A Phase II, Double-blinded, Randomized, Controlled Study to Evaluate the Efficacy and Safety of Vitalliver in Patients With Decompensated Cirrhosis

This study has been completed.
Sponsor:
Collaborator:
Vigconic (International) Ltd.
Information provided by:
Hospital Authority, Hong Kong
ClinicalTrials.gov Identifier:
NCT00562783
First received: November 20, 2007
Last updated: October 22, 2013
Last verified: October 2013
  Purpose

Cirrhosis is a diffuse lesion characterized by architectural distortion of the liver because of collagen deposition and development of nodules of regenerating hepatocytes. It is an irreversible change that results from diseases characterized by chronic liver injury (Fujimoto, 2000). Cirrhosis alters the pattern of blood flow through the liver and results in impaired perfusion of hepatic lobules with intrahepatic and extrahepatic shunting of blood. This deprives hepatocytes of uniform perfusion by arterial and portal venous blood resulting in both portal hypertension and other consequences of cirrhosis including impaired protein synthesis and altered drug metabolism. The histologic diagnosis of cirrhosis requires the presence of regenerative nodules or pseudolobules completely encircled by fibrosis such as congenital hepatic fibrosis can result in portal hypertension in the absence of cirrhosis (Anthony et al., 1977).

The events leading to the development of cirrhosis are generally those of chronic injury with hepatocyte destruction. Acute severe liver injury as in fulminant viral hepatitis does not result in cirrhosis and the liver generally returns to normal after recovery. Cirrhosis can be classified by macroscopic appearance, by cause, and by histologic appearance and location of liver damage. Micronodular cirrhosis is composed of uniform nodules less than 3 mm in diameter, whereas macronodular cirrhosis has varying size nodules greater than 3 mm diameter. Mixed nodular cirrhosis has nodules of both sizes. Some liver diseases such as alcoholic liver disease may present as micronodular cirrhosis and develop larger nodules with subsequent regeneration of hepatocytes. For this reason, many prefer etiologic classification (e.g., alcoholic cirrhosis). The designation of cirrhosis as post necrotic, biliary and portal are still commonly used and imply predominant histologic location of fibrosis.

Cirrhosis is an irreversible disease, and attempts should be made to stabilize the patient and to control the cause. Factors that indicate a poor outcome include an elevated prothrombin time that does not correct itself with parenteral vitamin K, upper gastrointestinal bleeding caused by varices, ascites refractory to therapy, increased age of the patient, sever malnutrition, spontaneous bacterial peritonitis, a pronounced increase of serum bilirubin in the absence of haemolysis, and heptocellular carcinoma (Yeh et al., 2003). In general, all causes of upper GI bleeding are associated with an increased mortality in patients with cirrhosis. For those with alcoholic cirrhosis who lack portal hypertension, survival is similar to an age-matched cohort if alcohol intake is stopped (Nakamura et al., 1991). If ethanol consumption continues, mortality is higher. Cirrhosis can be present without clinically significant complications and be identified only at autopsy or during evaluation of abnormal liver tests (Mendez et al., 2003). However, for many patients the disease is slowly progressive resulting in one or more complications. The clinical manifestations of cirrhosis are a result of altered hepatic blood flow through the liver with intrahepatic shunting causing impaired perfusion of hepatocytes or portal hypertension with shunting of blood around the liver though portosystemic communications. The major complications of portal hypertension include oesophageal or gastric varices, ascites, portosystemic encephalopathy, and hepatorenal-syndrome (Menon & Kamath, 2000). With impairment of hepatocyte perfusion or reduction of hepatocyte number, altered synthetic function can result in hypoalbuminemia, hypoprothrombinemia, and changes in drug metabolism.

Vitalliver is a Chinese medicine which is administered in the form of a suppository, which is uncommon for most Chinese medicines. Medications released from the suppositories are absorbed directly from the circulation around the rectum and then reach the liver via the portal vein.

Basic pharmacological studies have shown that Vitalliver has good immunomodulating functions, increases the activities of T-cells, B-cells and NK cells, therefore this formulation may have special values in treating liver diseases.


Condition Intervention Phase
Hepatitis B
Hepatitis C
Liver Cirrhosis
Drug: Vitaliver
Drug: Placebo
Phase 2

Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Single Group Assignment
Masking: Double-Blind
Primary Purpose: Treatment
Official Title: A Phase II, Double-blinded, Randomized, Controlled Study to Evaluate the Efficacy and Safety of Vitalliver in Patients With Decompensated Cirrhosis

Resource links provided by NLM:


Further study details as provided by Hospital Authority, Hong Kong:

Primary Outcome Measures:
  • The primary outcome for evaluating the clinical efficacy of Vitalliver is the Model for End Stage Liver Disease (MELD) score [ Time Frame: week 16 ]

Secondary Outcome Measures:
  • Child-Pugh's grading [ Time Frame: Week 16 ]
  • Quality of life variable [ Time Frame: Week 16 ]

Estimated Enrollment: 90
Study Start Date: January 2005
Study Completion Date: May 2006
  Eligibility

Ages Eligible for Study:   18 Years to 80 Years
Genders Eligible for Study:   Both
Criteria

Inclusion Criteria:

  • HBV or HCV related liver cirrhosis
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00562783

Locations
China
Queen Mary Hospital
Hong Kong, China
Sponsors and Collaborators
Hospital Authority, Hong Kong
Vigconic (International) Ltd.
Investigators
Principal Investigator: George Lau, Dr Department of Medicine, Queen Mary Hospital/ The University of Hong Kong
  More Information

Additional Information:
No publications provided

ClinicalTrials.gov Identifier: NCT00562783     History of Changes
Other Study ID Numbers: UW04-223 T/545, HARECCTR0500001
Study First Received: November 20, 2007
Last Updated: October 22, 2013
Health Authority: Hong Kong: Ethics Committee

Keywords provided by Hospital Authority, Hong Kong:
HBV
HCV
Liver cirrhosis

Additional relevant MeSH terms:
Hepatitis
Hepatitis A
Hepatitis B
Hepatitis C
Liver Cirrhosis
Digestive System Diseases
DNA Virus Infections
Enterovirus Infections
Flaviviridae Infections
Hepadnaviridae Infections
Hepatitis, Viral, Human
Liver Diseases
Picornaviridae Infections
RNA Virus Infections
Virus Diseases

ClinicalTrials.gov processed this record on October 23, 2014