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  • in reply to: Hard to treat Gt3 – Another stage of the journey #21468
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    • Guardian Angel
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    Gaj wrote:

    ……coconut oil? ugh!

    It’s either that or beef tallow <img style=ick:' />
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    in reply to: G1a relapse #21465
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    • Guardian Angel
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    I so hate this virus.

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    in reply to: Using Milk Thistle whilst on treatment. #21463
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    • Guardian Angel
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    It’s an anti inflammatory so it should help after treatment.

    The reason it was not recommended during interferon treatment is because interferon is PRO inflammatory. It’s how it elicits a reaction from the immune system. So Milk Thistle would work against it. It can also lower levels of some meds, but don’t ask me which because I don’t remember.

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    in reply to: Chlorcyclizine #21461
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    • Guardian Angel
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    Gaj wrote:

    *and be aware that the therapeutic dosage may differ from what is appropriate for use as an antihistamine.

    Dr F was thinking about using it so I asked Dr Dieterich if perhaps adding chlorcyclizine to DAAs could maybe increase success rate and would a dose of 75 mg at bedtime be enough in his opinion and he said….

    “While there is good invitro data there does not yet seem to be any human data for this so there is no dosage information or drug interaction data. So an abundance of caution would lead me to not recommend it yet. Good luck with it!”

    So I asked him if he thought a dose of 75mg would be enough and he said yes and to let him know how it went.

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    in reply to: Chlorcyclizine #21459
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    • Guardian Angel
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    Fitz, Dr Freeman was thinking about conducting a study using it.

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    in reply to: Red skin #21427
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    • Guardian Angel
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    I see it a different way Beaches.
    As Dr Ponzetto said sof IS a 5fluoro uracil-

    “Sofosbuvir is a phosphoramidate prodrug that is metabolized in the liver to β-d-2′-deoxy-2′-α-fluoro-2′-β-C-methyluridine-5′-monophosphate.”

    https://www.dovepress.com/changing-the-face-of-hepatitis-c-management-ndash-the-design-and-devel-peer-reviewed-article-DDDT

    Knowing exactly what you’re taking can help prevent, identify and treat side effects. For example, the literature says that skin redness can be helped by Pyridoxine (Vitamin B6). Obviously, everything should be checked with your doctor.

    https://books.google.com/books?id=CDADMzS0TKUC&pg=PA161&lpg=PA161&dq=5FU+and++cutaneousYHXuc2V0&hl=en&sa=X&ved=0ahUKEwi5qqnnhJLOAhUUT2MKHc4fArwQ6AEISTAG#v=onepage&q=5FU%20and%20%20cutaneous%20toxicity&f=false +toxicity&source=bl&ots=dNje7r1NGT&sig=RhgFPgLWtnXjAHO_po-

    in reply to: Red skin #21394
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    • Guardian Angel
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    One of the doctors on Research Gate says that since sofosbuvir is a 5fluoro uracil- like compound (5FU is a chemotherapy drug) then you can expect that side effects would be the same although in a much lesser degree, all side effects listed for 5FU are likely to appear….(and side effects include skin redness, plus delayed cancers and cardiac problems.)

    Here’s the conversation
    https://www.researchgate.net/post/any_suggested_papers_about_respiratory_side_effects_of_sofosbuvir

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    in reply to: Hard to treat Gt3 – Another stage of the journey #21314
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    • Guardian Angel
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    Gaj,
    “For people with genotype 3 though, the link between steatosis and the virus has now been definitively established. Up to 80% of people with genotype 3 have moderate to severe steatosis. It seems that that there is a complex interaction between the core protein of the genotype 3 strand of the virus and liver cells that leads to steatosis. This interaction is not seen in other genotypes. It also seems that the severity of steatosis in these patients is directly related to their viral load. The higher the viral load the greater the amount of steatosis.”

    Plus, the steatosis is around the portal areas, rather than in the middle of the lobules of the liver like the usual steatosis.

    http://hepatitiscnewdrugresearch.com/fatty-liver-and-hcv.html

    Reducing dietary saturated fat is associated with an increase in LDL-receptor abundance (which helps the virus multiply) of magnitude similar to the decrease in serum LDL-cholesterol (which is what happens with geno 3).

    So it looks like your new diet will have to include restriction of PUFAs in favor of big fat steaks, and eggs and bacon for breakfast instead of cereal, butter, coconut oil <img style=ick:' /> ….and treat during winter when chol is higher (because of seasonal variations in bile acids). :woohoo:

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    in reply to: My twinvir story #21306
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    Data shows that a 12 week is just as accurate as a 24 week test.

    But since you’ll probably continue to wonder, you could save the money and have a Qualitative Viral Load test at 24 weeks instead of monthly liver enzymes. It gives you a negative or positive result but I believe it’s cheaper than a Quantitative test. You can check with the lab in your country.

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    in reply to: Hard to treat Gt3 – Another stage of the journey #21293
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    Split dog, if you have genotype 1 which is associated with having insulin resistance and you’re overweight, then lowering your weight BEFORE you start treatment should help.

    Londongirl, thin people can also be insulin resistant and steatosis but obviously if you’re underweight then loosing weight would not be recommended. But diet can always be improved. I would concentrate on having less carbs and more protein if ok with your doc (since he’s the one familiar with your case).

    in reply to: Hard to treat Gt3 – Another stage of the journey #21219
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    • Guardian Angel
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    Gaj,
    I was thinking (yes, I know, I think too much)…what’s the one unique thing about genotype 3? The one thing that makes it different than all the others.

    The hepatic steatosis.

    So check out what I found…

    “Both the first and next generations of DAAs appear to be less effective against genotype 3 infections. Hepatic steatosis may be, at least in part, responsible for the persistently low rates of SVR associated with genotype 3. It may be that intrahepatic fat sequestration by the replicating virus reduces access of DAAs, thereby reducing the efficacy of these drugs.”

    And….

    “Importantly, lower baseline serum low-density lipoprotein (LDL) and lower expression of fatty acid metabolism and lipid transport genes at the end of treatment were associated with relapse, suggesting the relevance of host metabolism on treatment outcome with this DAA combination in genotype 1 HCV infection”

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4259863/

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    Gaj wrote:

    Although not able to access the full article yet, I see that 85% of them went on to acheive SVR after they had their liver transplant so presumably they became undetected? I wonder if having a compromised immune system prior to transplant was preventing them from clearing the stragglers that the DAAs hadn’t affected?

    Most of the patients weren’t able to finish treatment. Plus, they all used Ribavirin and people waiting for transplant are usually anemic so the Riba dose is usually lower. So this study taught us that suboptimal dosing and unfinished treatment in immunocompromised patients leads to small amounts of virus being left over. :lol:
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    GT2 wrote:

    It is easy to distinguish between those who have suffered from HCV and those who haven’t simply by the comments that they have posted.

    Oh come on, my answers weren’t that bad.
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    • Guardian Angel
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    Serg, I also think that you need to take into consideration whether you treated and failed treatment previously because studies have shown that may impact their health in the future.

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    Gaj wrote:

    Both the studies you list in the above quote are from 2004 and well prior to the development of modern DAAs such as Sofosbuvir, Ledipasvir, Daclatasvir, etc, etc. If you are going to cite studies to try to support your claims about the modern DAAs you need to provide more current information.

    Here’s a current one….

    HCV RNA Persists in Liver Explants of Most Patients Awaiting Liver Transplantation Treated With an Interferon-Free Regimen.

    http://www.ncbi.nlm.nih.gov/m/pubmed/27373513/#

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Viewing 15 posts - 1 through 15 (of 231 total)