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We hypothesize that atorvastatin will decrease HCV viral load in patients taking the medication.
Cholesterol is needed for HCV virion production. Cell culture studies have shown that atorvastatin (an HMG-CoA reductase inhibitor) decreases HCV viral replication. As atorvastatin has been proven to decrease heart attack and stroke in patients with high cholesterol, this medication is indicated for the treatment of elevated cholesterol in at risk individuals. Therefore we propose to study the effect atorvastatin has on the viral load of patients initiated on atorvastatin therapy for their elevated cholesterol.
Men and women ages 30 to 80 infected with HCV viremia whose physician has determined need cholesterol lowering medication will be recruited by the study investigators from Massachusetts General Hospital.
The study investigators will approach the potential subject after the referring doctor has ascertained that the potential subject is interested in meeting with the investigator.
Each subject who consents will undergo phlebotomy of 10 cc of blood three times. Once prior to the initiation of atorvastatin to measure the patients viral load. In addition, patients will undergo phlebotomy 4 and 12 weeks after the initiation of atorvastatin. The week 12 phlebotomy is required in all patients started on atorvastatin to monitor for side effects. Therefore patients who enroll in this study will undergo one additional phlebotomy. As part of our study an extra 10 cc of blood will be taken at these times to measure the patients HCV viral load.
Allocation: Non-Randomized, Control: Uncontrolled, Endpoint Classification: Efficacy Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment
20 mg of atorvastatin daily
Massachusetts General Hospital
Massachusetts General Hospital
Published on BioPortfolio: 2014-08-27T03:41:26-0400
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INFLAMMATION of the LIVER in humans due to infection by VIRUSES. There are several significant types of human viral hepatitis with infection caused by enteric-transmission (HEPATITIS A; HEPATITIS E) or blood transfusion (HEPATITIS B; HEPATITIS C; and HEPATITIS D).
A family of hepatotropic DNA viruses which contains double-stranded DNA genomes and causes hepatitis in humans and animals. There are two genera: AVIHEPADNAVIRUS and ORTHOHEPADNAVIRUS. Hepadnaviruses include HEPATITIS B VIRUS, duck hepatitis B virus (HEPATITIS B VIRUS, DUCK), heron hepatitis B virus, ground squirrel hepatitis virus, and woodchuck hepatitis B virus (HEPATITIS B VIRUS, WOODCHUCK).
A species in the genus HEPATOVIRUS containing one serotype and two strains: HUMAN HEPATITIS A VIRUS and Simian hepatitis A virus causing hepatitis in humans (HEPATITIS A) and primates, respectively.
INFLAMMATION of the LIVER in humans caused by HEPATITIS DELTA VIRUS, a defective RNA virus that can only infect HEPATITIS B patients. For its viral coating, hepatitis delta virus requires the HEPATITIS B SURFACE ANTIGENS produced by these patients. Hepatitis D can occur either concomitantly with (coinfection) or subsequent to (superinfection) hepatitis B infection. Similar to hepatitis B, it is primarily transmitted by parenteral exposure, such as transfusion of contaminated blood or blood products, but can also be transmitted via sexual or intimate personal contact.
INFLAMMATION of the LIVER in humans caused by HEPATITIS C VIRUS, a single-stranded RNA virus. Its incubation period is 30-90 days. Hepatitis C is transmitted primarily by contaminated blood parenterally, and is often associated with transfusion and intravenous drug abuse. However, in a significant number of cases, the source of hepatitis C infection is unknown.
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