In that context, here is another “component” of a possible multiprong antifibrotic cocktail.
Polyenylphosphatidylcholine (PPC)is just one example of an excellent, well published, NIH grant supported, human study supported, renowned research institution conducted, well respected researcher directed, several time AASLD presented (including a presentation in the grand auditorium, not just posters!), totally nontoxic – generally health enhancing, in combination with IFN SVR enhancing – see below, very available in high quality antifibrotic.
What is the answer to the following questions:
Why are two leading hepatologist, that I questioned in this regard, not aware of it at all?
How many remember that I discussed and described this particular component of antifibrotic measures here at this board about 12 month ago?
How many use this particular item or are at least aware of it?
Who understands the critical difference between “lecithin” and this particular compound?
The following paper is not referring to PPCs antifibrotic capacities, but to its enhancing features to reach SVR on IFN therapy in HCV. This was not a small study – 176 patients participated, it was conducted under strict Germany guidelines. And remember, these were early days- no riba was included. But it is a small but important timeless piece of reality uncovered and now long covered by library dust.Combine it with the above and draw your own conclusions.
Hepatogastroenterology. 1998 May-Jun;45(21):797-804.
Polyunsaturated phosphatidyl-choline and interferon alpha for treatment of
chronic hepatitis B and C: a multi-center, randomized, double-blind,
placebo-controlled trial. Leich Study Group.
Niederau C, Strohmeyer G, Heintges T, Peter K, Göpfert E.
Department of Medicine, Heinrich-Heine-University of Düsseldorf, Germany.
BACKGROUND/AIMS: Polyunsaturated phospatidyl-choline (PPC) has been shown to
reduce serum aminotransferases in experimental hepatitis. This multi-center,
randomized, double-blind, placebo-controlled trial evaluated the effects of PPC
in patients with chronic hepatitis B and C in combination with interferon alpha
2a or 2b. The diagnosis of chronic viral hepatitis was based on an abnormal serum
alanine aminotransferase (ALT) value (more than twice the upper value of normal),
viral replication and chronic hepatitis found on liver biopsy. METHODOLOGY:
Patients received 5 million I.U. (Hepatitis B) and 3 million I.U. (hepatitis C)
interferon s.c. thrice weekly for 24 weeks, respectively, and were randomly
assigned to additional oral medication with either 6 capsules of PPC (total daily
dose: 1.8 g) or 6 capsules of placebo per day for 24 weeks. Biochemical response
to therapy was defined as a reduction of ALT by more than 50% of pre-treatment
values. The responders were treated for further 24 weeks after cessation of
interferon therapy with either PPC or placebo. RESULTS: 176 patients completed
the study protocol (per-protocol population: 92 in the PPC and 84 in the placebo
group). A biochemical response (> 50% ALT reduction) was seen in 71% of patients
who were treated with PPC, but only in 56% of patients who received placebo (p <
0.05). PPC increased the response rate in particular in patients with hepatitis
C: 71% of those patients responded in the PPC group versus 51% in the placebo
group (p < 0.05). PROLONGED PPC THERAPY GIVEN TO RESPONDERS BEYOND THE CESSATION
OF INTERFERON THERAPY TENDED TO INCREASE THE RATE OF SUSTAINED RESPONDERS AT WEEK
48 IN PATIENTS WITH HEPATITIS C (41% VERSUS 15% IN THE CONTROL GROUP; p = 0.064).
In contrast, PPC did not alter the biochemical response to interferon in patients
with hepatitis B. PPC did not accelerate elimination of HBV-DNA, HBeAg and
HCV-RNA. CONCLUSIONS: In conclusion, PPC may be recommended in patients with
chronic hepatitis C in combination with interferon and after termination of
interferon in order to reduce the high relapse rate. PPC may not be recommended
for patients with chronic hepatitis B. In contrast to IFN and other antiviral
agents PPC does not carry major risks and is tolerated very well.