TY - JOUR
T1 - Intractable recurrent hepatitis A virus infection requiring repeated liver transplantation
T2 - A case report
AU - Park, G. C.
AU - Hwang, S.
AU - Yu, Y. D.
AU - Park, P. J.
AU - Choi, Y. I.
AU - Song, G. W.
AU - Jung, D. H.
AU - Ahn, C. S.
AU - Kim, K. H.
AU - Moon, D. B.
AU - Ha, T. Y.
AU - Lee, S. G.
PY - 2010/12
Y1 - 2010/12
N2 - Although hepatitis A virus (HAV) infection is usually self-limited, it may induce fulminant hepatitis. We present an unusual case of a 40-year-old, otherwise healthy man with intractable recurrent HAV infection requiring retransplantation after primary liver transplantation for HAV-associated fulminant liver failure. After the first living-donor liver transplantation, allograft function recovered uneventfully; however, beginning at 35 days, his serum total bilirubin concentration increased, reaching 40 mg/dL, with a slight increase in liver enzymes. Detection of genomic HAV RNA in serum at the time of graft dysfunction led to a diagnosis of recurrent HAV infection. Fifty-one days after the first transplant, he underwent a deceased donor retransplantation. His allograft function recovered; the patient was discharged from the hospital. Sixty-five days later, however, he was readmitted for colitis-like symptoms and was again treated for acute rejection, but died owing to overwhelming sepsis and persistence of HAV infection. These findings indicate that patients who undergo liver transplantation for HAV-associated liver disease may be at risk of HAV reinfection, particularly if they require anti-rejection therapy. Routine measurements of anti-HAV immunoglobulin M and HAV RNA during the early posttransplant period in HAV-associated liver transplant recipients may differentiate reinfection from an acute cellular rejection episode.
AB - Although hepatitis A virus (HAV) infection is usually self-limited, it may induce fulminant hepatitis. We present an unusual case of a 40-year-old, otherwise healthy man with intractable recurrent HAV infection requiring retransplantation after primary liver transplantation for HAV-associated fulminant liver failure. After the first living-donor liver transplantation, allograft function recovered uneventfully; however, beginning at 35 days, his serum total bilirubin concentration increased, reaching 40 mg/dL, with a slight increase in liver enzymes. Detection of genomic HAV RNA in serum at the time of graft dysfunction led to a diagnosis of recurrent HAV infection. Fifty-one days after the first transplant, he underwent a deceased donor retransplantation. His allograft function recovered; the patient was discharged from the hospital. Sixty-five days later, however, he was readmitted for colitis-like symptoms and was again treated for acute rejection, but died owing to overwhelming sepsis and persistence of HAV infection. These findings indicate that patients who undergo liver transplantation for HAV-associated liver disease may be at risk of HAV reinfection, particularly if they require anti-rejection therapy. Routine measurements of anti-HAV immunoglobulin M and HAV RNA during the early posttransplant period in HAV-associated liver transplant recipients may differentiate reinfection from an acute cellular rejection episode.
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U2 - 10.1016/j.transproceed.2010.09.151
DO - 10.1016/j.transproceed.2010.09.151
M3 - Article
C2 - 21168755
AN - SCOPUS:78650494399
VL - 42
SP - 4658
EP - 4660
JO - Transplantation Proceedings
JF - Transplantation Proceedings
SN - 0041-1345
IS - 10
ER -