HCV-associated liver cancer without cirrhosis

Mitri, Marco Di; Pisi, E; Poussin, Karine; Paterlini, P.; Bréchot, Christian; Baccarini, Paola; D’Errico, Antonietta; Grigiani, W.; Alberti, Alfredo; Pontisso, Patrizia; Simon, Nicole; Beaugrand, Michel

doi:10.1016/s0140-6736(95)90400-x

Cited by 266 publications

(132 citation statements)

References 22 publications

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“…RNA extraction, reverse transcription polymerase chain reaction, and nested polymerase chain reaction were performed as previously described. 16 Primers were designed according to HCV Sequence Database (http://hcv.lanl.gov) to an amplified NS3 region containing NS3…”

Section: Methodsmentioning

confidence: 99%

Selection of high-avidity CD8 T cells correlates with control of hepatitis C virus infection

et al. 2008

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E fficient control of viral infections in various animaland human models depends on a wide array of mechanisms affecting swiftness and strength of antiviral cellular and humoral immune responses. Diversity of such mechanisms is highlighted by analysis of immune responses elicited by hepatitis C virus (HCV) in humans. Control of acute HCV infection correlates with strong, sustained, and broad virus-specific cellular immunity mediated by both CD4 and CD8 T cells. By contrast, HCV persistence has been associated with transient T cell responses in infected donors. 1 Two nonmutually exclusive mechanisms could explain inefficient immune control of HCV in chronically infected patients. Mutations of several HCV epitopes, described both in chimpanzees and humans, can lead to decreased viral recognition by CD8 T cells. [2][3][4][5] Functional decline of HCV-reactive T cells resulting from progressive loss of interleukin-2 (IL-2)

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Section: Methodsmentioning

confidence: 99%

Selection of high-avidity CD8 T cells correlates with control of hepatitis C virus infection

et al. 2008

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“…July 6,1990, for end-stage liver disease caused by chronic non A non B hepatitis and alcohol abuse. Ultrasonography before transplantation did not show a focal lesion.…”

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confidence: 99%

De novo hepatocellular carcinoma in a hepatic allograft with recurrent hepatitis C cirrhosis

Saxena

Emre

et al. 1999

Liver Transpl

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We report a case of de novo hepatocellular carcinoma (HCC) in a patient with recurrent hepatitis C (HCV) and cirrhosis 7 years after orthotopic liver transplantation (OLT). This is a previously unreported observation in the natural history of posttransplantantion HCV infection and reiterates the strong oncogenic potential of HCV. Copyright 1999 by the American Association for the Study of Liver DiseasesA 63-year-old white man underwent OLT on July 6, 1990, for end-stage liver disease caused by chronic non A non B hepatitis and alcohol abuse. Ultrasonography before transplantation did not show a focal lesion. Serum alphafetoprotein level was 10.1 mg/mL (normal, 20 mg/mL). The donor was a 65-year-old woman in whom the HCV status was not determined at the time of organ donation. The preperfusion and postperfusion liver biopsy specimens obtained around the time of transplantation showed lipofuscinosis, a finding consistent with the age of the donor, but there was no evidence of hepatitis. The explanted liver, sectioned every 0.5 cm, showed micronodular cirrhosis, moderate lymphocytic septal inflammation, mild piecemeal necrosis, and areas of multiacinar collapse. There was no malignancy. The patient was started on cyclosporine, 125 mg twice daily; azathioprine, 100 mg four times daily; and prednisone, 20 mg four times daily. Six months later, he had biopsy-proven hepatitis and positive HCV RNA in the serum detected by reverse-transcriptase polymerase chain reaction. Over the next 6 months, the hepatitis progressed to stage III, in transition to cirrhosis. The azathioprine dose was reduced to 75 mg four times daily 12 months after OLT and to 50 mg four times daily at 18 months. Two years after OLT, the prednisone dose was reduced to 5 mg four times daily. Three and one half years later, he was maintained on cyclosporine, 75 mg twice daily, and prednisone, 5 mg four times daily every other day, with no evidence of rejection. Blood cyclosporine levels were maintained at 150 to 200 mg/mL. He remained clinically stable for the next 6 years, when he underwent a second OLT for a decompensated liver. Ultrasonography before transplantation showed cirrhosis with a 1.4-cm solid hypoechoeic mass. Serum alphafetoprotein level was 73.6 mg/ mL.The explanted liver showed chronic hepatitis and cirrhosis, with a well-demarcated, hemorrhagic, and focally necrotic 1.5-cm nodule in the right lobe. Microscopically, this was a welldifferentiated HCC arising in a macroregenerative nodule. Fluorescent in situ hybridization for X and Y chromosomes showed the tumor to be XX, confirming its de novo origin in the engrafted liver. The patient died of sepsis 75 days after the surgery.

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“…Chronic hepatitis C virus (HCV) infection has been identified as the causative agent of different chronic liver diseases as well as hepatocellular carcinoma (HCC) (IARC, 1994), even in the absence of cirrhotic lesions (De Mitri et al, 1995). HCV infection has been associated with certain extrahepatic manifestations, particularly mixed cryoglobulinaemia (MC), membranoproliferative glomerulonephritis, porphyria cutanea tarda and, possibly, autoimmune thyroiditis and Sjogren's syndrome (Gumber and Chopra, 1995).…”

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confidence: 99%