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my local doc said for me to go to the liver transplant doctor and get established with him.
He knows them and he said he doesn't believe that they will want to try treatment until after I have a transplant. Anyway more waiting I guess. I'm going to try to get in to see the transplant doc asap. Thanks for all the input. I'll keep y'all up on what the docs say.
plat ct of 85,000 is not to low to treat. I started tx with a 123,000 plat ct that dropped to 50,000 during tx. My hep said he did not get concerned til it gets down to the 30,000 range. Is your cirrhosis compensated or decompensated? Have you seen a hepatologist yet?
Also a stage 4 grade 2. My platelets bounce around between 80,000 and 100,000 just started a trial for relapsers, 85,000 would have just got me by.. Though you will need a good hepatologist to get you in, BTW from hepos i have talked with including my own 10% cure rate is a little low.... Best to you
Waiting to get an appointment with transplant doc in New Orleans. I will talk to him about treatment then. Thanks for the support and I'll keep y'all up on what they say.
I am in the relapser trial with boceprevir, and yes it states platelet level cut off is 100,000. But schering has a 10% lead-way so they on their own will let you be at 90,000. But the final decision rest with your hepatologist if he/she feels its safe at a lower level schering will go with it. Mine had no problem at 85,000 would he went to 80,000??? Not sure but i believe he would have.
This was a major concern for me so i had called the 888 number for the trial at clinicaltrials and then confirmed this info with my doctor. A CBC 30 days before my screening had me at 80,000. All become a mute point because the day of my screening my level was right at 100,000. Best to you
Also the trial requires an ultra sound, But my Hepo doesn't much care for the ultra sound and insteads has his patients have either a CT scan or MRI. Sense i had just had a upper gi and CT scan schering saw it is way and decided to drop the ultra scan requirement for patients that had the scan.
I'm not in any trial. I'm still waiting to talk to the transplant docs and see if they think I will be able to do any treatment before transplant. That's what really ***** for me is that I think I'm just going to have to sit around and do nothing until I get sicker and then get a transplant. Anyway, I'll keep y'all up on what the docs say. I started antidepressants so maybe they will take the edge off and everyone keeps telling me to just focus on 1 day at a time. I have ultrasound set up for tomorrow.
World J Gastroenterol. 2008 Nov 14;14(42):6467-72.
Antiviral therapy in hepatitis C virus cirrhotic patients in compensated and decompensated condition.
Iacobellis A, Ippolito A, Andriulli A.
"Casa Sollievo della Sofferenza" Hospital, IRCCS, viale Cappuccini 1, San Giovanni Rotondo 71013, Italy. a.***@****.
The main goals of treating cirrhotic patients with antiviral therapy are to attain sustained viral clearance (SVR), halt disease progression, and prevent re-infection of the liver graft. However, while the medical need is great, the use of interferon and ribavirin might expose these patients to severe treated-related side effects as a large proportion of them have pre-existing hematological cytopenias. We have reviewed potential benefits and risks associated with antiviral drugs in patients with liver cirrhosis, due to hepatitis C virus (HCV) infection. In cases presenting with bridging fibrosis or cirrhosis, current regimens of antiviral therapy have attained a 44%-48% rate of SVR. In cirrhotic patients with portal hypertension, the SVR rate was 22% overall, 12.5% in patients with genotype 1, and 66.7% in those with genotypes 2 and 3 following therapy with low doses of either Peg-IFN alpha-2b and of ribavirin. In patients with decompensated cirrhosis, full dosages of Peg-IFN alpha-2b and of ribavirin produced a SVR rate of 35% overall, 16% in patients with genotype 1 and 4, and 59% in those with genotype 2 and 3. Use of hematological cytokines will either ensure full course of treatment to be accomplished with and prevent development of treatment-associated side effects. Major benefits after HCV eradication were partial recovery of liver metabolic activity, prevention of hepatitis C recurrence after transplantation, and removal of some patients from the waiting list for liver transplant. Several observations highlighted that therapy is inadvisable for individuals with poor hepatic reserve (Child-Pugh-Turcotte score >= 10). Although SVR rates are low in decompensated cirrhotics due to hepatitis C, these patients have the most to gain as successful antiviral therapy is potentially lifesaving.
Best wishes,
Ev
He knows them and he said he doesn't believe that they will want to try treatment until after I have a transplant. Anyway more waiting I guess. I'm going to try to get in to see the transplant doc asap. Thanks for all the input. I'll keep y'all up on what the docs say.
This was a major concern for me so i had called the 888 number for the trial at clinicaltrials and then confirmed this info with my doctor. A CBC 30 days before my screening had me at 80,000. All become a mute point because the day of my screening my level was right at 100,000. Best to you
cando
World J Gastroenterol. 2008 Nov 14;14(42):6467-72.
Antiviral therapy in hepatitis C virus cirrhotic patients in compensated and decompensated condition.
Iacobellis A, Ippolito A, Andriulli A.
"Casa Sollievo della Sofferenza" Hospital, IRCCS, viale Cappuccini 1, San Giovanni Rotondo 71013, Italy. a.***@****.
The main goals of treating cirrhotic patients with antiviral therapy are to attain sustained viral clearance (SVR), halt disease progression, and prevent re-infection of the liver graft. However, while the medical need is great, the use of interferon and ribavirin might expose these patients to severe treated-related side effects as a large proportion of them have pre-existing hematological cytopenias. We have reviewed potential benefits and risks associated with antiviral drugs in patients with liver cirrhosis, due to hepatitis C virus (HCV) infection. In cases presenting with bridging fibrosis or cirrhosis, current regimens of antiviral therapy have attained a 44%-48% rate of SVR. In cirrhotic patients with portal hypertension, the SVR rate was 22% overall, 12.5% in patients with genotype 1, and 66.7% in those with genotypes 2 and 3 following therapy with low doses of either Peg-IFN alpha-2b and of ribavirin. In patients with decompensated cirrhosis, full dosages of Peg-IFN alpha-2b and of ribavirin produced a SVR rate of 35% overall, 16% in patients with genotype 1 and 4, and 59% in those with genotype 2 and 3. Use of hematological cytokines will either ensure full course of treatment to be accomplished with and prevent development of treatment-associated side effects. Major benefits after HCV eradication were partial recovery of liver metabolic activity, prevention of hepatitis C recurrence after transplantation, and removal of some patients from the waiting list for liver transplant. Several observations highlighted that therapy is inadvisable for individuals with poor hepatic reserve (Child-Pugh-Turcotte score >= 10). Although SVR rates are low in decompensated cirrhotics due to hepatitis C, these patients have the most to gain as successful antiviral therapy is potentially lifesaving.