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Discussion Starter · #1 ·
A 46-year-old man is known to have chronic hepatitis C virus (HCV) infection. He is a former IV drug user for more than 20 years who has been abstinent from drug use for 1 year. He is asking whether he should receive treatment for his HCV infection. He has a prior history of hepatitis B virus (HBV) and has positive antibody to HBV surface antigen. He was treated for tricuspid valve endocar-ditis 3 years previously. He has no other medical history.
He does not know when he acquired HCV. His laboratory studies show a positive HCV IgG antibody with a viral load of greater than 1 million copies. The virus is genotype 1. His AST is 62 U/L, and his ALT is 54 U/L. He undergoes liver biopsy, which demonstrates a moderate degree of bridging fibrosis. What do you tell him regarding his likelihood of progression and possibilities regarding treatment?

A. As he is infected with genotype 1, the likelihood of response to pegylated interferon and ribavirin is less than 40%.
B. Following 12 weeks of treatment, the expected viral load should be undetectable.
C. Given his normal liver enzymes on laboratory test-ing, he is unlikely to develop progressive liver injury.
D. If the patient elects to undergo treatment, the best regimen for individuals with genotype 1 disease is pegylated interferon and ribavirin for 24 weeks.
E. The presence of bridging fibrosis on liver biopsy is the most predictive factor of the development of cirrhosis over the next 10–20 years.
 

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I dont really know the answer.. but I know for a fact that once changes start in the liver the inevitable will be either cirrhosis or hepatocellular carcinoma unless treatment is indicated.. im not sure what is the length of treatment so.. I cant comment much.. I will probably be wrong tho
 

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Discussion Starter · #4 ·
The answer is E.

Much information has been gained in recent decades about the progression and treatment of chronic hepatitis C virus (HCV) infection. Chronic hepatitis develops in about 85% of all individuals affected with HCV, and 20–25% of these individuals will progress to cirrhosis over about 20 years. Among those infected with HCV, about one-third of individuals will have normal or near-normal levels of aminotransferases, although liver biopsy demonstrates active hepatitis in as much as one-half of patients. Moreover, about 25% of individuals with normal aminotransferase levels at one point in time will develop elevations in these enzymes later, which can lead to progressive liver disease. Thus, normal aminotransferase levels at a single point in time do not definitively rule out the possibility that cirrhosis can develop. Progression to end-stage liver disease in individuals with chronic HCV hepatitis is more likely in older individuals and in those with a longer duration of infection, advanced histologic stage and grade, genotype 1 infection, more complex quasi-species diversity, concomitant other liver disease, HIV infection, and obesity. Among these factors, the best prognostic indicator for the development of progressive liver disease is liver histology. Specifically, patients who have moderate to severe inflammation or necrosis including septal or bridging fibrosis have the greatest risk of developing cirrhosis over the course of 10–20 years. Indications for therapy in those with HCV include detectable levels of HCV RNA, portal or bridging fibrosis on liver biopsy, or moderate to severe hepatitis on liver biopsy. Contraindications to treatment are age greater than 60 years, mild hepa-titis on liver biopsy, and severe renal insufficiency. Standard therapy for HCV infection is pegylated interferon plus ribavirin. While genotypes 1 and 4 are less responsive to therapy than genotypes 2 and 3, the current research demonstrates a response rate of at least 40% for genotypes 1 and 4. Interestingly, even in individuals who fail to show a viro-logic or biochemical response, 75% will have histologic improvement on liver biopsy. The treatment course for genotypes 1 and 4 is a minimum of 48 weeks, whereas genotypes 2 and 3 can be treated for as little as 24 weeks. Once treatment has been started, a repeat HCV viral load should be assessed at 12 weeks. At this point, a 2-log drop in viral load is expected. Failure to achieve this level of response suggests that a sustained virologic response is unlikely to occur. With a drop of this magnitude, however, the likelihood of a sustained virologic response is about 66% at the end of therapy, and if the viral load is undetectable at 12 weeks, the chances of a sustained virologic response is more than 80%.
 
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