Aa
attention!the ignorance of doctors can generate monsters like this
these doctors have been so stupid and ignorant to go against all guidelines and doing a job none of our members would ever allow: use of all weak useless hbv antivirals to make all mutations resistance possible......
it is best to go for tdf directly and never risk mutations with all weak antivirals, this man accumulated 9 resistance mutations making all antivirals useless
http://www.ncbi.nlm.nih.gov/pubmed/24836314
J Clin Virol. 2014 Apr 12. pii: S1386-6532(14)00110-3. doi: 10.1016/j.jcv.2014.03.018. [Epub ahead of print]
Viral evolutionary changes during tenofovir treatment in a chronic hepatitis B patient with sequential nucleos(t)ide therapy.
Lee HW1, Chang HY1, Yang SY1, Kim HJ2.
Author information
Abstract
A 54-year-old man diagnosed with HBeAg-positive chronic hepatitis B (CHB) was treated with entecavir (ETV) 1mg/day following an initial unsuccessful lamivudine (LAM) treatment (rtL180M, rtM204V/I). Subsequently, virological breakthrough with ETV mutation (rtT184A/L) developed. The LAM and adefovir combination therapy was followed by virological breakthrough. The therapy had been switched to TDF monotherapy. However, this patient experienced virological breakthrough under TDF with a HBV strain bearing rtL80M, rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A, rtT184A/L, rtR153Q, and rtV191I combined mutations without rtA194T mutation. TDF resistance may emerge due to multi-site polymerase mutations rather than single-site polymerase mutation.
it is best to go for tdf directly and never risk mutations with all weak antivirals, this man accumulated 9 resistance mutations making all antivirals useless
http://www.ncbi.nlm.nih.gov/pubmed/24836314
J Clin Virol. 2014 Apr 12. pii: S1386-6532(14)00110-3. doi: 10.1016/j.jcv.2014.03.018. [Epub ahead of print]
Viral evolutionary changes during tenofovir treatment in a chronic hepatitis B patient with sequential nucleos(t)ide therapy.
Lee HW1, Chang HY1, Yang SY1, Kim HJ2.
Author information
Abstract
A 54-year-old man diagnosed with HBeAg-positive chronic hepatitis B (CHB) was treated with entecavir (ETV) 1mg/day following an initial unsuccessful lamivudine (LAM) treatment (rtL180M, rtM204V/I). Subsequently, virological breakthrough with ETV mutation (rtT184A/L) developed. The LAM and adefovir combination therapy was followed by virological breakthrough. The therapy had been switched to TDF monotherapy. However, this patient experienced virological breakthrough under TDF with a HBV strain bearing rtL80M, rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A, rtT184A/L, rtR153Q, and rtV191I combined mutations without rtA194T mutation. TDF resistance may emerge due to multi-site polymerase mutations rather than single-site polymerase mutation.
please advice me some antioxidants i am just taking tenofovir exercise daily and eat healthy low fat low salt diet
also is there a chance that i will be needimg a liver transplant in future although i am taking meds
also is there a chance that i will be needimg a liver transplant in future although i am taking meds
cirrhosis can be regressed, the fibrosis component is fully reverseable if liver is not too damaged
cirrhosis can be reversed too but very very few get complete reversal of histology too (nodules) after a very long time.i regressed fibrosis and slowly even nodules are getting less and less
of course the viruses must be stopped to get this result
cirrhosis can be reversed too but very very few get complete reversal of histology too (nodules) after a very long time.i regressed fibrosis and slowly even nodules are getting less and less
of course the viruses must be stopped to get this result
Depending on the timeline that might have limited availibility of antivirals,
they should not have started with lam
they should NOT have tried to treat a lam resistance with 1mg entecavir, this typically results in additional resistance mutations
then they should not have used adefovir, a weak antiviral due to its kidney toxicity dose limitations to combat the combo resistance.
There is of course a chance factor involved in mutant development.
But better antivirals should be used as soon as they become available and a treating professional should try to be fully informed about these issues.
they should not have started with lam
they should NOT have tried to treat a lam resistance with 1mg entecavir, this typically results in additional resistance mutations
then they should not have used adefovir, a weak antiviral due to its kidney toxicity dose limitations to combat the combo resistance.
There is of course a chance factor involved in mutant development.
But better antivirals should be used as soon as they become available and a treating professional should try to be fully informed about these issues.
what are the newer treatments in the market as yet?
rep9ac and myrcludex arenot they the cure for hbv and hdv
cant i want for these medicines till then i can use tenofovir to control the virus.
i have seen people like one of my relatives she had hep c got injection and severe fatigue also she was not able to clear the virus so i guess its useless maybe
i am also doing homeopathy treatment for my liver and i feel very energetic
the homeopathic doctor advised me to not go for interferon this is not good.
rep9ac and myrcludex arenot they the cure for hbv and hdv
cant i want for these medicines till then i can use tenofovir to control the virus.
i have seen people like one of my relatives she had hep c got injection and severe fatigue also she was not able to clear the virus so i guess its useless maybe
i am also doing homeopathy treatment for my liver and i feel very energetic
the homeopathic doctor advised me to not go for interferon this is not good.
okay thanks
one more thing my doctor says that cirhosis is irreversible is it true i dont know why he says this and being here on this forum just gives me courage that it really is
one more thing my doctor says that cirhosis is irreversible is it true i dont know why he says this and being here on this forum just gives me courage that it really is
most members here had manageable sides, mainly fatigue (fever only the first injection) from pegintf
you can try both ways but we dont know for sure if sequential boosts pegintf response on hbv+hdv, it is all a guess on hdv since there are very few studies
i think it is best to try tdf+pegintf as proposed by your doctor i think you have nothing to lose.the main treatment for hbv+hdv is pegintf afteral not tdf
you can try both ways but we dont know for sure if sequential boosts pegintf response on hbv+hdv, it is all a guess on hdv since there are very few studies
i think it is best to try tdf+pegintf as proposed by your doctor i think you have nothing to lose.the main treatment for hbv+hdv is pegintf afteral not tdf
fishoo is not interested in this:
i mean a long list of sides is reported on tdf and etv too but in the end only after you try it you find out
i mean a long list of sides is reported on tdf and etv too but in the end only after you try it you find out
fishoo is not interested in this but the cure rates since pegintf is the only one to cure hbv and hdv
sides can be none or few, heavy sides are unusual on hbv
sides can be none or few, heavy sides are unusual on hbv
Directly from their site:
http://www.pegasys.com/patient/for-patients/expect
The main complaints were always flu like symptoms and depression...
Here are the list of side effects:
blood problems. PEGASYS can affect your bone marrow and cause low red blood cell, low white blood cell, and platelet counts
thyroid problems
blood sugar problems. Some people may develop high blood sugar or diabetes
serious eye problems. PEGASYS may cause eye problems that may lead to vision loss or blindness
serious liver problems, worsening of liver problems, including liver failure and death
lung problems, including:
trouble breathing
pneumonia
inflammation of lung tissue
new or worse high blood pressure of the lungs (pulmonary hypertension). This can be severe and may lead to death
inflammation of your pancreas (pancreatitis)
inflammation of your intestines (colitis)
serious allergic reactions and skin reactions
effect on growth in children
nerve problems. People who take PEGASYS or other alpha interferon products with telbivudine (Tyzeka®) for hepatitis B can develop nerve problems such as continuing numbness, tingling, or burning sensation in the arms or legs (peripheral neuropathy)
http://www.pegasys.com/patient/for-patients/expect
The main complaints were always flu like symptoms and depression...
Here are the list of side effects:
blood problems. PEGASYS can affect your bone marrow and cause low red blood cell, low white blood cell, and platelet counts
thyroid problems
blood sugar problems. Some people may develop high blood sugar or diabetes
serious eye problems. PEGASYS may cause eye problems that may lead to vision loss or blindness
serious liver problems, worsening of liver problems, including liver failure and death
lung problems, including:
trouble breathing
pneumonia
inflammation of lung tissue
new or worse high blood pressure of the lungs (pulmonary hypertension). This can be severe and may lead to death
inflammation of your pancreas (pancreatitis)
inflammation of your intestines (colitis)
serious allergic reactions and skin reactions
effect on growth in children
nerve problems. People who take PEGASYS or other alpha interferon products with telbivudine (Tyzeka®) for hepatitis B can develop nerve problems such as continuing numbness, tingling, or burning sensation in the arms or legs (peripheral neuropathy)
what are the sideeffects of peg interferon
why not tdf first for three years and then try peg to boostup the response
why not tdf first for three years and then try peg to boostup the response
Thanks for the details. Where do you think the mistakes in treatment take place?
as can be seen, the addition of entecavir to tdf was able to bring the vl down into the hundreds from ten million after 12 weeks. longer combo treatment will likely further suppress the vl. also his alt has normalized. thus there is still hope for him.
he was indeed treated irresponsibly and inferior knowledge of medical professionals can be a real danger to the trusting patient.
he was indeed treated irresponsibly and inferior knowledge of medical professionals can be a real danger to the trusting patient.
yes you can also try this combo directly
tdf is active on hbv and pegintf on both hbv and hdv so the combo is correct
on hdv infection it is best to keep pegintf for more than 1 year
tdf is active on hbv and pegintf on both hbv and hdv so the combo is correct
on hdv infection it is best to keep pegintf for more than 1 year
2 Case report
The patient was a 54-year-old Korean man who first visited Chung-Ang University in July 2007. At a local clinic, LAM therapy was initiated when HBV viral load rapidly rose to 8.0 log10 copies/mL and alanine aminotransferase (ALT) was elevated to 82 IU/L (normal level ≤40 IU/L) at age 52. After 1 year, the HBV DNA level was lower than 5.1 log10 copies/mL as determined using the Hybrid Capture II HBV DNA assay (Digene Diagnostics, Bestivelle, MD, USA) and the ALT level was normal. However, after 2 years of continuous treatment, HBV DNA was detectable (5.7 log10 copies/mL) and ALT was slightly elevated to 46 IU/L. The patient was referred to our hospital for further evaluation. The laboratory data at the first visit were ALT 88 IU/L. The tests for HBeAg were positive. The serum HBV DNA level determined by the Amplicor™ Monitor PCR assay (lower limit of detection, 140 copies/mL; Roche Diagnostics, Basel, Switzerland) was 8.2 log10 copies/mL. HBV genotype was determined by INNOLiPA HBV Genotyping assay (Innogenetics, Belgium). He was infected with HBV genotype C. Because of the development of LAM mutation (rtL180M, rtM204V/I), the LAM regimen was replaced by entecavir (ETV) 1.0 mg/day monotherapy. However, virological breakthrough with ETV mutation (rtT184A/L) developed after 120 weeks. The therapy had been switched to LAM and ADV for 24 weeks. This led only to a temporary HBV DNA decline, which was soon followed by virological breakthrough, despite the lack of known ADV resistance mutations. The therapy had been switched to TDF 300 mg/day monotherapy for 1 year. He underwent regular follow-ups and performed with good compliance. However, the levels of HBV DNA and ALT rebounded from 3.8 log10 copies/mL and 23 IU/mL, respectively, at week 24 to 7.0 log10 copies/mL and 357 IU/mL, respectively, at week 48. The compliance was also confirmed during clinical breakthrough. Virological and biochemical breakthrough developed in spite of the lack of known rtA194T mutation (Fig. 1). Direct DNA sequence analysis of amplified PCR products from serum samples obtained at 14 different weeks of sequential therapy revealed the mutations shown in Table 1. Sequence analysis showed that rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A with a BCP mutation were detected continuously. The rtT184A/L mutation was detected intermittently. A longitudinal clonal analysis of HBV genomes was performed by evaluating a total of 50 clones from five different serum samples (Table 2). Samples 7, 10, and 12 were taken at development of virological and biochemical breakthrough of ETV, LAM + ADV, and TDF treatment, respectively. Sample 13 and 14 were taken at 3 and 9 months after ETV + TDF treatment. The dominant viral strain continuously revealed rtL80M, rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A, rtT184A/L, rtR153Q, and rtV191I mutations (Table 3). The new dominant viral strain was not detected in sample 12 at the development of TDF resistance. Its proportion in the quasispecies pool was slightly increased in sample 12 compared to in sample 7 and 10. In sample 14, the proportion of variants significantly decreased but variants did not disappear in spite of the combination treatment of ETV + TDF (Table 1). Although clinical data are lacking, European Association for the study of the Liver guideline recommend that in patients with multi-drug resistance, a combination of a nucleoside and a nucleotide (preferably tenofovir) should be used [6] and [7]. At 48 weeks, ETV 1.0 mg was added to TDF to decrease the risk of a hepatitis flare and to reduce the risk of subsequent TDF resistance. The serum HBV DNA level declined to 2.6 log10 copies/mL at week 60, and the serum ALT level remained normal.
The patient was a 54-year-old Korean man who first visited Chung-Ang University in July 2007. At a local clinic, LAM therapy was initiated when HBV viral load rapidly rose to 8.0 log10 copies/mL and alanine aminotransferase (ALT) was elevated to 82 IU/L (normal level ≤40 IU/L) at age 52. After 1 year, the HBV DNA level was lower than 5.1 log10 copies/mL as determined using the Hybrid Capture II HBV DNA assay (Digene Diagnostics, Bestivelle, MD, USA) and the ALT level was normal. However, after 2 years of continuous treatment, HBV DNA was detectable (5.7 log10 copies/mL) and ALT was slightly elevated to 46 IU/L. The patient was referred to our hospital for further evaluation. The laboratory data at the first visit were ALT 88 IU/L. The tests for HBeAg were positive. The serum HBV DNA level determined by the Amplicor™ Monitor PCR assay (lower limit of detection, 140 copies/mL; Roche Diagnostics, Basel, Switzerland) was 8.2 log10 copies/mL. HBV genotype was determined by INNOLiPA HBV Genotyping assay (Innogenetics, Belgium). He was infected with HBV genotype C. Because of the development of LAM mutation (rtL180M, rtM204V/I), the LAM regimen was replaced by entecavir (ETV) 1.0 mg/day monotherapy. However, virological breakthrough with ETV mutation (rtT184A/L) developed after 120 weeks. The therapy had been switched to LAM and ADV for 24 weeks. This led only to a temporary HBV DNA decline, which was soon followed by virological breakthrough, despite the lack of known ADV resistance mutations. The therapy had been switched to TDF 300 mg/day monotherapy for 1 year. He underwent regular follow-ups and performed with good compliance. However, the levels of HBV DNA and ALT rebounded from 3.8 log10 copies/mL and 23 IU/mL, respectively, at week 24 to 7.0 log10 copies/mL and 357 IU/mL, respectively, at week 48. The compliance was also confirmed during clinical breakthrough. Virological and biochemical breakthrough developed in spite of the lack of known rtA194T mutation (Fig. 1). Direct DNA sequence analysis of amplified PCR products from serum samples obtained at 14 different weeks of sequential therapy revealed the mutations shown in Table 1. Sequence analysis showed that rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A with a BCP mutation were detected continuously. The rtT184A/L mutation was detected intermittently. A longitudinal clonal analysis of HBV genomes was performed by evaluating a total of 50 clones from five different serum samples (Table 2). Samples 7, 10, and 12 were taken at development of virological and biochemical breakthrough of ETV, LAM + ADV, and TDF treatment, respectively. Sample 13 and 14 were taken at 3 and 9 months after ETV + TDF treatment. The dominant viral strain continuously revealed rtL80M, rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A, rtT184A/L, rtR153Q, and rtV191I mutations (Table 3). The new dominant viral strain was not detected in sample 12 at the development of TDF resistance. Its proportion in the quasispecies pool was slightly increased in sample 12 compared to in sample 7 and 10. In sample 14, the proportion of variants significantly decreased but variants did not disappear in spite of the combination treatment of ETV + TDF (Table 1). Although clinical data are lacking, European Association for the study of the Liver guideline recommend that in patients with multi-drug resistance, a combination of a nucleoside and a nucleotide (preferably tenofovir) should be used [6] and [7]. At 48 weeks, ETV 1.0 mg was added to TDF to decrease the risk of a hepatitis flare and to reduce the risk of subsequent TDF resistance. The serum HBV DNA level declined to 2.6 log10 copies/mL at week 60, and the serum ALT level remained normal.
hi stef my doctor says to increase my pletelet count through an injection and then he will try peginterferonon me
i dont know i dont feel he is doing right.
you told me that first tenefovir to boost up the response but he is directly onto the injection and tenofovir along with it is he doimg right should i change my doctor?
i dont know i dont feel he is doing right.
you told me that first tenefovir to boost up the response but he is directly onto the injection and tenofovir along with it is he doimg right should i change my doctor?
youtube article say absolutely nothing
the other is just an old report about treatments
the other is just an old report about treatments
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