Cholestatic hepatitis leading to hepatic failure in a patient with organ-transmitted hepatitis C virus infection
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Published on: October 21, 2017
Insights
Organ transmission of hepatitis C virus (HCV) caused subfulminant liver failure in a heart transplant patient. Early anti-HCV antibody tests were negative, highlighting diagnostic challenges in immunosuppressed individuals.
Area of Science:
- Hepatology
- Transplant Immunology
- Virology
Background:
- Heart transplant recipients are at risk for opportunistic infections and complications.
- Hepatitis C virus (HCV) infection can manifest differently in immunocompromised hosts.
- Subfulminant hepatic failure post-transplantation requires prompt diagnosis and management.
Observation:
- A 51-year-old heart transplant recipient developed progressive cholestatic liver injury.
- Initial investigations, including imaging and liver biopsy, mimicked large duct obstruction.
- HCV infection was confirmed late due to initially negative anti-HCV antibody tests and high HCV RNA levels.
Findings:
- Organ-transmitted HCV caused subfulminant hepatic failure with predominantly cholestatic features.
- Immunosuppression masked early serological detection of HCV infection.
- HCV RNA was detected in over 80% of hepatocytes, indicating significant viral replication.
Implications:
- Anti-HCV antibody testing may be unreliable for diagnosing HCV in immunosuppressed transplant patients.
- HCV should be considered in the differential diagnosis of cholestatic liver disease in transplant recipients.
- Early and sensitive viral load testing is crucial for timely HCV diagnosis and management in this population.
Abstract:
A 51-year-old heart transplant recipient who developed subfulminant hepatic failure because of organ-transmitted hepatitis C virus (HCV) infection is described. He presented with a predominantly cholestatic liver damage after heart transplantation. An extensive evaluation, including abdominal ultrasound and computed tomography scan and endoscopic retrograde cholangiopancreatography was unrevealing. Liver biopsy, however, was suggestive of a large duct obstruction with prominent portal and pericellular fibrosis, marked cholestasis, pericholangitis with marked ductular proliferation, and diffuse hepatocyte degeneration. Antibody to HCV (anti-HCV) was initially negative. He deteriorated in the ensuing 3 months. A repeat enzyme immunoassay-2 test for anti-HCV 4 months after initial presentation was weakly positive. Quantitation of serum HCV RNA by branched DNA assay revealed high level viremia, 547 x 10(6) genome equivalents per milliliter. Using in situ polymerase chain reaction, HCV RNA was detected in the cytoplasm in > 80% of the hepatocytes. The patient underwent interferon alfa therapy, and serum HCV RNA levels were reduced 20-fold after four doses. Unfortunately, the patient developed pulmonary aspergillosis and died. This case illustrates that in immunosuppressed patients anti-HCV is not a good marker for the diagnosis of HCV infection, and HCV can cause a progressive form of cholestatic liver disease mimicking a large duct obstruction.
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