I was transplanted in June 2000 - almost 7 1/3 years and I feel very good. I have read that the average lifespan for males is around 18 years from transplant and for females a few years longer. Those numbers may have been from the UK - I don't remember clearly but I think the numbers are close if not accurate. I know several people who were transplanted long before I was. I believe that the 7 year figure isn't even close to average. Mike
wow I didn't realize it had been that long since your TP - you seem to be doing remarkably well - Did you clear the virus prior to TP or after?
I was wondering about just hep c transplanted pt stat.I know lots of transplanted pt that are around for 20yrs and more but they were cured with the transplant whereas with hep c pt we are still fighting this virus within our body and use or try any method that will kill/retard this invading virus.
I cleared post transplant PSP.
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
thank-you for your comments.I'm sorry if I implied that HCV was the only dx that isn't "cured" by a transplant.My yearly boipsy showed cirrhosis 1 and activity 1.My Health care team feels treatment shouldn't start till staging is 2,I trust their judjment and have full confidience in them.I try not to worry about my condition and enjoy each day and expect to increase any data for longevity like you,your friends and all pts.I'm curious about the data.Have many more birthdays
This is from Clinical Care Options. A few days after transplant my surgeon told me not to trust anyone - even him. When we're under anesthesia we have to have trust but the rest of the time I check everything anyone tells me, if I have the time. I do not post this to upset you or to chip away at the confidence you have in your team but I do question their approach. If you are showing fibrosis after 16 months I don't see the upside of waiting for further liver deterioration. The numbers show that the predictive indicators with transplants who treat are roughly the same as non-transplants. A 2 log drop or undetectable at 12 weeks is a very strong positive predictor so you'd have a good idea if continuing treatment would be advisable and earlier PCRs would be even better and may save you enduring unsuccessful treatment time. Honestly, I don't get it. I don't know your overall situation and you may have contraindications but I certainly had several. I was treated for rejection 2 and maybe 3 times (I can't remember?) with intravenous steroids. I am diabetic and type 1b. Again, I don't want to upset you. I just think it is something that warrants research and thoughtful consideration.
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 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.
Here is a different view about treatment post transplant.
Fatal Liver Disease Despite Sustained Eradication of Recurrent Hepatitis C Virus Requiring Liver Retransplantation.
Transplantation. 82(2):286-288, July 27, 2006.
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.
I will question my medical team about starting Antiviral therapy. I'm type 1b,count 4.7 million.diabetic.AST 80,ALT 68,AP 113,INR 0.9,Bili 0.8 and Cr 0.8 GGT 416.All labs where stable till increases in AST,ALT,AP started increasing since 6/07. Never had a known rejection reaction.My team stated they don't follow GTT results.Will get back with update .
You're numbers look a lot better than mine looked 5 weeks post transplant. My bilirubin was out of range and my enzymes were in the hundreds. I wish you the best whichever way you go. I just think it is good to challenge your team occasionally. The squeaky wheel thing - you know. Be well, Mike
still would like to know that stat?