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Hello,
Your results look like this is an acute (recent) infection. This is because you HCV antibody is not present but virus has been confirmed by PCR.
But…
I can see you have previously treated. If you are well waiting would certainly be an option but cure should be simple.
Very low viral load suggests very weak form of virus.
YMMV
I like the pack of straws analogy for probability.
I explain 90% as being like pickingfrom a pack of 10 straws. 1 person gets the short one, 9 don’t.
When I grew up straws were more common than revolvers and Russian Roulette. The scene from the movie “The deer hunter” put me off that game. Great guitar tune though….
[video]https://youtube.com/watch?v=sA_qnNrVelc[/video]
YMMV
Hi Fitz,
Thanks for the I am my own trial info!
Hi Bob,
The HCV replicons take 6 weeks to break down so for anything to have use you need 6 weeks (ish). Monotherapy with anything like DAAs is a bad idea. For chlorocyclizine it probably won’t hurt because it is host based but it is unlikely to be effective.
YMMV
Hi Paul,
Sorry to hear that. Sadly 95% is not 100% branded or generic.
It’s not as simple as “just take this for that many weeks”. It really is some thing to discuss with someone expert at length with past treatments and response, fibrosis, other medications, as well as your budget to consider. There is quite a lot of information on the forum about retreatment so rather than repeat it here please type “retreatment” and “relapse” into the search box to find the relevant stuff. Here are a couple of good threads to get started…
http://fixhepc.com/forum/retreatment-corner.html
http://fixhepc.com/forum/fixhepc-admin/1047-options-for-retreatment.html
YMMV
Hi Oscar,
Unless you are near death sick I would adopt a waiting brief on this. Really, even if you are very unwell, and have a MELD > 15 I would treat with DAAs first and see where you are then.
The mechanism of action is caspase inhibition preventing apoptosis which is natural cell death, used for many purposes including killing cancer cells. It would be surprising (to me at least) if this medication did not result in higher HCC rates in cirrhotics.
YMMV
Hi Serg,
I was sitting in the room when this was presented:
In the Italian study, medical records of 344 HIV-negative patients with HCV related cirrhosis, who did not have active HCC, were analysed. All patients had received treatment with one of the following DAA combinations: sofosbuvir and simeprevir (34%), 3D combination* (22%), sofosbuvir and ribavirin (17%), sofosbuvir and daclatasvir (16%) and sofosbuvir and ledipasvir (10%). Occurrences of HCC were assessed by comparing baseline enhanced-ultrasonography and MRI/CT-scans with those taken during the six month post treatment follow-up.
Sustained virologic response was achieved in 89% of patients at 12 weeks post treatment. At 24 weeks post treatment, active HCC was detected in 7.6% of all patients (n=26) without a history of HCC – deemed to be a ‘standard rate’ by the study authors. However, in the 59 patients who had a previous history of HCC, a ‘high rate’ of 29% (n=17) redeveloped the condition.
Which is not the study you are looking at. The upshot was that in cirrhotics the headline numbers were:
1) 7.6% for all participants (26/344)
2) 29% for those who had previously had an HCC (17/59)
3) 3.1% for participants who had not had an HCC before (26-17=9)/(344-59=285) ie 9/285All participants were assessed with MRI for current HCC prior to starting, and patients with a past history of HCC were not excluded.
Unfortunately although Interferon may provide some HCC protection when it comes to all cause death patients who have a second round of interferon have a 9.7% mortality rate compared to 6.4% taking placebo so the interferon adds ~ 3.3% mortality, and you still have the HCC risk from the cirrhosis.
YMMV
Interferon is anti lots of things. Anti-cancer and anti-viral being two. Unfortunately it makes people feel sick.
The problem for you Serg, it that it’s not the drugs that cure Hep C that cause the problem, which I believe is likely to be real. It’s the curing the cell death by curing the Hep C, so now, or at any time in the future, treatment will present this risk, but, the evidence suggests fibrosis is progressive (after all you start at F0) and that only cirrhotics are impacted. You could extrapolate and suggest more cirrhosis == more risk, after all cirrhosis is a line in the sand – under this number and you are not, over and you are. Risk, like fibrosis is likely to be a spectrum.
http://www.medsci.org/v03p0047.htm
Studies have estimated the 3, 5, and 10-year survival rates of compensated cirrhosis to be 96%, 91%, and 79%, respectively. [51] . The cumulative probability of an episode of clinical decompensation is 5% at 1 year, and increases to 30% at 10 years from the diagnosis of cirrhosis. [51-53] Once decompensated cirrhosis occurs, the 5-year survival rate falls to 50%. [51] The time from HCV infection to cirrhosis is dependent on multiple factors, and cannot be predicted in an individual patient. Virtually all HCV-related HCC occurs among patients with cirrhosis. In a meta-analysis of 21 case-control studies, the risk for HCC was increased 17-fold in HCV-infected patients compared to HCV-negative controls. [54] The results of several retrospective trials show a moderate decrease in the risk of developing HCC among HCV patients treated with interferon. [55-58] This benefit appears to be greater in patients with a sustained viral response rather than non-responders to interferon treatment. [59]
There are no right answers, only informed speculation. My expectation is that the HCC risk post DAA treatment will just be a blip, and that it will drop back to the 3% untreated rate (from the 7%).
One thing that seems to getting missed is that most of that 7% was made up of 21% of people who HAD PREVIOUSLY HAD AN HCC.
YMMV
Hi A.L,
Please read this – it’s informed, balanced and passed peer review:
http://onlinelibrary.wiley.com/doi/10.1111/liv.13157/full
Pharma spends 1.3% of gross revenues on R&D and 25% on marketing. They are laying waste to the public purse (both government and insurance) while not delivering what we, as in the world, need ie more new novel antibiotics. I think I use the words “strangling the goose that lays the golden eggs” and like it or not, it is totally accurate.
At the moment health care costs are increasing by 7% pa in most of the western world. GDP growth is 3%. That 4% annual gap means healtcare budgets DOUBLE – in real terms – within 20 years (they will on the current trajectory quadruple in actual dollar value).
In Australia healthcare costs 9.8% of GDP. Double that and we get to 20% (what it currently is in the USA) but that 9.8% is also 28.6% of consolidated revenue – so double that and over 1/2 our budget is going on health which leads to what do we give up to fund it? Education, roads, ports, prisons? The money has to come from somewhere.
And what is the major line item in the health budget? Pharma.
Sofosbuvir existed for 10 years before Gilead bought it as a nearly done deal, and would have hit the market regardless, at a lower price and with the direct result that some of the 500,000 HCV patients who died last year (about the same number that got treated) would be alive and well, enjoying time with family and friends.
Gilead are one of the worst examples, but far from the only one. I also recommend this short letter to you, and the 2 minute video from Bloomberg at the end:
http://fixhepc.com/blog/item/30-a-new-plan-for-pbs-pricing-negotiations.html
Do you want know the worst thing about SVR?
Chances are you’re going to live long enough to see the western health system implode under the weight of the sort of greed that would make even Gordon Gecko blush.
YMMV
Hi CD here from HepCBC. Thanks to all for sharing your stories. We are getting a lot of requests from people who want to import treatment, and our biggest problem (here in BC and I suppose the rest of Canada) is getting a physician to oversee the treatment (bloodwork, monitoring for complications –for example, I am cured now!!!! —Harvoni–but my 4th clinical trial was with Zepatier and it triggered atrial fibrillation and I was pulled off although it was working against the hep). So, how does a person who successfully imports the drugs into Canada proceed via getting blood work done? Here in BC everything is done through Pharmacare… or, is there a private pay option?
Have you considered having HepCBC doing this:
Spend about $10,000 on a Cepeid Gene Xpert I II or IV (does 1,2, or 4 simultaneous tests)
http://www.cepheid.com/en/cepheid-solutions-uk/systems/genexpert-systems/genexpert-ii
Then for about $30 you can buy the disposable cartridges:
http://www.cepheid.com/en/cepheid-solutions-uk/clinical-ivd-tests/virology/xpert-hcv-viral-load
And by charging $50-100-150 for the test (as say a donation because you’re not a path lab) patients can have a PCR viral load in about 1 hour and you can pay for the nurse to draw the blood.
Then the ordinary bloods can be done by any doctor under the pretext of a check up.
There is not a huge amount of monitoring required for patients not using ribavirin.
YMMV
8 August 2016 at 10:21 am in reply to: Just emailed dr Freeman about fixing my father-in-law’s HepC #21960I have never seen Dr. Freeman at gp2u.com.au. You click on his name and ALWAYS get this “Sorry, no appointments are available for Dr James Freeman. Been trying daily for 2 months. Sent two emails to him at his request and never heard from him. I know he’s busy but can these other doctors on there also get you a prescription?
Hi Tommy,
Yes, I do tend to get booked out quickly, and yes the other doctors can and do prescribe HCV meds.
According to my email, you sent 1 email on 11th of Jun which I replied to on 12th Jun as follows (maybe it ended up in your SPAM) and did not get a reply. The offer remains open
——
Hi Tommy,what time zone are you in and when are you available. It is 4.39pm here so 8 hours before now to 4 hours after would be the window.
Yes we need your bloods and you can just email them here.
You need to register as a patient here: https://gp2u.com.au/register so I can book you in. Let me know your username.
Kind Regards
James
Dr James Freeman
——
YMMV
Hi Bob,
Platelet numbers (and others) relate to
1) Production Rate
2) Lifespan
3) Destruction RateWith you it’s likely that the production rate is normalish (may be a bit low as an unusual DAA side effect). Platelet lifespan is short so not likely to be an issue which brings us to destruction…..
You have varices because of increase portal pressures from cirrhosis. Your spleen will also be swollen and it destroys the platelets.
With luck it will settle off the meds.
YMMV
Those who cannot remember the past are condemned to repeat it
– George Santayana
Across the course of history there have been some bad things happen. People in power, and alive at the time have put in place “red tape” to try to prevent future generations having the same issues. Over time memory fades and the voices for change gather momentum.
Take BREXIT for example. As imperfect as the European Union might be the 70 year period of relative peace and prosperity that follows WWII has no parallel in history. Prior to that European countries were routinely at war with each other.
Take Donald Trump as another example, his nationalism and plan for a wall to keep Mexicans out – the parallels to Hitler pre WWII should be evident to any student of history.
Take the whys and wherefores of the US housing meltdown: http://www.huffingtonpost.com/robert-weissman/deregulation-and-the-fina_b_82639.html
Here’s a great article from the Harvard Business Review: https://hbr.org/2009/07/shareholders-first-not-so-fast
In the 1950s and 1960s, the stakeholder was king. CEOs saw their role as one of balancing the interests of the various groups that touched their companies—customers, employees, suppliers, shareholders, and the community at large. This reflected the executives’ sophisticated understanding not only of their role as stewards of the valuable resources entrusted to them but also of their own enlightened self-interest: Each of these groups was essential for organizational success. What was true then is even more so today, in an age of knowledge work, outsourcing, global supply chains, and activist interest groups.
YMMV
For retreatment in GT1 DAA failures 3 drugs are better than 2. For 2 drugs Sof+Vel would be the current best choice.
Options for 3D treatment include:
Sof+Dac+Simeprevir (about $4500 for 12 weeks)
Sof+Dac+Asunaprevir (about $3000 for 12 weeks)Or for those who can access branded meds via insurance
Viekira pac + Sofosbuvir
Zepatier + SofosbuvirWith the sofosbuvir as a generic for under $1000 for 12 weeks
All can be +/- ribavirin for a 4th weaker agent.
YMMV
Liver inflammation – killing liver cells – kills cancer cells and normal cells so it is not entirely surprising that treating the HCV, and the damage it is causing, has this result.
It’s important to remember that in the absence of treatment liver cell death, liver failure and decompensated cirrhosis is the outcome.
Treating early, before cirrhosis, is a good option.
With cirrhosis the alternative to treatment is allowing the disease to run its course, and that tends to end badly once this stage is reached.
YMMV
Dr Freeman, I have been wondering about the potential for patients who do not achieve SVR to stay on current generation DAAs until newer more effective regimens come along.
It is certainly possible. With Hep B and HIV – where long term treatment is normal we do see resistance emerge in some patients.
Entecavir monotherapy (one drug only) seems to work happily for years, unlike lamivudine where resistance happens faster.
Lesson 1 – better drugs work better for longer
Lesson 2 – montherapy requires only a mono mutation and then we have a “Houston I think we have a problem” RAV (Resistance Associated Variant)
With HIV monotherapy saw more rapid development of resistance. This almost certainly relates to the fact that HIV is based on single stranded RNA, which is genetically unstable, but HBV is based on double stranded DNA which is inherently much more genetically stable.
Lesson 3 – with RNA viruses mutations happen faster, so monotherapy is a relatively bad idea
With HIV the appearance of resistance is less rapid if we get really good viral supression ie if it ain’t duplicating, it ain’t mutating (actually I expect the weaker mutants probably get a free ride piggy back off the more fit virus because a virus, during duplication, is really just a sea of chemical floating around in proximity, so has no way to tell if (say) this NS5B came from Arthur or Martha)
Lesson 4 – in patients who rapidly become UND there is very little opportunity for mutations and breakthrough
With drugs like tenofovir (at least in the current TDF form) there are long term issues (bones and kidneys) and for drugs in general there are virtually none with no unwanted side effects. Sofosbuvir has not been used long term in people so we really don’t know what the long term impacts might be.
Lesson 5 – as soon as you depart markedly from the trials you are into the area of human experimentation with you as the participant.
Viekira pac is the combination of an NS3/4A, NS5A and weaker than Sofosbuvir NS5B and needs both a booster (that inhibits metabolism of one bit) and Ribavirin to work in GT1a, but even though it might be viewed as 4 weaker drugs mixed into a chemical soup, the overall results are as good as Harvoni.
HAART (Highly Active Anti Retroviral Therapy) for HIV uses combinations of 3 or 4 drugs and the evidence is that doing this is capable of supressing HIV more or less indefinitely.
Lesson 6 – 1+1 might equal 2 but 1+1+1 > 3 and the experience with HIV is that 3-4 drugs is better than 2 so you probably don’t just want to do Sofosbuvir+Daclatasvir (which is the rational economy option), but should also be looking at either an NS3/4 or something experimental like chlorcyclizine to get a 3rd agent working for you
DAAs only get out of Phase 2 at the end of 2011, so there has only be 4 years or scale use, and really it’s more like 3.
Lesson 7 – if you can wait for retreatment it’s not a bad option. There will always be better drugs around the corner and other people can be the guinea pigs. If you can’t wait – F4, psychological then I would be chasing 3D (3 drug treatment) or failing that Sof+Vel which is the best 2D regimen available now. Zepatier + Sof, V-pac + Sof look good if you can get the branded stuff on insurance and then add Sof generic, but I would still be going for cure.
And as a last thought, I do know of a couple of patients doing long term DAAs because they were so sick when they started they don’t want to risk stopping. So wait if that’s reasonable, go hard on retreatment if it’s not, buy yes you can go long term.
YMMV
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