Research supported antifibrotics - do they exist?

[Hepatitis Researcher]

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.

[St. George]

Wouldn't you agree that the small percentage of people who may develop a food sensitivity to it would be offset by the releif of symptoms many would attain from it, not to mention the protection it would afford the liver.  Have  you heard of Glisodin in your research?

[St. George]

here is a link explaining in depth the functions of glisodin Sod in the body and are backed by clinical studies.  Also, glisodin doesn't displace nitrous oxide as stated in my previous post, but rather modulates it.

http://www.glisodin.com/glisodin_monograph.php

[Hepatitis Researcher]

Glisodin is Superoxide Dismutase from Melons bound to a gliadin protein carrier. The Gliadin is a protein with multiple acidic Glutamic acid side chain molecules, that renders it undigestable in the stomach/upper intestines. This way the SOD is protected frorm digestion and a small amount of it is penetrating the intestinal wall possibly by some leaky gut phenomenon.

It is unfortunately burdened with the risk of developing a food allergy type of reaction to it.

[St. George]

Here is a link with info pertaining to nattokinase and its effect on fibrin.

http://www.raysahelian.com/nattokinase.html

[St. George]

oh ,and also a naturally occuring enzyme which may be purchased named nattokinase.  Read up on it.

[St. George]

I happened upon a substance about a year ago through my studies in chiropractic college when I was experiencing extreme liver inflamation from the disease.  It is a patented substance called Glisodin.  It is an enterically protected form of S.O.D (superoxide dismutase).  SOD is one of the   main antioxidants the body produces naturally along with glutathione.  SOD in the body displaces extra Nitric oxide and renders it harmless which in turn reduces inflamation.  The problem with SOD is that when taken  orally stomach acids neutralize it and make it usesless but that is where Glisodin comes in.  It has a clinically tested delivery system that in studies raised Glisodin levels in older humans to levels seen in young adults.  Up until Glisodi SOD was only useful when delivered  by sub q injection because it bypassed the perils of the stomach.  I received so much releif from my symptoms whithin days of taking this substance.   I beleive that this product could be useful as an anti fibrotic agent.