Atorvastatin, L-Carnitine and Non-Alcoholic Steatohepatitis (NALCAT)

This study is currently recruiting participants. (see Contacts and Locations)
Verified May 2014 by Tehran University of Medical Sciences
Sponsor:
Information provided by (Responsible Party):
Tehran University of Medical Sciences
ClinicalTrials.gov Identifier:
NCT01617772
First received: June 8, 2012
Last updated: May 6, 2014
Last verified: May 2014

June 8, 2012
May 6, 2014
January 2013
December 2015   (final data collection date for primary outcome measure)
improvement in liver stiffness [ Time Frame: 2 years ] [ Designated as safety issue: No ]
As measured by Fibroscan
Same as current
Complete list of historical versions of study NCT01617772 on ClinicalTrials.gov Archive Site
  • improvement in liver enzyme levels [ Time Frame: 2 years ] [ Designated as safety issue: No ]
  • Adverse drug events [ Time Frame: 2 years ] [ Designated as safety issue: Yes ]
Same as current
Not Provided
Not Provided
 
Atorvastatin, L-Carnitine and Non-Alcoholic Steatohepatitis
Comparison the Effectiveness of L-Carnitine With Atorvastatin in Non-Alcoholic Steatohepatitis (NASH)

The aim of the present study was to compare the effects of simvastatin and L-carnitine coadministration versus simvastatin, L-Carnitine monotherapy on liver enzymes ( AST,ALT ) and liver elasticity in NASH patients.

Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of disease ranging from steatosis to steatohepatitis (nonalcoholic steatohepatitis, NASH) to cirrhosis. Statins are competitive inhibitors of HMG CoA reductase, the rate-limiting step in cholesterol biosynthesis. They occupy a portion of the binding site of HMG CoA, blocking access of this substrate to the active site on the enzyme. A reduction in intrahepatic cholesterol leads to an increase in LDL receptor turnover that results from an enhanced rate of hepatic LDL receptor cycling. On the other hand recent studies have implicated several important cellular processes and signaling pathways that are affected by abnormal lipid metabolism, resulting in specific biochemical, histological, and clinical changes associated with NAFLD.

Maybe statins, as lipid lowering agents, and through their effect in reduction of intrahepatic cholesterol, can affect the abnormal lipid metabolism in NASH.

L- carnitine, can improve the outcome of NASH, because it reduces lipid levels, limits oxidative stress, and modulates inflammatory responses . It performs a number of essential intracellular and metabolic functions, such as fatty acid transport, detoxification of potentially toxic metabolites, regulation of the mitochondrial acyl-Co A / CoA ratio, and stabilization of cell membranes. It has a pivotal role in the transport of long chain fatty acids across the inner mitochondrial membrane.

Interventional
Phase 2
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Factorial Assignment
Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor)
Primary Purpose: Treatment
Non-alcoholic Steatohepatitis
  • Drug: Atorvastatin
    Atorvastatin 20 mg
  • Drug: L-Carnitine
    1000mg L-carnitine
  • Drug: Placebo
    Identically looking placebo
  • Experimental: Atorvastatin
    20mg atorvastatin daily
    Intervention: Drug: Atorvastatin
  • Experimental: Carnitine
    1000mg L-carnitine daily
    Intervention: Drug: L-Carnitine
  • Experimental: Atoral
    1000mg L-carnitine and 20mg atorvastatin
    Interventions:
    • Drug: Atorvastatin
    • Drug: L-Carnitine
  • Placebo Comparator: Placebo
    Identically looking placebo
    Intervention: Drug: Placebo
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
440
February 2016
December 2015   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • NASH diagnosed on the basis of the following criteria:

    1. Imaging techniques showing evidence of hepatic steatosis
    2. Increased ALT above 1.5 times normal (normal: 20 IU/L for women, 30 for men) on two occasions three months apart.

Exclusion Criteria:

  • Patients with hepatitis B or C
  • ALT > 300 IU/L
  • Participants presenting one or more causes commonly associated with secondary NAFLD (drugs, surgical procedures, environmental toxins, or total parenteral nutrition)
  • Alcohol ingestion greater than 40 gr per week
  • Abnormal Lipid profile (TG>500 , LDL>160)
  • Patients with hypertension, diabetes mellitus, coronary heart disease
  • Fibroscan score more than 7.9 kp
  • pregnancy, lactation
  • Drug addiction
  • Reynolds Risk Score > 10%
  • Not consenting to the study
Both
40 Years to 60 Years
No
Contact: Shahin Merat, Professor +98 917 117 3966 merat@tums.ac.ir
Contact: Reza Malekzadeh, Professor +98 912 111 4139 malek@ams.ac.ir
Iran, Islamic Republic of
 
NCT01617772
DDRI/90.10
Yes
Tehran University of Medical Sciences
Tehran University of Medical Sciences
Not Provided
Study Chair: Reza Malekzadeh, MD Tehran University of Medical Sciences
Tehran University of Medical Sciences
May 2014

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP