Fibrosing cholestatic hepatitis (FCH) is characterized by ballooning degeneration of hepatocytes with periportal fibrosis and abundant accumulation of viral antigen in the cytoplasm [1,2]. In recipients of solid‐organ transplants, FCH may result in rapidly progressive liver failure with mild abnormalities of serum aminotransferase levels. Clinically, most reported cases of FCH in transplant recipients are related to hepatitis B (HBV) or hepatitis C (HCV) infections, but its association with other hepatotoxic viruses has not previously been described [3,4]. With a respiratory route of transmission parvovirus B19 (B19) is the only member of the family Parvoviridae known to be a common cause of human infections worldwide. In healthy adults and children, B19 infections can cause erythema infectiosum and polyarthropathy syndromes [5]. It may also induce aplastic anaemia and liver dysfunction, which may range from mild biochemical abnormalities to liver failure [6–8]. We previously described a case of B19‐related acute hepatitis in an immunosuppressed patient with a renal transplant [9]. The pathologic changes in hepatic infections by B19, however, have not been well described. In the normal host, B19 is eliminated following production of specific IgG and IgM antibodies, which coincides with the disappearance of the virus from circulation. In renal transplant recipients, persistent B19 infections can be found along with serum positive for viral DNA even after intravenous immunoglobulin (IVIG) treatment [10–12]. We report here the first case of FCH possibly related to a persistent B19 infection in a renal transplant recipient undergoing immunosuppressive therapy.
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Shan et al. (2001) studied this question.
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