liver transplant

[Bucklaroo]

I had a liver transplant and am starting treatment tomorrow. Just wondering anyone had a transplant and beeing or been treated. How all  went??

[couchpotato]

My husband had a liver transplant in Nov. '04 and started tx 2 weeks ago. So far, so good. No major complaints, the usual aches and pains. Couple of other people here with transplants also, Mike Simon being one.

Good luck and chin up
Mattie

[Jeff88]

I had a liver transplant in 2002. I am on tx now wk 20. Sx are usual, fatique,
rash, irritability (riba rage). They also depend on type of interferon, pegasys is usually easier on you than infergen.

I saw Dr a few days ago. His concern is the danger of rejection. Interferon busts the immune system and it may result in rejection. Hopefully you are seeing a good dr who will keep you on the right amount of antirejection. It is all individual.

Best of luck with your treatment. Jeff.

[couchpotato]

Are you showing any signs of rejection? Big fear for me. Before tx was the hcv affecting your new liver?

Be well
Mattie

[Bucklaroo]

Yes the hep was killing my new liver already stage 2 chriosis. Also my enzimes had elevated from 77 to 300 in 1 month. Hoping the tx will clear these problems up
Thanks for the concern

[couchpotato]

Do you mind me asking when you had your TP? Husbands enzymes and blood work has all be perfect and TP center wanted to wait till his hep started affecting things before they wanted to treat, but he insisted on doing it before. Rejection is their main concern with tx. BTW he is geno type 2, so on a short course, which is a blessing.

I wish you well
Mattie

[BThompson4]

Know what you mean about the hep c (geno 1a) hitting hard after transplant.  I did great for a year and a half (enzymes in the 20s, normal bilirubin-- all liver numbers normal) after my Jan. 2001 transplant and then my viral load shot up and enzymes stayed around 100 and bilirubin jumped to an average of 2.5-3.0.  

Got to F2 fibrosis by June 2005, but now have "no significant fibrosis" per my biopsy taken during week 36 of treatment (150 mcg ped-intron and 1200 mg/daily riba), so my liver has benefited greatly from treatment so far.  Now in week 48; undetectable at week 22 so I am going 72 weeks.  Sides have been a pain but manageable.

I think immunosupression is increased a little during treatment.  I have been lucky and have never had any sign of rejection in the three of four biopsies I've had post transplant and the one done during treatment.

Hope you do well on treatment.  This board is a great source of information; lots and lots of help and good advice from the great people here.  Love to see your enzymes go down, something that is pretty common even early in treatment.

[hommeworks]

Watch that treatment **** 18months after my very  very successful transplant, my new liver showed stage1. My Dr. said getting on treatment early could stem the geno 1-b march and recover the stage 1 liver damage. Six months later I'm in a battle for my life with PTLD. Non-Hodgkins lymphoma. Its in my abs and in my brain. Simultanoius chemo and radiation treatment. Several near death deliveries to the hospital in coma. Watch that **** its poison.

[mikesimon]

I treated and have been SVR since June 2004. It took me three treatment tries and the last one was for 73 weeks but it was worth it. I had rejections shortly after transplant but never during treatment and I treated for almost 3.5 years. I have read that rejection can occur as a result of interferon but I know several transplant recipients who've treated and none had any rejection problems. And some are SVR which is encouraging. Good luck, Mike

[mikesimon]

Liver Transplantation in Hepatitis C Virus Patients - Outcomes, Antiviral Strategies, Detection and Immunosuppression
(http://www.medscape.com/viewarticle/555660_3)

HCV is the single most common indication for liver transplantation in the US [15]. Recurrent HCV-related cirrhosis is accelerated in the immunosuppressed individual and develops in 8-44% of patients within 5-7 years [16].

The best strategy to prevent severe posttransplant recurrence of HCV is to eliminate the virus before transplantation. Antiviral therapy of HCV with interferon and ribavirin is, however, difficult to tolerate, and is associated with poor response rates in patients with decompensated cirrhosis [17]. The International Liver Transplant Society Consensus Conference suggested that patients with decompensated cirrhosis and a MELD score of less than 18 could be considered for antiviral therapy [18].

The mainstay of antiviral therapy for HCV after liver transplantation remains the combination of interferon and ribavirin. A recent systematic review of interferon-based combination antiviral therapy for HCV after liver transplantation showed pooled sustained viral response rates of 24% (95% confidence interval 20-27%) for regular interferon + ribavirin and 27% (95% confidence interval 23-31%) for pegylated interferon + ribavirin [19]. Discontinuation rates were 24-26%, although dose reductions were performed in up to 60%. No therapeutic advantages were seen for pegylated interferon as compared to regular interferon, as is seen in nontransplant HCV infection. More research is needed to evaluate the etiologies of this poor response with pegylated interferon after liver transplantation and to improve response rates/reduce the high relapse rates. Longer-term studies are lacking to see if the sustained responders have reduction in fibrosis over time. Trials of novel better tolerated antiviral agents (protease inhibitors) with and without interferon are needed in transplant patients in an attempt to improve the dismal outcomes associated with recurrent HCV disease.

Retransplantation of HCV-infected recipients continues to be debated. Retransplantation within 1 year of primary transplantation is associated with significantly reduced survival compared to later retransplants. In a retrospective study of 131 HCV-positive liver transplant recipients, the mean survival time from the time of retransplantation was 9.6 ± 3.3 months when retransplantation was in the first year and 24.5 ± 7.5 months when retransplantation took place after a longer interval [20].

An exciting development has been in the use of gene array technologies to identify gene expression patterns that may be associated with early progression to fibrosis [21]. In patients with early liver fibrosis due to HCV infection posttransplant, genes associated with the interferon-mediated antiviral system and the antigen-presenting and cytotoxic response to HCV infection were not upregulated in response to HCV infection. In the future, these patterns may be useful for early detection of 'rapid fibrosers'.

At present it remains difficult to differentiate HCV recurrence from allograft rejection by histopathology, since venous endotheliitis, bile duct inflammation and portal inflammation are present in both. Several studies have evaluated various markers in liver tissue to differentiate allograft rejection from recurrent HCV. One such marker is C4d staining of hepatic tissue which has been shown to be positive in rejection, but not in recurrent HCV. The deposition of C4d in portal capillaries and on sinusoidal endothelial cells is a marker of activated humoral immunity and activated complement cascade. Its role in demonstrating rejection in renal and cardiac transplant patients is well established [22]. In one study of 97 liver transplant recipients, 67.7% with rejection displayed C4d staining in the liver biopsy compared to only 11.8% of patients with HCV reinfection and 6.9% of controls [23]. Two other smaller studies have reported similar results with C4d staining [24,25]. Larger prospective studies with multiple comparison groups are needed to identify the accuracy of this test.

In recent years the rate of severe recurrence of HCV after transplantation appears to have increased [26]. Factors identified for more severe recurrence include multiple steroid pulses for treatment of rejection, rapid steroid tapering, high pretransplant HCV viral load, older donor age and increased histological activity early after transplant in the first year [27-33]. With increasing trends to accept older donors, this problem may be compounded in HCV positive recipients [34,35].

More potent recent immunosuppressants such as tacrolimus and mycophenolate may be detrimental for HCV [26,36]. Recent intriguing reports have shown that cyclosporine may have an additive antiviral effect on HCV when combined with interferon - an effect that is not seen with tacrolimus [37]. This study as well as others have also shown an antiviral effect of cyclosporine in HCV replicon models [37,38]. Azathioprine has also been shown to have an anti-HCV effect in the replicon model [39]. Most studies, however, have reported no differences between cyclosporine and tacrolimus in HCV outcomes posttransplantation [40-42]. Confirming the potential for specific immunosuppressant combinations to have a salutary effect on HCV progression in liver transplant recipients awaits better clinical trials of appropriate power and duration.
Previous Page
Section 3 of 7
Next Page: Hepatocellular

[savitri]

i am suffering frm primary bilary liver chriosis & treatment is gng since 2003,their is sum improvement but still skin tone has not cleared & its getting darker,there is also burning sensation in my feets & pain in my legs............do suggest wht is to be done...........

[savitri]

i am suffering frm primary bilary liver chriosis & treatment is gng since 2003,their is sum improvement but still skin tone has not cleared & its getting darker,there is also burning sensation in my feets & pain in my legs............do suggest wht is to be done...........

[Dayzdreamer]

I know a friend that had a liver transplant. The trasplant went well. After 9 months she showed the HCV again. Was put on a 24 month treatment and was one of the lucky ones that cleared the virus. She was genotype 1a.  If you didn't know you would think there was nothing wrong with her.

Each individual is different and no one knows what will happen until you try it and find out. I wish you the best in your treatment to clear the virus.