Aa
transplants and cirrhosis
why does a clean transplanted liver go to cirrhosis so quickly when the recipient has HCV
I agree this is an extremely complex subject and I think each individual patient
also has his/her unique reasons.
My husband received his liver transplant in June, 2012. He was 66 years of age at the time. His donor was a young female of about 28. (May she rest in peace). His surgeon told me after the 6 hr surgery that the liver was "perfect".
Not long after we found out he was positive for CMV (the donor was positive and he was negative). They put him on Valcyte, which he took for many months. We also found out the HCV had returned after being undetected for 8 months prior to transplant. Two months after surgery we found out he had a blockage of the hepatic artery which led to significant bile duct damage.
They repaired the blockage with a vein from his leg but the damage to the billary tree we were told could not be repaired. They inserted two stents which worked for about five months until he was hospitalized for a bacterial infection. They removed the stents and decided not to replace them as they felt it was too risky for the bacterial infection (one of those superbugs) to return. That was 10 months ago. He started having symptoms of HE again 3 months later which has progressed to the point where he has been hospitalized twice, most recently two weeks ago. They did a liver biopsy then only to find his new liver now has cirrhosis, only a year and a half after transplant.
The pathologist said he believes the cirrhosis is half because of complications related to the billary tree damage and half due to the Hep C infection.
He has a followup appt with his doctor tomorrow. The plan is to start him on Sovaldi + Ribavirin for 24 weeks in January.
Your question was:
"why does a clean transplanted liver go to cirrhosis so quickly when the recipient has HCV"
My answer is transplants are very complicated surgeries. Things often happen that require follow-up "clean-up" procedures. Having recurrent HCV
certainly doesn't help the situation.
I'm sure that's why his doctor tried to rid him of the virus before transplant wth the triple treatment with Incivik despite him having Stage 4 Cirrhosis. Unfortunately, it didn't work and he decompensated.
Hopefully with the new treatments, having recurrent HCV after transplant will be a thing of the past very soon.
I hope the details of my husband's story will be helpful to someone out there.
Nan
also has his/her unique reasons.
My husband received his liver transplant in June, 2012. He was 66 years of age at the time. His donor was a young female of about 28. (May she rest in peace). His surgeon told me after the 6 hr surgery that the liver was "perfect".
Not long after we found out he was positive for CMV (the donor was positive and he was negative). They put him on Valcyte, which he took for many months. We also found out the HCV had returned after being undetected for 8 months prior to transplant. Two months after surgery we found out he had a blockage of the hepatic artery which led to significant bile duct damage.
They repaired the blockage with a vein from his leg but the damage to the billary tree we were told could not be repaired. They inserted two stents which worked for about five months until he was hospitalized for a bacterial infection. They removed the stents and decided not to replace them as they felt it was too risky for the bacterial infection (one of those superbugs) to return. That was 10 months ago. He started having symptoms of HE again 3 months later which has progressed to the point where he has been hospitalized twice, most recently two weeks ago. They did a liver biopsy then only to find his new liver now has cirrhosis, only a year and a half after transplant.
The pathologist said he believes the cirrhosis is half because of complications related to the billary tree damage and half due to the Hep C infection.
He has a followup appt with his doctor tomorrow. The plan is to start him on Sovaldi + Ribavirin for 24 weeks in January.
Your question was:
"why does a clean transplanted liver go to cirrhosis so quickly when the recipient has HCV"
My answer is transplants are very complicated surgeries. Things often happen that require follow-up "clean-up" procedures. Having recurrent HCV
certainly doesn't help the situation.
I'm sure that's why his doctor tried to rid him of the virus before transplant wth the triple treatment with Incivik despite him having Stage 4 Cirrhosis. Unfortunately, it didn't work and he decompensated.
Hopefully with the new treatments, having recurrent HCV after transplant will be a thing of the past very soon.
I hope the details of my husband's story will be helpful to someone out there.
Nan
Although this subject isn't completely understood we do know some factors that affect the transplant recipient.
The age of the donor is one factor. The older the donor the more severe the recurrent disease. The studies I have seen generally use 40 years as a cutoff point after which age the HCV recurrence is more severe. And it gets worse as the donor age gets higher - >50 and >60 years of age. My understanding is that this problem with older donor age isn't seen in liver transplants for non-HCV diseases.
The condition of the donor liver is also a factor and the longer the ischemic time the more severe the disease recurrence.
The immunosupression of the transplant recipient is another important factor. Steroid use can exacerbate the disease post transplant and particularly in those patients treated with bolus steroid intravenous injections for acute organ rejection. We know that a significant contributing factor in liver damage is due to the immune mediated response and the fact that the patient is immune compromised will affect that dynamic - and I readily admit that I don't fully understand this complex subject.
A higher viral load post transplant is another factor associated with disease severity. Diabetes in another negative factor.
The IL-28B gene polymorphism TT is associated with more severe HCV recurrence and poorer graft survival than CT or CC.
Genotype 1b is also associated with more severe HCV recurrence.
It's an extremely complex subject and the good news is that with the new treatment options available and more on the horizon transplants recipients hopefully can achieve SVR before significant histological damage occurs.
The age of the donor is one factor. The older the donor the more severe the recurrent disease. The studies I have seen generally use 40 years as a cutoff point after which age the HCV recurrence is more severe. And it gets worse as the donor age gets higher - >50 and >60 years of age. My understanding is that this problem with older donor age isn't seen in liver transplants for non-HCV diseases.
The condition of the donor liver is also a factor and the longer the ischemic time the more severe the disease recurrence.
The immunosupression of the transplant recipient is another important factor. Steroid use can exacerbate the disease post transplant and particularly in those patients treated with bolus steroid intravenous injections for acute organ rejection. We know that a significant contributing factor in liver damage is due to the immune mediated response and the fact that the patient is immune compromised will affect that dynamic - and I readily admit that I don't fully understand this complex subject.
A higher viral load post transplant is another factor associated with disease severity. Diabetes in another negative factor.
The IL-28B gene polymorphism TT is associated with more severe HCV recurrence and poorer graft survival than CT or CC.
Genotype 1b is also associated with more severe HCV recurrence.
It's an extremely complex subject and the good news is that with the new treatment options available and more on the horizon transplants recipients hopefully can achieve SVR before significant histological damage occurs.
My uneducated guess would be that the immune suppressants needed to keep a transplant patient from rejecting the liver would compromise the immune system and allow the virus to replicate more quickly and keep the body from putting up a good fight against the hepatitis. But, I have no basis for that and it is just a guess.
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