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Item Does providing routine liver volume assessment add value when performing CT surveillance in cirrhotic patients?(Springer, 2019-07-29) Patel, Milan; Puangsricharoen, Pimpitcha; Arshad, Hafiz Muhammad Sharjeel; Garrison, Sam; Techasatian, Witina; Ghabril, Marwan; Sandrasegaran, Kumar; Liangpunsakul, Suthat; Tann, Mark; Medicine, School of MedicineBackground: The measurement of liver volume (LV) is considered to be an effective prognosticator for postoperative liver failure in patients undergoing hepatectomy. It is unclear whether LV can be used to predict mortality in cirrhotic patients. Methods: We enrolled 584 consecutive cirrhotic patients who underwent computerized topography (CT) of the abdomen for hepatocellular carcinoma surveillance and 50 age, gender, race, and BMI-matched controls without liver disease. Total LV (TLV), functional LV (FLV), and segmental liver volume (in cm3) were measured from CT imaging. Cirrhotic subjects were followed until death, liver transplantation, or study closure date of July 31, 2016. The survival data were assessed with log-rank statistics and independent predictors of survival were performed using Cox hazards model. Results: Cirrhotic subjects had significantly lower TLV, FLV, and segmental (all except for segments 1, 6, 7) volume when compared to controls. Subjects presenting with hepatic encephalopathy had significantly lower TLV and FLV than those without HE (p=0.002). During the median follow up of 1,145 days, 112 (19%) subjects were transplanted and 131 (23%) died. TLV and FLV for those who survived were significantly higher than those who were transplanted or dead (TLV:1740 vs 1529 vs 1486, FLV 1691 vs 1487 vs 1444,p <0.0001). In the Cox regression model, age, MELD score, TLV or FLV were independent predictors of mortality. Conclusion: Baseline liver volume is an independent predictor of mortality in subjects with cirrhosis. Therefore it may be useful to provide these data while performing routine surveillance CT scan as an important added value. Further studies are needed to validate these findings and to better understand their clinical utility.Item Liver Stiffness Measurements in Patients with Non‐cirrhotic Portal Hypertension – The Devil is In the Details(AASLD, 2018) Vuppalanchi, Raj; Mathur, Karan; Pyko, Maximillian; Samala, Niharika; Chalasani, Naga; Medicine, School of MedicineNon‐cirrhotic portal hypertension (NCPH) is often a diagnostic challenge due to signs and symptoms of portal hypertension that overlap with cirrhosis. The etiology of NCPH is broadly classified as prehepatic, hepatic (pre‐sinusoidal and sinusoidal) and post‐hepatic.1 Some common etiologies of NCPH encountered in clinical practice include portal vein thrombosis (prehepatic) and nodular regenerative hyperplasia (NRH) (hepatic).Item Prioritization of Therapeutic Targets and Trial Design in Cirrhotic Portal Hypertension(Wiley, 2019-03) Abraldes, Juan G.; Trebicka, Jonel; Chalasani, Naga; D’Amico, Gennaro; Rockey, Don C.; Shah, Vijay H.; Bosch, Jaime; Garcia-Tsao, Guadalupe; Medicine, School of MedicinePortal hypertension (PH) is the main driver of cirrhosis decompensation, the main determinant of death in patients with cirrhosis. PH results initially from increased intrahepatic vascular resistance. Subsequently, increased inflow from splanchnic vasodilation and increased cardiac output lead to a further increase in portal pressure (PP). Reducing PP in cirrhosis results in better outcomes. Removing the cause of cirrhosis might improve PP. However, this is a slow process and patients may continue to be at risk of decompensation. Additionally, for some chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD), etiological treatments are not yet available. Therefore, there is a need to develop better therapies specifically aimed at reducing PP. For over 35 years, the mainstay of such therapy has been the use of nonselective beta‐blockers (NSBBs) that act by reducing portal venous inflow. Recently, many drugs (mainly targeting intrahepatic mechanisms) have shown promise in preclinical and early clinical studies and may act alone or synergistically with NSBBs in reducing PP in cirrhosis. The objective of this position paper is to propose a novel framework for the design of clinical trials (phase 1, 2, and 3) in patients with cirrhosis and PH and to prioritize targets and pharmacological therapies in this setting. We have focused the discussion on patients with compensated cirrhosis. The paper summarizes discussions held at The American Association for the Study of Liver Diseases (AASLD) Industry Colloquium in January 2018, with the participation of clinical and translational investigators, regulatory professionals, and industry partners.Item Update in the Treatment of the Complications of Cirrhosis(Elsevier, 2023-07) Abradles, Juan G.; Caraceni, Paolo; Ghabril, Marwan; Ghabril, Marwan; Guadalupe , Garcia-Tsao; Medicine, School of MedicineCirrhosis consists of 2 main stages: compensated and decompensated, the latter defined by the development/presence of ascites, variceal hemorrhage, and hepatic encephalopathy. The survival rate is entirely different, depending on the stage. Treatment with nonselective β-blockers prevents decompensation in patients with clinically significant portal hypertension, changing the previous paradigm based on the presence of varices. In patients with acute variceal hemorrhage at high risk of failure with standard treatment (defined as those with a Child-Pugh score of 10-13 or those with a Child-Pugh score of 8-9 with active bleeding at endoscopy), a pre-emptive transjugular intrahepatic portosystemic shunt (TIPS) improves the mortality rate and has become the standard of care in many centers. In patients with bleeding from gastrofundal varices, retrograde transvenous obliteration (in those with a gastrorenal shunt) and/or variceal cyanoacrylate injection have emerged as alternatives to TIPS. In patients with ascites, emerging evidence suggests that TIPS might be used earlier, before strict criteria for refractory ascites are met. Long-term albumin use is under assessment for improving the prognosis of patients with uncomplicated ascites and confirmatory studies are ongoing. Hepatorenal syndrome is the least common cause of acute kidney injury in cirrhosis, and first-line treatment is the combination of terlipressin and albumin. Hepatic encephalopathy has a profound impact on the quality of life of patients with cirrhosis. Lactulose and rifaximin are first- and second-line treatments for hepatic encephalopathy, respectively. Newer therapies such as L-ornithine L-aspartate and albumin require further assessment.