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Hepatitis C: Latest Guidelines From the NIH

Hepatitis C: Latest Guidelines From the NIH

The most common blood-borne infection in the United States, hepatitis C is also one of the leading causes of chronic liver disease in this country. About 35,000 new hepatitis C virus (HCV) infections are diagnosed each year; by 2015, the number of persons with documented HCV infection is expected to have increased 4-fold from what it was in 1990.

Fortunately, the increase in newly diagnosed infections has been paralleled by tremendous growth in our understanding of HCV. In 1997, the NIH issued a consensus statement that for the past 5 years has defined the standard of care with respect to the diagnosis, treatment, and prevention of HCV infection.1 The recent advances in knowledge of the disease led the NIH in 2002 to hold a second Consensus Development Conference and issue updated recommendations.2 Highlights from these guidelines are presented here. (The consensus statement may be viewed in its entirety at http://www. consensus.nih.gov.)

NATURAL HISTORY
Infection with HCV may be caused by any of 6 viral genotypes. Genotype 1 accounts for at least 70% of infections in the United States.

Acute infection. HCV RNA may be detected 1 to 3 weeks after exposure and is present by the time symptoms develop. HCV antibodies are present in only 50% to 70% of patients by the time symptoms develop but can be detected in 90% of patients 3 months after exposure. The acute infection is rarely fulminant.

Chronic infection. Chronic hepatitis C develops in up to 85% of infected persons. Women and those infected at a younger age are more likely to clear their infection. African American men appear to be the least likely to clear the infection.

In patients who remain infected, the proportion of those in whom cirrhosis develops within 20 years varies from between 2% and 4% in women and children to between 20% and 30% in transfused patients.

HIV or hepatitis B virus (HBV) coinfection appears to hasten the progression of liver disease. In addition, there is strong evidence that significant alcohol use (equivalent to 4 beers a day in men or 2 beers a day in women) accelerates the course of the disease. Lower levels of alcohol consumption may also be detrimental.

Neither viral load nor genotype appears to alter the progression of HCV infection-although genotype 1 is associated with a lower rate of responseto treatment.

HCV infection accounts for one third of the cases of hepatocellular carcinoma (HCC) in the United States. HCC develops almost exclusively in patients with cirrhosis. Risk factors for HCC are largely the same as those for cirrhosis.

ASSESSMENT
Multiple tests are available to diagnose and monitor HCV infection. These include enzyme immunoassays (EIAs), recombinant immunoblot assays (RIBAs), qualitative and quantitative HCV RNA assays, and liver biopsy.

Serologic tests. An EIA detects antibodies to HCV. It is easy to perform, reproducible, and suitable for screening persons at risk. Third-generation EIAs have very high sensitivity and specificity. In immunocompetent patients with clinical liver disease or risk factors for HCV infection, a negative result on an EIA excludes chronic hepatitis C. Supplemental testing with an RIBA is still useful in some set-tings. [Editor's note: For an extended discussion of EIAs and RIBAs, see Dr Sofair's article, "Apparently Healthy Man With History of Injection Drug Use: The Initial Approach," CONSULTANT, February 2002, page 157.]

Use an FDA-approved qualitative HCV RNA assay to confirm the presence of chronic infection in patients with a positive result on an EIA or in whom early infection is suspected. These tests can detect viral loads as low as 50 to 100 IU/mL. Transcription-mediated amplification assays can detect viral loads as low as 5 IU/mL but have not yet been approved by the FDA for clinical use. A single positive response to an HCV RNA assay confirms active HCV infection. A single negative result does not exclude viremia; the test must be repeated to rule out a transient decline in viral titer that is below the limits of detection. Once active infection has been confirmed, repeated RNA testing is unnecessary except to document clearance of the infection.

Quantitative HCV RNA assays (quantitative polymerase chain reaction or branched DNA) may be useful in predicting outcome of therapy, which is more likely to be favorable in patients with a low viral load.

Liver biopsy. Although biopsy rarely detects other unsuspected liver diseases, the procedure provides valuable information on which to base treatment decisions. Patients with normal alanine aminotransferase levels and little or no fibrosis on biopsy have a favorable prognosis and may opt to defer treatment.

Because of the shorter treatment duration and more favorable outcome in patients with genotype 2 or genotype 3 infection, a pretreatment biopsy may not always be necessary in such persons.

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