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Research supported antifibrotics - do they exist?

The problems of treatment failure for SOC/IFN nonresponders and the possibility of reducing future supercombo-SVRchances by introducing archived resistance mutations when using "Pseudomonotherapy" - (that is here defined as using  a single  antiviral agent that is not protected against resistance development by its combo with an IFN/riba component (IFN by definition in this scenario is not sufficiently effective in reducing viral replication so that all the burden to tame the adaptive quasispecies evolution falls on the antiviral)) together with the 61% and 65% SVR rates for the latest triple modality in Geno 1s, have raised concern and the awareness for the need for alternate/additional treatment modalities in many HCV patients and their health care providers. Waiting for future antiviral developments is one route frequently recommended, but for the patients  in current need, our repertoire of additional meaningful approaches needs to be carefully reevaluated. Using antifibrotics to halt fibrosis progression is one concept not proven in large trials but it might well be effective in many, because the mechanisms for fibrosis generation are not intrinsically linked to HCV persistence, but rather to secondary response mechanisms evoked in the chronically inflamed liver, with the stellate cell activation holding center stage in this scenario. The following is one of several possible add on modalities.
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144210 tn?1273088782
So the article from 2003 says it isn't helpful after all? No benefit in taking PPC? What's the scoop?
Avatar universal
the 2003 article on PPC was interesting but i am not sure if that particular study would accurately reflect the anti fibrotic potential of PPC because the population of the 789 patients in the study were alcoholics (hx of average 16 drinks/day) and when baseline liver biopsy taken the alcohol intake among paticipants were about 2.5 drinks/day including the hcv positive participants.
in conclusion this study may not reflect the potential anti-oxidant potential of PPC on a patient who has 0 intake of alcohol?

i also could not find literature on MP1021 and would love a english translation of this link if you are up to the task. also are you presently on this and have any personal biochemical or biopsy changes as evidence of its anti fibrotic claims?

thank you for your info.
Avatar universal
thank you for the info on PPC.

i would think that anti fibrotic therapeutic regimes would be quite an important adjunct to liver disease in general and hcv in particular. sigh...i wish we had more evidenced based therapeutics in this area!
my question is this...how does one evaluate the true ingredients and bioavailabilty of PPC products? there are so many scams out there.

also if you have time (certainly our tx docs do not) could you give several clinically interesting anti fibrotic therapeutics that have some promise for many non responders in F3-4 class that are in limbo with failed treatments. we need more answers for these ones! for instance there was some excitement over sulfasalazine a while back. i feel a desperate need for some positive therapies to benefit this population of heppers.

best regards
Avatar universal
It would be naive to assume that PPC by itself can halt the progression of fibrosis. But it certainly is one very useful component of a multiprong/complex approach in that direction.
To get a good feel for the overall effect of a substance, you need to study many publications in its regard and this substance has the power to contribute a certain degree of hepatocyte protection and reduction of stress signaling onto the stellate system by combining an effect on membrane fluidity and functionality with the local, membrane bound availibility of choline and methyl groups. You could consider it a membrane bound betaine or Trimethylglycine with improved lateral mobility due to its polyunsaturated membrane anchor.The alcoholics trial is dealing with a difficult patient population with doubtful compliance, particularly in a long term trial and more so when the simplest method to halt progresion vom alcoholic liver fibrosis is to stop drinking. So you have an ill defined behaviour in your trial groups, a secondary very strong result influencing variable ( voluntary drinking restriction) and - equally important - the limitations of the semiquantitative nature of determination of fibrosis degree ("measuring fibrosis") by the use of liver biopsy. In the end the picture is blurred to the extent, that you see "no statistical significant effect".
All in all there is too much evidence in favor of its possible contribution to antifibrosis, combined with its overall health beneficial effects and total nontoxicity as to not make it an oblkigatory component of an antifibrotic cocktail.
92903 tn?1309904711
Not much more to report - just the stuff above, plus cod liver oil, and a probiotic, oh and SAMe - but I haven't been taking that lately - just forgetting to. Sometimes I end up with a full spectrum multi-vitamin instead of the liver formula.

The why part is just trying to improve the old Stage 4 liver.  
144210 tn?1273088782
per HR's last post. That is good enough for me, I'm getting PPC.
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