhosis has long been clinically divided into “compensated” and “decompensated” disease, with an estimated 12-year survival in compensated disease and 2-year survival in decompensated disease. Additional clinical stratifications have been proposed, including a five-stage model progressing from cirrhosis without portal hypertension (hepatic venous pressure gradient below 10 mm Hg) to cirrhosis with portal hypertension, and then cirrhosis complicated by bleeding or other decompensating events. These clinical stages correspond to a step-wise increase in mortality and, with the presence of more than one decompensating event, the five-year mortality approaches 90%. The major complications of cirrhosis include varices with or without hemorrhage, ascites, hepatic encephalopathy, immune dysfunction, renal impairment, and hepatocellular carcinoma. Liver transplantation has provided an avenue to alter the course and outcomes in chronic liver disease, with graft survival rates that reach 80% at 5 years.  This review contains 4 figures, 6 tables and 51 references Key Words: natural history, cirrhosis, mortality, hepatocellular carcinoma, acute-on-chronic liver failure

scholarly journals Results of liver and spleen endoscopic ultrasonographic elastography predict portal hypertension secondary to chronic liver disease

2020 ◽  
Vol 08 (11) ◽  
pp. E1623-E1632
Author(s):  
Carlos Robles-Medranda ◽  
Roberto Oleas ◽  
Miguel Puga-Tejada ◽  
Manuel Valero ◽  
Raquel Del Valle ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Predictive Value ◽  
Strain Ratio ◽  
Chronic Liver ◽  
Spleen Stiffness ◽  
Eus Elastography ◽  
Sensitivity Specificity

Abstract Background and study aims Assessment of endoscopic ultrasonography (EUS)-elastography of the liver and spleen may identify patients with portal hypertension secondary to chronic liver disease. We aimed to evaluate use of EUS-elastography of the liver and spleen in identification of portal hypertension in patients with chronic liver disease. Patients and methods This was a single-center, diagnostic cohort study. Consecutive patients with liver cirrhosis and portal hypertension underwent EUS-elastography of the liver and spleen. Patients without a history of liver disease were enrolled as controls. The primary outcome was diagnostic yield of liver and spleen stiffness measurement via EUS-elastography in prediction of portal hypertension secondary to chronic liver cirrhosis. Cutoff values were defined through Youden’s index. Overall accuracy was calculated for parameters with an area under the receiver operating characteristic (AUROC) curve ≥ 80 %. Results Among the 61 patients included, 32 had cirrhosis of the liver. Liver and spleen stiffness was measured by the strain ratio and strain histogram, with sensitivity/(1 − specificity) AUROC values ≥ 80 %. For identification of patients with cirrhosis and portal hypertension, the liver strain ratio (SR) had a sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of 84.3 %, 82.8 %, 84.4 %, and 82.8 %, respectively; the liver strain histogram (SH) had values of 87.5 %, 69.0 %, 75.7 %, and 83.3 %, respectively. EUS elastography of the spleen via the SR reached a sensitivity, specificity, PPV, and NPV of 87.5 %, 69.0 %, 75.7 %, and 83.3 %, respectively, whereas the values of SH were 56.3 %, 89.7 %, 85.7 %, and 65.0 %, respectively. Conclusion Endoscopic ultrasonographic elastography of the liver and spleen is useful for diagnosis of portal hypertension in patients with cirrhosis.

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