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Supplements to compliment Interferon treatment
Hi all,
To all the Interferon patient out there, is there any supplement we should take with Interferon mono therapy and any we should avoid.
Thank you.
To all the Interferon patient out there, is there any supplement we should take with Interferon mono therapy and any we should avoid.
Thank you.
i m already using green coffee, but vdr needs to be fully activated hbv is blocking vdr already too much by nagalase secretion
where are the studies about green coffee and vdr?are they reliable?if so i ll stop it
Look here for some ideas:
http://www.lef.org/protocols/infections/hepatitis_b_08.htm
What I personally tried with success (I have chronic hep B, but I take no PEG):
Green coffee - works well, but it will lower Na (if one has that problem) and too much chlorogenic acid will block the VDR -> leading to more future problems (same for vit D3), according to mpkb.org
(HBsAG - coffee studies: http://www.medhelp.org/posts/Hepatitis-B/Chlorogenic-Acid/show/1947296)
Coffee enemas (with green coffee) - works well (but be careful at the procedure in order not to hurt yourself)
phyllantus - works well, but lowers Na as well
Milk Thistle - works well, but it is high in oxalates, if one has problems.
If you want to supplement minerals, ionic form is the best way. I use labcatal (in Europe).
Also, Q10 seems to boost HB Antibodies production (http://www.ncbi.nlm.nih.gov/pubmed/10416052)
http://www.lef.org/protocols/infections/hepatitis_b_08.htm
What I personally tried with success (I have chronic hep B, but I take no PEG):
Green coffee - works well, but it will lower Na (if one has that problem) and too much chlorogenic acid will block the VDR -> leading to more future problems (same for vit D3), according to mpkb.org
(HBsAG - coffee studies: http://www.medhelp.org/posts/Hepatitis-B/Chlorogenic-Acid/show/1947296)
Coffee enemas (with green coffee) - works well (but be careful at the procedure in order not to hurt yourself)
phyllantus - works well, but lowers Na as well
Milk Thistle - works well, but it is high in oxalates, if one has problems.
If you want to supplement minerals, ionic form is the best way. I use labcatal (in Europe).
Also, Q10 seems to boost HB Antibodies production (http://www.ncbi.nlm.nih.gov/pubmed/10416052)
i think this applies to pegintf mono only, with the sequential treatment there were no differences about this, to note genotype D is all precore and bcp mutants, it is extremely rare to have hbeag positive after 15-20yo
test for mutation may be a add on test before interferon.
Published on Friday, 04 May 2012 00:00
Written by Liz Highleyman
Chronic hepatitis B patients who do not have 2 common HBV mutations are more likely to achieve undetectable viral load and HBsAg loss when treated with pegylated interferon, according to study findings presented at the 47th International Liver Congress (EASL 2012) last month in Barcelona.
Hepatitis B virus (HBV) may carry variations in the "precore" and "core promoter" regions of its genome, which affect production of hepatitis B "e" antigen (HBeAg). Prior research has shown that these mutations are associated with more severe disease progression and poorer response to treatment compared with wild-type, or non-mutated, virus.
HBeAg loss in people who start out HBeAg positive is a measure of treatment success, along with undetectable HBV DNA viral load and hepatitis B surface antigen (HBsAg) loss; 1 study saw an HBeAg loss rate of 30% among patients treated with pegylated interferon. However, people who experience HBeAg loss still often have detectable HBV DNA and positive HBsAg, indicating that they are not cured.
Milan Sonneveld from Erasmus Medical Center in Rotterdam and colleagues performed a study to look at the relationship between the presence of precore/core promoter mutations and HBV DNA, HBeAg, and HBsAg persistence during interferon treatment.
The analysis included 214 HBeAg positive chronic hepatitis B patients treated with pegylated interferon alfa-2b (PegIntron); about half also received lamivudine (3TC; Epivir) for 52 weeks. Most (78%) were men, three-quarters were white, 19% were Asian, and the mean age was 34 years. Approximately one-third had HBV genotype A, 9% had genotype B, 14% had genotype C, and 40% had genotype D.
Participants were classified at baseline as having either only wild-type HBV or non-wild-type virus with detectable precore and/or core promoter mutations. Treatment response was evaluated 6 months after completion of therapy (week 78), with long-term follow-up at 3 years.
Results
Precore and/or core promoter mutations were detected in 64% of patients, with frequencies varying substantially across different genotypes:
Genotype A: 69% wild-type, 7% precore, 24% core promoter, 0% both mutations;
Genotype B: 26%, 68%, 0%, and 5%, respectively;
Genotype C: 24%, 7%, 45%, and 24%, respectively;
Genotype D: 11%, 40%, 18%, and 32%, respectively.
At baseline, participants with only wild-type virus had significantly higher levels of HBV DNA (9.20 vs 8.86 log copies/mL), HBeAg (2.81 vs 2.33 log IU/mL), and HBsAg (4.53 vs 4.28 log IU/mL) than those with precore/core promoter mutations.
Participants with only wild-type HBV were significantly more likely than those with mutations to respond to treatment by all measures at 78 weeks:
Undetectable HBV DNA (<400 copies/mL): 20% vs 2%, respectively;
HBsAg loss: 18% vs 2%, respectively;
HBeAg loss: 42% vs 32%, respectively;
Combined response of HBeAg loss + HBV DNA < 10,000 copies/mL: 34% vs 11%, respectively.
After 3 years of follow-up, response rates were higher overall, and wild-type virus still predicted better response:
Undetectable HBV DNA: 78% vs 25%, respectively;
HBsAg loss: 61% vs 13%, respectively;
Sustained HBeAg loss: 87% vs 80% (no longer significant).
In a multivariate analysis, exclusively wild-type HBV at baseline was the strongest pre-treatment predictor of 78-week outcomes:
HBV DNA undetectability: odds ratio (OR) 7.93, or about 8-fold higher likelihood;
HBsAg clearance: OR 4.64, or nearly 5-fold higher;
Combined response: OR 2.90, or about triple likelihood.
Alanine aminotransferase (ALT) level had a minimal effect on treatment response among patients with wild-type virus compared with a nearly linear association for those with precore/core promoter mutations.
"Precore and core promoter mutants may be detected in a majority of HBeAg positive chronic hepatitis B patients," the investigators concluded. "Presence of mutants before [pegylated interferon treatment] is association with treatment failure."
"Patients with only wild-type virus have a high probability of virological response and HBsAg clearance through long-term follow-up," they continued. "Assessment of presence of mutants can help select patients with the highest probability of response [to pegylated interferon]."
During the question period, Sonneveld suggested that these findings may indicate that HBV with precore/core promoter mutations survive better in cells, and are perhaps less targeted by T-cells.
In a related study, Sonneveld's group also analyzed the relationship between precore/core promoter mutations and HBeAg levels and seroconversion in 138 HBeAg positive chronic hepatitis patients treated the nucleoside/nucleotide analogs lamivudine, adefovir (Hepsera), entecavir (Baraclude), and/or tenofovir (Viread).
They found that the presence of precore/core promoter mutations was associated with lower HBeAg levels and higher probability of HBeAg seroconversion. However, these mutations also predisposed patients to persistent HBV replication or HBeAg relapse after seroconversion, as was the case with pegylated interferon.
5/4/12
Published on Friday, 04 May 2012 00:00
Written by Liz Highleyman
Chronic hepatitis B patients who do not have 2 common HBV mutations are more likely to achieve undetectable viral load and HBsAg loss when treated with pegylated interferon, according to study findings presented at the 47th International Liver Congress (EASL 2012) last month in Barcelona.
Hepatitis B virus (HBV) may carry variations in the "precore" and "core promoter" regions of its genome, which affect production of hepatitis B "e" antigen (HBeAg). Prior research has shown that these mutations are associated with more severe disease progression and poorer response to treatment compared with wild-type, or non-mutated, virus.
HBeAg loss in people who start out HBeAg positive is a measure of treatment success, along with undetectable HBV DNA viral load and hepatitis B surface antigen (HBsAg) loss; 1 study saw an HBeAg loss rate of 30% among patients treated with pegylated interferon. However, people who experience HBeAg loss still often have detectable HBV DNA and positive HBsAg, indicating that they are not cured.
Milan Sonneveld from Erasmus Medical Center in Rotterdam and colleagues performed a study to look at the relationship between the presence of precore/core promoter mutations and HBV DNA, HBeAg, and HBsAg persistence during interferon treatment.
The analysis included 214 HBeAg positive chronic hepatitis B patients treated with pegylated interferon alfa-2b (PegIntron); about half also received lamivudine (3TC; Epivir) for 52 weeks. Most (78%) were men, three-quarters were white, 19% were Asian, and the mean age was 34 years. Approximately one-third had HBV genotype A, 9% had genotype B, 14% had genotype C, and 40% had genotype D.
Participants were classified at baseline as having either only wild-type HBV or non-wild-type virus with detectable precore and/or core promoter mutations. Treatment response was evaluated 6 months after completion of therapy (week 78), with long-term follow-up at 3 years.
Results
Precore and/or core promoter mutations were detected in 64% of patients, with frequencies varying substantially across different genotypes:
Genotype A: 69% wild-type, 7% precore, 24% core promoter, 0% both mutations;
Genotype B: 26%, 68%, 0%, and 5%, respectively;
Genotype C: 24%, 7%, 45%, and 24%, respectively;
Genotype D: 11%, 40%, 18%, and 32%, respectively.
At baseline, participants with only wild-type virus had significantly higher levels of HBV DNA (9.20 vs 8.86 log copies/mL), HBeAg (2.81 vs 2.33 log IU/mL), and HBsAg (4.53 vs 4.28 log IU/mL) than those with precore/core promoter mutations.
Participants with only wild-type HBV were significantly more likely than those with mutations to respond to treatment by all measures at 78 weeks:
Undetectable HBV DNA (<400 copies/mL): 20% vs 2%, respectively;
HBsAg loss: 18% vs 2%, respectively;
HBeAg loss: 42% vs 32%, respectively;
Combined response of HBeAg loss + HBV DNA < 10,000 copies/mL: 34% vs 11%, respectively.
After 3 years of follow-up, response rates were higher overall, and wild-type virus still predicted better response:
Undetectable HBV DNA: 78% vs 25%, respectively;
HBsAg loss: 61% vs 13%, respectively;
Sustained HBeAg loss: 87% vs 80% (no longer significant).
In a multivariate analysis, exclusively wild-type HBV at baseline was the strongest pre-treatment predictor of 78-week outcomes:
HBV DNA undetectability: odds ratio (OR) 7.93, or about 8-fold higher likelihood;
HBsAg clearance: OR 4.64, or nearly 5-fold higher;
Combined response: OR 2.90, or about triple likelihood.
Alanine aminotransferase (ALT) level had a minimal effect on treatment response among patients with wild-type virus compared with a nearly linear association for those with precore/core promoter mutations.
"Precore and core promoter mutants may be detected in a majority of HBeAg positive chronic hepatitis B patients," the investigators concluded. "Presence of mutants before [pegylated interferon treatment] is association with treatment failure."
"Patients with only wild-type virus have a high probability of virological response and HBsAg clearance through long-term follow-up," they continued. "Assessment of presence of mutants can help select patients with the highest probability of response [to pegylated interferon]."
During the question period, Sonneveld suggested that these findings may indicate that HBV with precore/core promoter mutations survive better in cells, and are perhaps less targeted by T-cells.
In a related study, Sonneveld's group also analyzed the relationship between precore/core promoter mutations and HBeAg levels and seroconversion in 138 HBeAg positive chronic hepatitis patients treated the nucleoside/nucleotide analogs lamivudine, adefovir (Hepsera), entecavir (Baraclude), and/or tenofovir (Viread).
They found that the presence of precore/core promoter mutations was associated with lower HBeAg levels and higher probability of HBeAg seroconversion. However, these mutations also predisposed patients to persistent HBV replication or HBeAg relapse after seroconversion, as was the case with pegylated interferon.
5/4/12
no calcium and no diaries products, diaries are dangerous even without hbv unless sources are from animals in the wild and fed with no pesticiades or food not fresh or processed.they must have no antibiotics or ormones too....this is very difficult to find for those living in big cities so may be better to cut this complitely.
as to diaries on d3 supplements it is best to cut them, d3 will absorbed all calcium from other nutrients
your d3 is ok if you dont mean to use for therapeutic use, i mean boost your immune response towards hbv or boost intf response
What about supplements like selenium, zinc and calcium?
in heptech for cirrhosis doses are:
sel 400mcg daily
zinc 30mg daily
calcium none
be sure sources are natural because the synthetic ones are toxic at certain levls while the natural ones are much better and less toxic in case of overdo
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