s necessary to change it now since Epivir works well with me (my DNA is 200 copies). But he was worried about resistance and mutation. Do I have to listen to him? I got Viread today but I am not sure I would start taking it from today.
-Natalie
p.s.: Do you guys drink coffee? I started drinking coffee about 4 months ago...Do you think coffee would make my liver stressed???
(20) The T69S insertion mutations, associated with resistance to multiple nucleoside analogues, are associated with resistance to tenofovir as well. Tenofovir resistance conferred by the T69S mutation or by multiple thymidine analogue resistance mutations appears to be multiplied if the M184V mutation is replaced by wild-type.(21) The K65R mutation, which may be selected by prior nucleoside analogue therapy, is associated with a modest decrease in sensitivity to tenofovir.
Hi, I don't know the answer -- but since both CML and Gleevec toxicity produce anemia because of marrow suppression, maybe it's not possible to tell the difference. E.g., both would show a low reticulocyte count.
This full text paper on anemia from Gleevec https://onlinelibrary.wiley.com/doi/full/10.1002/ajh.23879 shows that other signs such as red blood cell size can vary, so that doesn't seem to help. Sorry.
Objectives
The aim of this study was to characterise a novel HBV pattern which shows resistance to lamivudine, adefovir dipivoxil and entecavir using in vitro phenoyping assay.
Study design
A male 36 years old patient diagnosed with anti HBe-positive chronic hepatitis B (CHB) had received lamivudine treatment for 7 years following an initial unsuccessfull interferon treatment. The therapy had been switched to adefovir and then to entecavir when breakthrough occcured during each treatment.
Is it possible that after taking gleevec for only two weeks WBC droped from 36.7 to 7? All other blood counts are also came back to normal range. Could doctor make mistake in diagnosis of CML? Maybe I should get seg second opinion?
What is the risk of double pc mutation at g1896a and c1858t combined with bcp mutation at a1762T and G1764A with Genotype C. It seems I am really @#$$@#$ . Will these 2 combinations create antiviral resistance?
I was diagnosed with CML and given Gleevec 400 ml. After taking gleevec for 2 weeks doctor took additional blood test. My WBC dropped from 36.5 to 7.1 and all other blood counts came down to normal range. I'm wondering if gleevec could give such fast hematological response or I was possibly misdiagnosed originally. I don't and didn't have any symptoms, my spleen and liver weren't enlarged, no enlarged lymph. Should I get second opinion asap? Please, help me.
three patients infected with HBV genotype C had the rtM204V + rtL180M mutations associated with lamivudine (LMV) resistance. Four patients had the rtI233V mutation that may reduce sensitivity to adefovir, and three patients had the rtM250L/V mutation typical of entecavir resistance. LMV compensatory mutations rtL80V and rtV173L were seen in two and one patients, respectively.
After two weeks on 400mlg gleevec my WBC droped from 36.5 to 7.1. My doctor told to come for additional test in two weeks. Now my WBC is 1.3 and absolute neutrophils count is 0.04. I was told to stay home on antibiotics. How long it may take for my counts to clime back to safe range. And of course, I'm off gleevec right now. Does it seem that dose of 400mlg is too high for me.
because etv is still active on many strains except those resistant for which tdf will work, after sometime stable on the combo yo may go tdf only, maybe they keep the combo to avoid any possible mutation of resistance to tdf too, etv will protect you from that being active on tdf resistance strains
However, this patient experienced virological breakthrough under TDF with a HBV strain bearing rtL80M, rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A, rtT184A/L, rtR153Q, and rtV191I combined mutations without rtA194T mutation. TDF resistance may emerge due to multi-site polymerase mutations rather than single-site polymerase mutation.
Ann8 just like with hepsera, if a primary resistance mutation to Tenofovir would occur, the simultaneous LAM will suppress the propagation of this mutated species, preventing it to get to higher numbers. This always is based of course on the assumption that no a priory LAM mutation is in existence. Thus now after many years it is now routinely recommended to start hepsera together with LAM.
Recently I asked the study nurse at my site to ask for the viral mutation data from my prove 3 bloods.
I became low detectable during week 8 and it went up by week 12.
My last draw I was told would include a virus sequencing (to determine the mutuations I think).
I would like to have this info it could be important to know for my next attempt (if it is a protease tx and if there are the strong resistant virus type I can forget about it).
take tenofovir immediately, if you have finiancial problems or cannot have it in nigeria you can look for tenvir generic from cipla
also combo with nitazoxanide if you find lam mutation resistance, both tenofovir and nitazoxanide are active against lam mutants
lam resistance muattion can lower response to other drugs this is why i suggested combo tnf+ntz
in theory ntz is active against all mutations since acts on immune system, not the virus, by now we have vitro studies on lam and adv mutatio
Am on Gleevec 400mg, now having problems with blisters on the palm. What can I do about it?
A COMPLEX HBV QUASISPECIES IN RT AND HBSAG CHARACTERIZES PATIENTS WITH ACUTE HEPATITIS B: A REFINED UDPS ANALYSIS Print
M. Aragri1, N. Coppola2, C. Alteri1, C. Minichini2, A. Battisti1, C. Sagnelli3, M.C. Bellocchi1, M.A. Pisaturo2, R. Salpini1, M. Starace2, F. Continenza4, D. Armenia1, L. Carioti1, M. Pollicita1, E. Sagnelli2, C.F. Perno1,5, V.
I wonder if being bc / pc mutation will cause fast resistance to telb. Will it also create polymerase resistance? I feel like I might need to choose between the lesser of 2 evils.
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