Fibrosing cholestatic hepatitis in patient with HIV and hepatitis B

Fang, JaneW.S.; Wright, T L; Lau, J. N.

doi:10.1016/0140-6736(93)92160-u

Cited by 71 publications

(33 citation statements)

References 4 publications

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“…Case reports have suggested that HIV may accelerate the course of HCV-related as well as HBV-related liver disease in selected patients (3,20). A large prospective study of hemophiliacs also suggests that HIV accelerates the clinical course of HCV-related liver disease and that liver failure produces significant morbidity and mortality in patients coinfected with HCV and HIV (4).…”

Section: Discussionmentioning

confidence: 96%

Hepatitis C in Hiv–Infected Patients With and Without Aids: Prevalence and Relationship to Patient Survival

et al. 1994

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Background: Limited information is available about the prevalence of hepatitis C virus in patients with human immunodeficiency virus in relation to specific risk factors or about the influence of hepatitis C virus coinfection on survival. This retrospective study addressed these questions. Methods: The study population consisted of 512 predominantly non-intravenous drug-using male homosexuals, 224 of whom had AIDS. Samples positive for hepatitis C virus antibody by second-generation enzyme immunoassay were further tested by means of strip immunoblot assay, and for hepatitis C virus RNA by means of polymerase chain reaction amplification. A randomly selected set of enzyme immunoassay-negative samples was also tested for hepatitis C virus RNA and, if hepatitis C virus RNA positive, by a second-generation recombinant immunoblot assay. Results: The prevalence of hepatitis C virus infection unaccounted for by intravenous drug use or transfusion was 11.7% by enzyme immunoassay, and 87% of sera positive by enzyme immunoassay were also positive by second-generation recombinant immunoblot assay or hepatitis C virus RNA analysis. Hepatitis C virus RNA was detectable in 53% of enzyme immunoassay-positive samples but in only about 1% of enzyme immunoassay-negative samples. Hepatitis C virus coinfection did not influence survival of HIV-infected patients with or without manifestations of AIDS. Conclusions: Hepatitis C virus infection in nontransfused, non-intravenous drugusing patients with HIV infection is several times more prevalent than in volunteer blood donors, suggesting homosexual transmission of hepatitis C virus. About

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Section: Discussionmentioning

confidence: 96%

Hepatitis C in Hiv–Infected Patients With and Without Aids: Prevalence and Relationship to Patient Survival

et al. 1994

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“…[1][2][3][4] It has been closely associated with immunosuppression within the setting of liver transplantation, whereas a direct cytopathic effect of massively accumulated hepatitis B virus (HBV) antigens has been implicated in its pathogenesis. FCH has been reported sporadically in other immunocompromised patients infected with HBV, including renal graft recipients, [5][6][7][8][9][10] as well as a few transplant patients with hepatitis C virus (HCV) infection, in particular in 4 liver transplant recipients, 11 1 heart transplant recipient, 12 and recently in 1 renal transplant recipient. 13 These observations indicate FCH does not exclusively occur in liver allografts and HBV is not the only hepatotropic virus involved in the pathogenesis.…”

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confidence: 99%

Fibrosing cholestatic hepatitis in renal transplant recipients with hepatitis C virus infection

et al. 1999

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Fibrosing cholestatic hepatitis (FCH) has been described as a specific manifestation of hepatitis B virus (HBV) infection in liver allograft recipients characterized by a rapid progression to liver failure. Only sporadic cases have been reported in other immunocompromised groups infected with HBV and in a few transplant recipients with hepatitis C virus (HCV) infection. We present the occurrence of FCH in 4 HCV-infected renal transplant recipients within a series of 73 renal transplant recipients with HCV infection followed up closely serologically and with consecutive liver biopsies. All 4 patients received the triple-immunosuppressive regimen (azathioprine, cyclosporine A, methylprednisolone). The interval from transplantation to the appearance of liver dysfunction was 1 to 4 months and to histological diagnosis, 3 to 11 months. The biochemical profile was analogous to a progressive cholestatic syndrome in 3 patients, whereas the fourth patient had only slightly increased alanine aminotransferase and ␥-glutamyl transferase (␥GT) levels. Liver histological examination showed the characteristic pattern of FCH in 2 patients, whereas the other 2 patients had changes compatible with an early stage. All patients were anti-HCV negative at the time of transplantation, whereas 2 patients, 1 with incomplete and 1with complete histological FCH features, seroconverted after 3 and 31 months, respectively. The patients were HCV RNA positive at the time of the first liver biopsy and showed high serum HCV RNA levels (14 to 58 ؋ 10 6 Eq/mL, branched DNA). HCV genotype was 1b in 3 patients and 3a in 1 patient. After histological diagnosis, immunosuppression was drastically reduced. Two patients died of sepsis and liver failure 16 and 18 months posttransplantation, whereas the seroconverted patients showed marked improvement of their liver disease, which was histologically verified in 1 patient. In conclusion, FCH can occur in HCV-infected renal transplant recipients. It seems to develop as a complication of a recent HCV infection during the period of maximal immunosuppression and is associated with high HCV viremia levels. There are indications that drastic reduction of immunosuppression may have a beneficial effect on the outcome of the disease.

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“…9 The risk of developing FCH is increased if HCV or HBV patients are co-infected with HIV. [5][6][7] The histopathological changes are characterized by (i) extensive periportal and/or perisinusoidal fibrosis, (ii) marked hepatocyte ballooning (swelling), (iii) severe intracellular and canalicular cholestasis, (iv) minimal infiltration by inflammatory cells, and (v) cholestasis accompanied by an extensive periportal ductular reaction as has been noted in this patient. The distribution and severity of fibrosis is variable, it ranges from minimal, thin periportal, and perisinusoidal collagen fibers, to a diffuse and extensive periportal and panlobular pericellular distribution.…”

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confidence: 95%

“…Clinically, FCH has a rapid course characterized by severe jaundice, coagulopathy and hepatic encephalopathy, and death may ensue within 4-6 weeks of onset. 1 It was originally described by Davies et al in 1991 in a hepatitis B virus (HBV)-infected recipients of liver allografts 2 and has been reported in chronic hepatitis B or C patients who are under immunosuppression, 3,4 in patients with acquired immunodeficiency syndrome (AIDS) co-infected with hepatitis C virus (HCV) or HBV, [5][6][7] in renal transplant recipient with cytomegalovirus (CMV) infection, 8 and in those who have chemotherapy-induced immunosuppression. 9 The risk of developing FCH is increased if HCV or HBV patients are co-infected with HIV.…”

mentioning

confidence: 99%

Fatal Hepatitis C in a Renal Transplant Recipient on Immunosuppression: Fibrosing Cholestatic Hepatitis

2012

Journal of Clinical and Experimental Hepatology

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Fibrosing cholestatic hepatitis in patient with HIV and hepatitis B

Cited by 71 publications

References 4 publications

Hepatitis C in Hiv–Infected Patients With and Without Aids: Prevalence and Relationship to Patient Survival

Hepatitis C in Hiv–Infected Patients With and Without Aids: Prevalence and Relationship to Patient Survival

Fibrosing cholestatic hepatitis in renal transplant recipients with hepatitis C virus infection

Fatal Hepatitis C in a Renal Transplant Recipient on Immunosuppression: Fibrosing Cholestatic Hepatitis

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