When do HCV antibodies disappear

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Critical Care Ask The Expert

Hepatitis C Antibodies

Medscape Critical Care 3(1), 2002. © 2002 Medscape Portals, Inc

Question

If a patient who has hepatitis C is cured, when do the hepatitis C

antibodies disappear from his blood?

Almariah, MD

Response

from Reardon, MD, 05/09/2002

Hepatitis C virus (HCV) accounts for 70% of chronic hepatitis and 30% of

end-stage liver disease (ESLD) in the United States. The incubation period

of the acute infection is 7-8 weeks, with 25% of patients developing

symptoms and jaundice. Anti-HCV antibodies are usually measurable by

enzyme-linked immunosorbent assay (ELISA) after the onset of symptoms.

Immunocompromised patients such as transplant recipients or hemodialysis

patients may have an impaired antibody response.[1,2] Confirmatory assays

such as the recombinant immunoblot assay (RIBA-2) for HCV antigens and

polymerase chain reaction (PCR) for HCV-RNA can aid in diagnosis of HCV

infection. HCV-RNA can be found in the serum of acutely infected patients

within days of exposure and may be present for months prior to the

development of anti-HCV antibodies.[3,4]

Less than 15% of patients with HCV infection have a spontaneous cure.

Normalization of serum aminotransferases and disappearance of anti-HCV

antibodies do not indicate clearance of the infection. In a study of a

cohort of Irish women infected with HCV via contaminated anti-D

immunoglobulin in 1977, 47.1% of 68 women who had spontaneous clearance of

HCV still had anti-HCV antibodies 18 years after the initial infection.[5]

Resolution of HCV infection is defined as the persistent loss of HCV-RNA

during long-term follow-up. Documentation of persistent loss of HCV-RNA will

confirm that the patient does not have intermittent viremia indicating

ongoing infection.

HCV infection causes chronic hepatitis in 85% of patients. The rate of

spontaneous clearance of HCV after 6 months of infection is low. Treatment

of chronic HCV infection for selected patients includes combination

interferon and ribavirin. The goal of treatment is a sustained virologic

response, which is defined as a persistent absence of detectable HCV-RNA in

the serum for more than 6 months after cessation of treatment. The sustained

virologic response rate with combination interferon and ribavirin is 30% to

40%.[6]

References

Pereira BJ, Levey AS. Hepatitis C infection in dialysis and renal

transplantation. Kidney Int. 1997;51:981-999.

Lau JY, GL, Brunson ME, et al. Hepatitis C virus infection in kidney

transplant recipients. Hepatology. 1993;18:1027-1031.

Farci P, Alter HJ, Wong D, et al. A long-term study of hepatitis C virus

replication in non-A, non-B hepatitis. N Engl J Med. 1991;325:98-104.

Beld M, Penning M, van Putten M, et al. Low level of hepatitis C virus RNA

in serum, plasma, and periperal blood mononuclear cells of injecting drug

users during long antibody-undetectable periods before seroconversion.

Blood. 1999;94:1183-1191.

Barrett S, Goh J, Couglan B, et al. The natural course of hepatitis C virus

infection after 22 years in a unique homogenous cohort: spontaneous viral

clearance and chronic HCV infection. Gut. 2001;49:423-430.

The National Institutes of Health Consensus Development Conference.

Management of hepatitis C. Hepatology. 1997;26(suppl 1):S1-S9.

Reardon, Reardon, MD, Assistant Professor of

Medicine, Pulmonary and Critical Care Medicine, Boston University School of

Medicine; Associate Director of the Medical Intensive Care Unit, Department

of Internal Medicine, Boston Medical Center, Boston, Massachusetts

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To Print: Click your brower's PRINT button.

NOTE: To view the article with Web enhancements, go to:

http://www.medscape.com/viewarticle/432543

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Critical Care Ask The Expert

Hepatitis C Antibodies

Medscape Critical Care 3(1), 2002. © 2002 Medscape Portals, Inc

Question

If a patient who has hepatitis C is cured, when do the hepatitis C

antibodies disappear from his blood?

Almariah, MD

Response

from Reardon, MD, 05/09/2002

Hepatitis C virus (HCV) accounts for 70% of chronic hepatitis and 30% of

end-stage liver disease (ESLD) in the United States. The incubation period

of the acute infection is 7-8 weeks, with 25% of patients developing

symptoms and jaundice. Anti-HCV antibodies are usually measurable by

enzyme-linked immunosorbent assay (ELISA) after the onset of symptoms.

Immunocompromised patients such as transplant recipients or hemodialysis

patients may have an impaired antibody response.[1,2] Confirmatory assays

such as the recombinant immunoblot assay (RIBA-2) for HCV antigens and

polymerase chain reaction (PCR) for HCV-RNA can aid in diagnosis of HCV

infection. HCV-RNA can be found in the serum of acutely infected patients

within days of exposure and may be present for months prior to the

development of anti-HCV antibodies.[3,4]

Less than 15% of patients with HCV infection have a spontaneous cure.

Normalization of serum aminotransferases and disappearance of anti-HCV

antibodies do not indicate clearance of the infection. In a study of a

cohort of Irish women infected with HCV via contaminated anti-D

immunoglobulin in 1977, 47.1% of 68 women who had spontaneous clearance of

HCV still had anti-HCV antibodies 18 years after the initial infection.[5]

Resolution of HCV infection is defined as the persistent loss of HCV-RNA

during long-term follow-up. Documentation of persistent loss of HCV-RNA will

confirm that the patient does not have intermittent viremia indicating

ongoing infection.

HCV infection causes chronic hepatitis in 85% of patients. The rate of

spontaneous clearance of HCV after 6 months of infection is low. Treatment

of chronic HCV infection for selected patients includes combination

interferon and ribavirin. The goal of treatment is a sustained virologic

response, which is defined as a persistent absence of detectable HCV-RNA in

the serum for more than 6 months after cessation of treatment. The sustained

virologic response rate with combination interferon and ribavirin is 30% to

40%.[6]

References

Pereira BJ, Levey AS. Hepatitis C infection in dialysis and renal

transplantation. Kidney Int. 1997;51:981-999.

Lau JY, GL, Brunson ME, et al. Hepatitis C virus infection in kidney

transplant recipients. Hepatology. 1993;18:1027-1031.

Farci P, Alter HJ, Wong D, et al. A long-term study of hepatitis C virus

replication in non-A, non-B hepatitis. N Engl J Med. 1991;325:98-104.

Beld M, Penning M, van Putten M, et al. Low level of hepatitis C virus RNA

in serum, plasma, and periperal blood mononuclear cells of injecting drug

users during long antibody-undetectable periods before seroconversion.

Blood. 1999;94:1183-1191.

Barrett S, Goh J, Couglan B, et al. The natural course of hepatitis C virus

infection after 22 years in a unique homogenous cohort: spontaneous viral

clearance and chronic HCV infection. Gut. 2001;49:423-430.

The National Institutes of Health Consensus Development Conference.

Management of hepatitis C. Hepatology. 1997;26(suppl 1):S1-S9.

Reardon, Reardon, MD, Assistant Professor of

Medicine, Pulmonary and Critical Care Medicine, Boston University School of

Medicine; Associate Director of the Medical Intensive Care Unit, Department

of Internal Medicine, Boston Medical Center, Boston, Massachusetts

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