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Good luck and chin up
Mattie
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.
Be well
Mattie
Thanks for the concern
I wish you well
Mattie
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.
(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.
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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.