Portal Pressure, Presence of Gastroesophageal Varices and Variceal Bleeding

García–Tsao, Guadalupe; Groszmann, J M D Roberto; Fisher, Ronald P.; Conn, Harold O.; Atterbury, Colin E.; Glickman, Morton G.

doi:10.1002/hep.1840050313

Cited by 848 publications

(387 citation statements)

References 15 publications

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“…The normal HVPG is 3-5 mmHg. The HVPG and changes in HVPG that occur over time have predictive value for the development of esophagogastric varices, 15,16 the risk of variceal hemorrhage, [17][18][19] the development of non-variceal complications of portal hypertension, 17,20,21 and death. 19,[21][22][23] Single measurements are useful in the prognosis of both compensated and decompensated cirrhosis, while repeat measurements are useful to monitor response to pharmacological therapy and progression of liver disease.…”

Section: Evaluation Of Portal Hypertensionmentioning

confidence: 99%

“…Patients with cirrhosis and gastroesophageal varices have an HVPG of at least 10-12 mm Hg. 15,24 Gastroesophageal varices are present in approximately 50% of patients with cirrhosis. Their presence correlates with the severity of liver disease (Table 2); while only 40% of Child A patients have varices, they are present in 85% of Child C patients.…”

Section: Natural History Of Varicesmentioning

confidence: 99%

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Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis

et al. 2007

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Section: Evaluation Of Portal Hypertensionmentioning

confidence: 99%

Section: Natural History Of Varicesmentioning

confidence: 99%

Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis

et al. 2007

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“…Actually, it has been shown to correlate with survival, decompensation, and development of collaterals. 15,16 These considerations suggest that HVPG could be used as a quantitative marker of disease progression in patients with chronic hepatitis C. 17 This would be particularly relevant in liver transplant recipients with HCV infection recurrence.…”

Section: Hronic Hepatitis C Virus (Hcv) Infection Leadingmentioning

confidence: 99%

Hepatic venous pressure gradient identifies patients at risk of severe hepatitis C recurrence after liver transplantation

et al. 2006

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Liver biopsy is essential in the follow-up of HCV-infected liver transplant recipients. The aim of this study was to prospectively compare percutaneous (PLB) versus transjugular liver biopsy (TLB) in the assessment of liver damage. We also explored the diagnostic value of hepatic venous pressure gradient (HVPG) to identify patients at risk of severe HCV disease recurrence after liver transplantation (LT). One hundred sixteen paired PLB and TLB (with HVPG measurement) were performed 3 or 12 months after LT in 80 patients. Concordance for necroinflammation and fibrosis was fair or good, particularly 1 year after LT (kappa > 0.6). At this point, a significant positive association was seen between the median HVPG and the fibrosis stage C hronic hepatitis C virus (HCV) infection leading to liver cirrhosis and hepatocellular carcinoma is the main indication for liver transplantation (LT) in Western countries and Japan. 1 Regretfully, recurrence of HCV infection is universal after LT, 2 and disease progression is significantly faster in immunosuppressed than in immunocompetent individuals. In liver transplant recipients, chronic HCV infection may lead to cirrhosis in as much as 30% of individuals only 5 years after LT. [3][4][5] Once liver cirrhosis is established, the cumulative probability of developing clinical decompensation is close to 50% 1 year after diagnosis and, more importantly, survival after decompensation is extremely short. 6 As a result of this accelerated course of HCV infection, longterm graft and patient survival are significantly reduced in patients undergoing LT for HCV-related cirrhosis compared with other groups. 7 Frequent liver biopsies are essential to monitor HCV-induced liver damage and are part of the routine follow-up of HCV-infected liver transplant recipients. Early histological damage after transplantation correlates with long-term outcome; in fact, the presence of significant liver fibrosis in 1-year liver biopsies identifies patients at high risk of graft loss. 3,8 In addition, assessment of liver damage is relevant to adopt therapeutic decisions, particularly because of the low efficacy and high incidence of adverse events of current antiviral therapy in this group of patients. 3,9,10

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“…9 Cirrhosis of liver leads to portal hypertension and the development of portal-systemic collaterals. 10 The increased hepatic and collateral resistances to an increased portal blood flow maintain portal hypertension. 11 Recently, a possible role of endothelins in the pathophysiology of portal hypertension has been suggested.…”

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confidence: 99%

Endothelin–1 Induces Vasoconstriction on Portal–Systemic Collaterals of Portal Hypertensive Rats

et al. 2001

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Cirrhosis of liver leads to portal hypertension and the development of portal-systemic collaterals. 10 The increased hepatic and collateral resistances to an increased portal blood flow maintain portal hypertension. 11 Recently, a possible role of endothelins in the pathophysiology of portal hypertension has been suggested. ET-1 was found to induce hepatic vasoconstriction and subsequently increase portal venous resistance. 4,12 In addition, ET-1 could stimulate contraction of hepatic stellate cells to increase intrahepatic resistance. 13 In vitro experiments also showed that ET-1 produced contraction of rat portal vein. 14 Furthermore, the mesenteric expressions of ET A and ET B receptors and ET-1-induced vasoconstriction were significantly enhanced in partially portal veinligated (PVL) rats. 5 Recently, it has been shown that bosentan, a nonselective endothelin receptor antagonist, significantly reduced the portal pressure of portal hypertensive rats. 15 However, it is not clear if ET-1 could modulate portal pressure by a direct constrictive effect on the collateral vessels of portal hypertensive rats.The aims of this study were to investigate the vascular activity and the receptor-mediated effects of ET-1 on the portalsystemic collaterals of portal hypertensive rats. The regulation of nitric oxide (NO) and prostaglandin on the effects of ET-1 was also evaluated. MATERIALS AND METHODSMale Sprague-Dawley rats weighing 280 to 300 g at the time of surgery were used for experiments. The rats were housed in a plastic cage and allowed free access to food and water. All rats were fasted for 12 hours before operation. In all experiments, the investigators adhered to the American Physiological Society Guiding Principles for the Care and Use of Laboratory Animals.A prehepatic portal hypertensive animal model was created as previously reported. 16 Anesthesia was performed with ketamine HCl (100 mg/kg body weight, intramuscularly). In brief, the portal vein was isolated and a 3-0 silk ligature was tied around both the portal vein and an adjacent 20-gauge blunt-tipped needle. The needle was then removed and the vein allowed to reexpand. A second loose ligature was left around the portal vein with 2 endings of the ligature placed on each side in the abdominal cavity. The abdomen was then closed and the animal was allowed to recover. Perfusion studies were performed in overnight-fasted rats 10 to 13 days after the operation, at which time an extensive collateralization of the portal system was fully established. 17 The body weights of rats were measured on the day of perfusion studies.Abbreviations: ET-1, endothelin-1; PVL, portal vein-ligated; NO, nitric oxide; NNA, n -nitro-L-arginine; INDO, indomethacin.From the Divisions of

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Portal Pressure, Presence of Gastroesophageal Varices and Variceal Bleeding

Cited by 848 publications

References 15 publications

Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis

Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis

Hepatic venous pressure gradient identifies patients at risk of severe hepatitis C recurrence after liver transplantation

Endothelin–1 Induces Vasoconstriction on Portal–Systemic Collaterals of Portal Hypertensive Rats

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