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Prevalence and outcome of hepatitis C infection among heart transplant recipients
N N Zein1, C G McGreger, N K Wendt
1Division of Gastroenterology, Mayo Clinic and Foundation, Rochester, Minn, USA.
Insights
Hepatitis C virus infection can occur in heart transplant recipients without detectable antibodies. This infection may lead to severe cholestatic liver disease, hepatic failure, and death, highlighting the need for vigilant monitoring in these patients.
Area of Science:
- Hepatology
- Transplant Surgery
- Infectious Diseases
Background:
- Hepatitis C virus (HCV) infection poses risks for organ transplant recipients, potentially causing severe illness and death.
- Immunosuppression in transplant patients can mask HCV infection, preventing antibody development.
- Understanding HCV prevalence and clinical outcomes in heart transplant recipients is crucial.
Purpose of the Study:
- To determine the prevalence of Hepatitis C virus infection in heart transplant recipients.
- To identify clinical syndromes associated with HCV infection post-heart transplantation.
Main Methods:
- Collected sera from 59 heart transplant recipients and their donors.
- Tested pre- and post-transplantation samples for HCV antibodies using recombinant immunoblot assay.
- Utilized reverse transcriptase polymerase chain reaction to detect HCV RNA.
Main Results:
- HCV RNA was detected in 7% (4/59) of post-transplantation serum samples; only one patient was antibody-positive.
- Two infected patients received organs from HCV RNA/antibody-positive donors; two possibly acquired infection post-transplant.
- One patient developed progressive, fatal cholestatic liver disease due to HCV infection after transplantation.
Conclusions:
- Hepatitis C virus infection can occur in heart transplant recipients without detectable antibodies.
- Severe cholestatic liver disease is a potential complication of HCV infection following heart transplantation.
Background:
Hepatitis C virus infection is common in organ transplant recipients, and can be associated with significant morbidity and mortality. A unique feature of this infection among immunosuppressed patients is that it can progress without the development of hepatitis C virus antibodies.
Methods:
To define the prevalence of hepatitis C virus infection in patients undergoing heart transplantation and identify clinical syndromes associated with hepatitis C virus infection in heart transplant recipients, we collected sera from 59 consecutive heart transplant recipients and their donors. Samples were tested before and after transplantation for hepatitis C virus antibodies with the use of a second-generation recombinant immunoblot assay and for hepatitis C virus RNA by means of reverse transcriptase polymerase chain reaction.
Results:
Four of 59 patients (7%) had hepatitis C virus-RNA detected in posttransplantation serum samples; but only one of these was anti-hepatitis C virus antibody positive. Two of the four patients with hepatitis C virus RNA detected after transplantation received organs from donors who were positive for hepatitis C virus RNA/anti-hepatitis C virus. One of these two recipients tested positive for hepatitis C virus antibody and hepatitis C virus RNA before transplantation. The other two patients received organs from hepatitis C virus negative donors and possibly acquired infection after transplantation from blood or immunoglobulin preparations. One patient was anti-hepatitis C virus positive before transplantation but had no detectable hepatitis C virus RNA, and hepatitis C virus infection did not develop after transplantation. Progressive hepatitis C virus-induced cholestatic liver disease that led to hepatic failure and death after heart transplantation occurred in one of the four patients.
Conclusion:
Hepatitis C virus infection may occur after heart transplantation in the absence of anti-hepatitis C virus antibodies, and a syndrome of severe cholestatic liver disease may complicate heart transplantation in the presence of hepatitis C virus infection.