Related Articles

Hepatitis C.

Semin Liver Dis. 2009 Feb;29(1):53-65

Authors: Burra P

Hepatitis C virus (HCV) is a leading cause of end-stage liver disease worldwide and the most common indication for liver transplantation in the United States and Europe. HCV nearly always recurs in liver-transplanted patients, and 10 to 25% of them develop cirrhosis within 5 to 10 years. One of the strategies suggested to limit virological HCV recurrence is pretransplant antiviral treatment, but studies are warranted on the pharmacokinetics of antiviral drugs in cirrhotic patients, the benefits of fixed or escalating antiviral drug dosage schedules, the duration of the treatment, and the indications for using growth factors. Several risk factors are associated with a more aggressive recurrent HCV and early allograft failure, such as an older donor age. The relationship between immunosuppression and fibrosis progression in HCV recurrence remains uncertain. Concerning the antiviral treatment, treating established recurrent disease with a combination of interferon and ribavirin has been the mainstay of management to date, but when it is best to start and how to manage the side effects are still controversial issues. Antiviral treatment should be started once the disease has been confirmed by a biopsy when the fibrosis develops, providing that ongoing acute or chronic rejection, biliary obstruction, vascular damage, autoimmune diseases and sepsis, and any other standard contraindications for antiviral therapy, have been excluded. HCV recurrence after liver transplantation may well lead to graft failure and become an indication for retransplantation, but this is done in a relatively small number of cases, accounting for only 3 to 5% of retransplanted patients, since retransplantation is associated with much worse results than primary liver transplant procedures. We must be prepared for the fact that increasing numbers of HCV-positive recipients with allografts failing due to recurrent HCV will be asking to be retransplanted-and we do not know yet how to respond to this request.

PMID: 19235659 [PubMed - indexed for MEDLINE]

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Budd-Chiari syndrome.

Semin Liver Dis. 2008 Aug;28(3):259-69

Authors: Plessier A, Valla DC

Primary Budd-Chiari syndrome is related to thrombosis of hepatic veins or the terminal portion of the inferior vena cava. This rare disease is usually caused by multiple concurrent factors, including acquired and inherited thrombophilias. Half of the patients with primary Budd-Chiari syndrome are affected with a myeloproliferative disease, the recognition of which is largely based on the assessment of V617F Janus tyrosine kinase 2 (JAK2) mutation in peripheral granulocytes. A diagnosis of Budd-Chiari syndrome should be considered in any patient presenting with acute or chronic liver disease, as clinical manifestations are extremely diverse. Spontaneous outcome in symptomatic patients is poor. Diagnosis can be made in most patients noninvasively when imaging shows venous obstruction and/or collaterals. A treatment strategy is recommended where anticoagulation is given first, followed by angioplasty when appropriate, then TIPS in patients not responding to previous measure, and finally liver transplantation. This strategy has achieved 5-year survival rates close to 90%.

PMID: 18814079 [PubMed - indexed for MEDLINE]

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