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*dip*
I don't have the numbers for HCV transplants off hand but I think yours is a relevant question. I think it is obviously much better to clear the virus, preferably before transplant but, if not, after transplant. The numbers I have see suggest that roughly 20% of HCV transplant recipients who don't treat will progress to fibrosis/cirrhosis within 5 years of transplant. I know several people who haven't progressed and one in particular who was transplanted in 1996 for HCV and never treated and has a low viral load and no liver damage. He was a type 1b. And there are autoimmune diseases that are not always cured with transplantation - Primary Sclerosing Cholangitis come immediately to mind since my friend has that disease. She has colitis as well so the grass isn't always greener. Have you ever treated? I know a lot of centers have been reluctant to initiate treatment but I believe the tide is changing somewhat. When I was done in 2000 the general consensus was that HCV transplants did as well without treatment as those transplanted for other underlying diseases but that is not the thinking today. Had I not become so ill immediately after my transplant I would probably not have treated. I started treatment about 6 weeks post transplant but I didn't really have a choice. My enzymes were flying as soon as I recovered from surgery. So I treated and treated and treated again and finally reached SVR. That's about all I know about it but I will try and find some hard numbers for you. Be well, Mike
See: http://www.tiny.cc/lxffl
When to Initiate Antiviral Treatment of HCV Recurrence Following Liver Transplantation
Nezam H. Afdhal, MD, FRCPI:
One of the main concerns in liver transplantation recipients is the recurrence of HCV posttransplantation. In fact, approximately 20% of patients develop aggressive fibrotic disease resulting in cirrhosis and other liver complications. This has led to a debate as to when to initiate interferon-based therapy in liver transplantation recipients with HCV recurrence: Should it be broadly used in patients with early disease or should treatment be delayed until patients have more advanced disease?
Carrion and colleagues[21] randomized a group of 54 posttransplantation patients with HCV recurrence and mild fibrosis scores of F0-F2 to no therapy or to peginterferon/ribavirin antiviral therapy for 48 weeks (Capsule Summary). A third group of 27 patients with advanced liver disease (fibrosis score F3-F4) also received antiviral therapy for 48 weeks. Patients underwent a liver biopsy at baseline and at Week 72.
Generally, the investigators showed that patients who responded to antiviral therapy by achieving a SVR and/or alanine aminotransferase normalization had a reduction in the degree of liver injury, indicated by decreased fibrosis on the biopsy and a reduced hepatic venous pressure gradient (HVPG). For patients with mild fibrosis at baseline, only 26% of treated patients demonstrated an advance in fibrosis by ≥ 1 stage compared with 70% of untreated patients (P = .0001). The investigators concluded that clinicians should consider administering antiviral therapy early in patients with HCV recurrence posttransplantation.
In my opinion, this study was fairly well done with good histology and HVPG measurements. The findings suggest that achieving an SVR with peginterferon/ribavirin posttransplantation predicts a significant improvement in morbidity, such as the effect seen on HVPG. A limitation of the study is that no information is available regarding the effect of treatment on survival or retransplantation rates, but this type of information takes years to accrue. Using a reduction in portal pressure as a surrogate for these outcomes is reasonable. As such, this is a very positive study, albeit somewhat small, and warrants larger multicenter studies in the posttransplantation population.
Kris V. Kowdley, MD, FACP:
These data are indeed encouraging. There is an inherent paradox in our current approach to recurrent hepatitis C among posttransplantation patients: Clinicians tend to treat patients with the most rapid and severe fibrosis most aggressively, and yet these individuals may be the least likely to respond to treatment. In my opinion, if treatment is initiated, then it should be done early rather than waiting until the patients have rapid and progressive fibrosis, as is the typical practice. This well-designed study suggests that patients with advanced fibrosis might benefit the least from treatment, as only 18.5% of these individuals achieved an SVR on peginterferon/ribavirin and 54.0% developed fibrosis progression despite treatment. The results of several similar long-term, randomized trials that are currently ongoing will be of great interest.
Josep M. Llovet, MD:
It is difficult to perform this type of randomized trial with a large number of patients posttransplantation, so data from small but well-designed studies such as this are important.
Fatal Liver Disease Despite Sustained Eradication of Recurrent Hepatitis C Virus Requiring Liver Retransplantation.
Brief Reports
Transplantation. 82(2):286-288, July 27, 2006.
Mukherjee, Sandeep
Abstract:
Liver retransplantation for recurrent hepatitis C is usually not recommended for patients with early, severe disease. As it is difficult to predict which patients are at risk, interferon-based therapies are often used after histological confirmation of recurrent disease. Unfortunately, this treatment is poorly tolerated, costly and often unsuccessful. Three patients are described who developed decompensated cirrhosis requiring retransplantation despite sustained viral eradication. With the exception of one patient who developed post transplant nonalcoholic steatohepatitis, no etiology was identified in the others. All were retransplanted and remain hepatitis C negative at a mean follow-up of 25.6 months. Despite a lack of alternatives, the reflexive urge to use interferon-based therapy for recurrent hepatitis C in an attempt to prevent retransplantation at all costs should be resisted, particularly as recent studies suggest onset of recurrent disease after initial transplant does not predict onset of recurrence following retransplantation.
(C) 2006 Lippincott Williams & Wilkins, Inc.