View clinical trials related to Liver Cirrhosis.
Filter by:• Main objectives and outcome measures. 1. Establish prevalence of and factors contributing to fatty liver disease and liver fibrosis in patients with psoriasis. Fatty liver disease diagnosed via ultrasound. Liver fibrosis diagnosed by liver biopsy or non-invasive tests of fibrosis including transient elastography, ultrasound, serum markers of fibrosis including procollagen-3-N-terminal peptide (P3NP). 2. Evaluate non-invasive markers of liver fibrosis in the psoriasis population. Namely transient elastography, standard liver function tests and P3NP. 3. Evaluate the impact of psoriasis disease severity and comorbidities including metabolic syndrome on response to treatment in patients with psoriasis. Data on co-morbid disease collected through questionnaires and review of medical records. Response to treatment assessed using psoriasis area and severity index (PASI) physician global assessment (PGA) and dermatology life quality index (DLQI). - Study population: 380 patients with moderate to severe psoriasis will be prospectively recruited to the study. - Chief investigator: Professor Jonathan Barker. Co-investigator: Professor Catherine Smith - Sponsor/funding organization: Pfizer and Biomedical Research Centre (BRC) at Guys and St Thomas Hospitals Trust
The development of ascites in the natural history of cirrhosis heralds a worsening of the prognosis to 50% survival at 2 years, and this deteriorates to 30-50% at 1 year when the ascites becomes refractory to medical therapy. Hemodynamic alterations and their relation to neurohumoral systems are essential in pathophysiology of ascites formation. The theory that best explain the ascites formation and sodium retention in cirrhotics is portal hypertension leading to splanchnic arterial vasodilatation leading to underfilling of arterial circulation which is sensed by the arterial and the cardiopulmonary receptors leading to sympathetic nervous system activation and activation of the anti-natriuretic factors (RAAS and arginine vasopressin), resulting in sodium and water retention. The therapeutic options available for patients with refractory ascites are serial therapeutic paracentesis, liver transplantation and transjugular intrahepatic portosystemic shunts.Vasopressin V2 receptor antagonists antagonize the antidiuretic effects of vasopressin at the V2 receptor located in the renal collecting duct, they increase free water clearance, and thus may be helpful in mobilizing excess water in conditions associated with water retention including cirrhosis. The use of V2 receptor antagonists in cirrhosis with ascites has been shown to be safe and efficacious. Midodrine, an alpha adreno receptor agonist by causing splanchnic vasoconstriction has been used in hepatorenal syndrome (HRS) and for control of ascites in patients with refractory or recurrent ascites. It is possible that vasoconstrictors and aquaretics (V2 receptor antagonists) by acting at different sites in combination may reverse some of the pathogenic events that results in refractory or recurrent ascites.There are no reports on the use of combination of midodrine and tolvaptan in the patients with cirrhosis with ascites. Therefore, we plan to study the role of midodrine, tolvaptan and their combination on systemic hemodynamics, renal functions and control of ascites in patients with cirrhosis and refractory or recurrent ascites.
The purpose of this study is to evaluate the safety and efficacy of multiple infusions of mononuclear bone marrow cells in patients with chronic liver diseases.
30% of ketamine users complain of abdominal discomfort. Long-term ketamine use is associated with hepatotoxicity and pathologic changes to the biliary tract. Yet the prevalence of gastrointestinal and hepatobiliary pathologies in ketamine users has not been well-described. The investigators plan to recruit a large number of ketamine users based on referrals from different Psychiatry clusters in Hong Kong and to investigate the underlying cause of abdominal discomfort, describe the prevalence of different gastrointestinal and hepatobiliary pathologies and describe their long-term outcome.
Multicentric, observational and prospective study with two groups of treatment: Refractory ascites and non-refractory ascites. All patients should be prescribed beta-adrenergic blockers as primary or secondary profilaxis for variceal bleeding.
The purpose of this study is to determine whether transjugular intrahepatic portosystemic shunt (TIPS) combined with large spontaneous portosystemic shunts embolization are effective in the prevention of hepatic encephalopathy (HE).
The purpose of this study is to test the safety and determine the maximum safe dose of an experimental drug called LDE225 (hedgehog inhibitor) in people with liver cancer. We have identified hedgehog dysregulation as a novel mechanism for hepatocarcinogenesis and hepatic fibrosis/cirrhosis. Therefore, we hypothesize that the hedgehog inhibitor may be an ideal drug target for treating both hepatocellular carcinoma (HCC) and Child-Pugh A cirrhosis (CPA).
Hepatorenal syndrome (HRS) is a common cause of acute kidney injury (AKI) in cirrhotic patients and has a one month survival rate of 50% and a 3 month survival rate of 20%. The leading theory behind HRS is selective vasoconstriction of renal vasculature in the setting of decreased systemic vascular resistance. Patients with liver cirrhosis suffer from a large degree of third spacing in the form of peripheral edema and ascites. In addition treatment with multiple drugs, including diuretics puts these patients at higher risks of prerenal AKI and ischemic acute tubular necrosis (ATN). AKI occurring due to HRS, prerenal AKI and ischemic or nephrotoxic ATN have different pathophysiologic mechanisms and are treated differently with significantly different outcomes. While renal perfusion is expected to be reduced in HRS and prerenal AKI, it is normal or increased in ATN. Prerenal AKI has the most favorable prognosis among these pathologies and treatment simply consists of volume expansion with blood, albumin, crystalloids or colloids. In clinical practice vasoactive agents such as midodrine and octreotide are used to increase the tone of splanchnic vessels and to improve renal perfusion. These interventions would not affect renal function in cases with ATN. Unfortunately, the diagnostic criteria proposed by the International Club for Ascites (ICA) for HRS are not specific and do not always exclude patients with other forms of acute kidney injury. Therefore, availability of a simple diagnostic tool for measurement of renal blood flow (RBF) at the bedside would be of great value in management of cases with cirrhosis of the liver presenting with acute reduction in kidney function. However, currently, there are no practical and simple tools available for this purpose. Contrast enhanced ultrasonography (CEU) involves the intravenous injection of gas-filled microbubbles to enhance the ultrasound image of the organs and mainly to assess tissue vascularity and blood flow. We and others have used CEU to assess changes in RBF in response to physiologic stimuli and therapeutic interventions. Here we propose a prospective, pilot diagnostic study to validate the use of CEU, in assessing RBF in cirrhotic patients with AKI, and to assess the utility of CEU to differentiate between causes of AKI in cirrhotic patients. Our hypothesis is that CEU will show arteriolar vasoconstriction and decreased blood flow in the renal cortex in patients with HRS which would not change in response to volume expansion. On the contrary, patients with prerenal AKI will have reduced RBF which will increase after volume expansion. Finally, those with ATN will not have a reduced RBF at baseline. We plan to enroll 25 patients with liver cirrhosis and acute kidney injury who are admitted to the University of Virginia hospital into the study. CEU will be performed on all subjects to measure baseline RBF. CEU will be repeated in all subjects within 24 hours after volume expansion with at least 1gm/kg of albumin (up to 100 gm/day) to assess a potential change. Hourly urine output and serum creatinine will be monitored for potential renal response to the volume expansion as part of clinical care. For the subgroup of subjects who receive treatment with combination therapy with albumin, midodrine, and octreotide (AMO) RBF assessment with CEU will be repeated after at least 48 hours of receiving this combination. Renal response will be assessed by monitoring urine output and serum creatinine monitored as part of clinical care. All subjects will have measurements of fractional excretion of sodium (FENa) and urea (FEUrea) and urine microscopy as a part of their routine clinical care (work up of AKI). The results of these tests and the response to volume expansion will be used to categorize subjects into three categories of AKI (HRS, prerenal AKI, ATN). Correlations between RBF and its changes between different therapeutic interventions and renal diagnosis will be tested in this study.
This study will be used to train an algorithm using Methacetin breath test (MBT) measures and to select a cut-off to determine presence or absence of Clinically Significant Portal Hypertension (CSPH) as defined by Hepatic Venous Gradient Pressure (HVPG) ≥ 10mmHg,
This is a double-blind, multicenter study involving patients with chronic HCV infection who had a liver transplantation; developed HCV-related liver fibrosis and/or incomplete cirrhosis; achieved a sustained virologic response (SVR) following anti-HCV therapy; but still have fibrosis and/or incomplete cirrhosis on liver biopsy to see if treatment with IDN-6556 is better than placebo in reversing or stopping the progression of the damage to the new liver caused by HCV.