Portal Hypertension and Related Complications: Diagnosis and Management

Simonetto, Douglas A.; Liu, Mengfei; Kamath, Patrick S.

doi:10.1016/j.mayocp.2018.12.020

Cited by 163 publications

(118 citation statements)

References 83 publications

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“…Portal hypertension is defined by a hepatic venous pressure gradient of 6 mmHg or more, and in the clinical scenario of cirrhosis, it is characterized by complications, such as ascites, variceal bleeding, and hepatic encephalopathy in advanced cases . In cirrhosis, portal hypertension results from the increased collagen deposition and formation of regenerative nodules, which eventually lead to an increase in portal pressure . These changes are followed by compensatory splanchnic vasodilation, which will further increase portal flow and continue to worsen portal pressure (as predicted by Ohm’s law).…”

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confidence: 99%

Clinical Outcomes of Portosystemic Shunts on the Outcome of Liver Transplantation

et al. 2020

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Spontaneous portosystemic shunts (SPSSs) have been associated with worse clinical outcomes in the pre-liver transplantation (LT) setting, but little is known about their post-LT impacts. Our aim was to compare LT candidates with and withoutSPSSs and assess the impact of SPSSs on patient mortality and graft survival in the post-LT setting. Patients 18 years or older with abdominal imaging done prior to LT were included. Exclusion criteria were the presence of pre-LT surgical shunts, LT indications other than cirrhosis, and combined solid organ transplantations. SPSSs were classified as absent, small, or large according to their maximum diameter (8 mm). Multiple variables that could influence the post-LT course were extracted for analysis. Patient and graft survival were estimated using the Kaplan-Meier method and were compared between groups using a log-rank test. The project received institutional review board approval. We extracted data from 326 patients. After comparing patients without SPSS or with small or large SPSSs, no statistical difference was found for overall patient survival: no SPSS (n = 8/63), reference; small SPSS (n = 18/150), hazard ratio (HR), 1.05 (95% confidence interval [CI], 0.45-2.46); and large SPSS (n = 6/113), HR, 0.60 (95% CI, 0.20-1.78); P = 0.20. Also, no difference was found for graft survival: no SPSS (n = 11/63), reference; small SPSS (n = 21/150), HR, 0.80 (95% CI, 0.38-1.70); large SPSS (n = 11/113), HR, 0.59 (95% CI, 0.25-1.40); P = 0.48. Similarly, no statistical significance was found for these variables when comparing if the graft used was procured from a donation after circulatory death donor versus a donation after brain death donor. In conclusion, the previously described association between SPSSs and worse clinical outcomes in pre-LT patients seems not to persist once patients undergo LT. This study suggests that no steps to correct SPSS intraoperatively are necessary. Liver Transplantation 26 693-701 2020 AASLD.Portal hypertension is defined by a hepatic venous pressure gradient of 6 mmHg or more, and in the clinical scenario of cirrhosis, it is characterized by complications, such as ascites, variceal bleeding, and hepatic encephalopathy in advanced cases. (1) In cirrhosis, portal hypertension results from the increased collagen deposition and formation of regenerative nodules, which eventually lead to an increase in portal pressure. (2) These changes are followed by compensatory splanchnic vasodilation, which will further increase portal flow and continue to worsen portal pressure (as predicted by Ohm's law). The presence of these complications leads to clinical deterioration, with some series describing up to 80% 5-year mortality if 2 complications were present concomitantly, (3) which also results in cost increases due to frequent hospital admissions. (4) A complication in the setting of portal hypertension is the formation of spontaneous portosystemic shunts (SPSSs). These are channels that form as the portal rOdriguez et al.

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confidence: 99%

Clinical Outcomes of Portosystemic Shunts on the Outcome of Liver Transplantation

et al. 2020

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“…5 Gastroesophageal varices, variceal hemorrhage, ascites, hepatic encephalopathy, and hepatorenal syndrome are common and direct consequences of clinically significant portal hypertension, which lead to significant morbidity and mortality. 6,7 The increased intrahepatic resistance in cirrhosis and changes in perisinusoidal space are mediated by the transdifferentiation of…”

Section: Introductionmentioning

confidence: 99%

Endothelin-1 in portal hypertension: The intricate role of hepatic stellate cells

Ezhilarasan

2020

Exp Biol Med (Maywood)

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Portal hypertension is one of the most important cirrhosis-associated complications of chronic liver disease, leading to significant morbidity and mortality. After chronic liver injury, hepatic stellate cells reside in the perisinusoidal space activted and acquire a myofibroblast-like phenotype. The activated hepatic stellate cells act as both sources as well as the target for a potent vasoconstrictor endothelin-1. Activation of hepatic stellate cells plays a vital role in the onset of cirrhosis by way of increased extracellular matrix production and the enhanced contractile response to vasoactive mediators such as endothelin-1. In fibrotic/cirrhotic liver, activated hepatic stellate cells produce endothelin-1 leading to an imbalance between pro and antifibrotic factors responsible for enormous extracellular matrix synthesis. Thus, extracellular matrix deposition in the perisinusoidal space further augments liver stiffness and elevates the vascular tone and portal hypertension. Portal hypertension is a complex process modulated by several cell types like hepatic stellate cells, liver sinusoidal endothelial cells, Kupffer cells, injured hepatocytes, immune cells, and biliary epithelial cells. Therefore, targeting a single cell type may not be useful for regression of cirrhosis and portal hypertension. Nevertheless, numerous findings indicate that functionally liver sinusoidal endothelial cells and hepatic stellate cells closely regulate the sinusoidal blood flow via synthesis of several vasoactive molecules including endothelin-1, and hence targeting these cells with novel pharmacological agents may offer promising results. Impact statement Portal hypertension is pathologically defined as increase of portal venous pressure, mainly due to chronic liver diseases such as fibrosis and cirrhosis. In fibrotic liver, activated hepatic stellate cells increase their contraction in response to endothelin-1 (ET-1) via autocrine and paracrine stimulation from liver sinusoidal endothelial cells and injured hepatocytes. Clinical studies are limited with ET receptor antagonists in cirrhotic patients with portal hypertension. Hence, studies are needed to find molecules that block ET-1 synthesis. Accumulation of extracellular matrix proteins in the perisinusoidal space, tissue contraction, and alteration in blood flow are prominent during portal hypertension. Therefore, novel matrix modulators should be tested experimentally as well as in clinical studies. Specifically, tumor necrosis factor-α, transforming growth factor-β1, Wnt, Notch, rho-associated protein kinase 1 signaling antagonists, and peroxisome proliferator-activated receptor α and γ, interferon-γ and sirtuin 1 agonists should be tested elaborately against cirrhosis patients with portal hypertension.

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“…When cirrhosis is diagnosed, varices are present in about 30%-40% of compensated patients and 60% present with ascites. [7][8] Stigmann et al first introduced the technique of endoscopic band legation. This mechanical method of obliterating variceal with elastic O-ring https://doi.org/10.29309/TPMJ/2020.27.…”

Section: Introductionmentioning

confidence: 99%

Variceal band ligation and its outcome: A single tertiary care centre study.

Anjum

Gul²,

Rasool

et al. 2020

TPMJ

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Objectives: To determine the frequency of complications after esophageal variceal band ligation in patients of decompensated chronic liver disease. Study Design: Descriptive Case study Setting: Department of Gastroenterology Lahore General Hospital, Lahore. Period: June 2015 to June 2016. Material & Methods: In the present study, the cases of both genders and age more than 20 years having esophageal variceal of any grade on variceal screening esophagogastroduodenoscopy and duration of decompensated liver cirrhosis of at least 6 months or more were included. Esophageal variceal band ligation was performed using a multiband ligation device (Six-shooter, Wilson-Cook Inc., Winston-Salem, NC) and up to 6 bands were placed per session and next session was performed at 2 week intervals until esophageal varices were eradicated, which was defined as a complete disappearance of varices and/or the presence of a varix being too small to be ligated. All patients were followed every month regarding complications in terms of ulcer bleed and esophageal strictures. Results: In this study there were total 720 cases out of which 450 (62.5%) were males and 270 (37.5%) females. The mean age of the subjects was 33.504±4.00 years, mean duration of cirrhosis was 9.086±2.54 months and mean weight was 72.44±13.78Kg. Ulcer bleed was seen in 6.9% patients and esophageal strictures was seen in 2.5% patients. Conclusion: Complications of esophageal variceal band ligation are not that common and amongst them ulcer bleed is the salient one. Both ulcer bleed and esophageal stricture are significantly associated with varices more than 2.

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Portal Hypertension and Related Complications: Diagnosis and Management

Cited by 163 publications

References 83 publications

Clinical Outcomes of Portosystemic Shunts on the Outcome of Liver Transplantation

Clinical Outcomes of Portosystemic Shunts on the Outcome of Liver Transplantation

Endothelin-1 in portal hypertension: The intricate role of hepatic stellate cells

Variceal band ligation and its outcome: A single tertiary care centre study.

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