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Add -on of peg interferon to a stable nucleoside, hbsag loss 40%
Add -on of peg interferon to a stable nucleoside regimen led to loss of HBs Ag in chronic hepatitis HBe Ag negative patients
D. Ouzan1; G. Penaranda2; H. Joly1; H. Khiri2; P. Halfon2
1. Institut Arnault Tzanck, Saint-Laurent du Var, France.
2. Laboratoire ALPHABIO, Marseille, France.
Objectives: Suppression of HBV viral load by nucleoside treatment reduces disease progression but requires indefinite treatment. Hbs Ag loss is a rare event after long term treatment with analogues therapy. In HBe Ag negative patients peg interferon alpha 2a for 96 weeks improved the sustained responses rate versus 48 weeks. It is of interest to know whether the addition of peg interferon for 96 weeks to a stable nucleoside therapy will reduce quantitative HBs-Ag which may follow by HBs Ag loss.
Methods: We analyzed HBs Ag levels of 10 patients who received additional peg
D. Ouzan1; G. Penaranda2; H. Joly1; H. Khiri2; P. Halfon2
1. Institut Arnault Tzanck, Saint-Laurent du Var, France.
2. Laboratoire ALPHABIO, Marseille, France.
Objectives: Suppression of HBV viral load by nucleoside treatment reduces disease progression but requires indefinite treatment. Hbs Ag loss is a rare event after long term treatment with analogues therapy. In HBe Ag negative patients peg interferon alpha 2a for 96 weeks improved the sustained responses rate versus 48 weeks. It is of interest to know whether the addition of peg interferon for 96 weeks to a stable nucleoside therapy will reduce quantitative HBs-Ag which may follow by HBs Ag loss.
Methods: We analyzed HBs Ag levels of 10 patients who received additional peg
The paper said very little about the other 8. Wonder whether they are still on treatment?
Gilead has just entered into an agreement with Globelmmune:
"Gilead Sciences Inc. said Monday it will work with GlobeImmune Inc. to develop a new hepatitis B treatment that includes Gilead's drug Viread."
Some commenters say this is usually a ploy to extend the patent?
N.B. GlobeImmune seems to have a therapeutic DNA vaccine for HBV?
Gilead has just entered into an agreement with Globelmmune:
"Gilead Sciences Inc. said Monday it will work with GlobeImmune Inc. to develop a new hepatitis B treatment that includes Gilead's drug Viread."
Some commenters say this is usually a ploy to extend the patent?
N.B. GlobeImmune seems to have a therapeutic DNA vaccine for HBV?
pattern for tenofovir look like will expire in 2017 US and 2018 Europe (http://en.wikipedia.org/wiki/Gilead_Sciences)
cn you check when their patents expire in europe?
I will check and if found an answer I came back with an answer.
I will check and if found an answer I came back with an answer.
this is interesting and for sure everybody want to understand why this was happening.
what about the other 8 ? they are in the same situation?
HBsAg loos and HBsAg seroconversion is the same or HBsAg seroconversion means HBsAg loos + HBsAb ?
what about the other 8 ? they are in the same situation?
HBsAg loos and HBsAg seroconversion is the same or HBsAg seroconversion means HBsAg loos + HBsAb ?
I agree, this paper is interesting. It ties in with your idea of using interferon to lower HBsAg. I remain cautious because the sample is small, only 10 persons. From an Asian perspective, I also want to know the genotypes of the hbv.
Have a read of this paper:
HBV Treatment Induced HBsAg Seroconversion to Anti-HBs in 9 Asian-American Patients: Experience in a Community Clinic
H. Lee1; K. Hu1; S. Tonthat1
1. GI/Hepatology, U.C. Irvine, Irvine, CA, United States.
Background: Although HBeAg seroconversion to anti-HBe has been a standard treatment endpoint for HBeAg+ patients, patients who achieve this endpoint have a 20-40% relapse rate over a 5 year period. HBsAg seroconversion appears to be a more durable endpoint of HBV treatment than HBeAg seroconversion, but it is difficult to achieve. Several natural history cohorts of HBV patients have shown a low incidence of spontaneous HBsAg seroconversion, approximately 0.5-1.0% per year. Registration trials of HBeAg+ patients on tenofovir DF have shown 10.8% of patients achieve HBsAg loss and 7.7% of patients seroconvert to anti-HBs over 4 years. However, HBsAg loss was not seen in Asian patients or in HBeAg-negative patients.
Aim: To assess the probability and durability of HBsAg seroconversion in Asian-American patients treated with standard of care (SOC) nucleos(t)ide analogue oral agents in a community clinic.
Methods: A retrospective chart review of patients with CHB, who received nucleos(t)ide therapy from a single Irvine, CA clinic from 2008-2010.
Results: We identified nine Asian-American patients on treatment with nucleos(t)ide analogs who achieved HBsAg seroconversion. 4/9 (44%) were male, 8/9 (89%) were HBeAg negative at baseline, and the median age was 48 y.o. 4/9 patients were started on therapy by their primary physician, and their baseline viral load and ALT were not available. For the five patients with complete data, the median starting HBV DNA level was 69,392 IU/ml, and median ALT level was 53 U/L. 6/9 patients were treated with tenofovir (one of whom had lamivudine + TDF), 2 were treated with entecavir (ETV), and 1 was treated with adefovir (ADV). All nine patients achieved a normal ALT and undetectable HBV DNA on treatment. Treatment was discontinued in one patient when he achieved a HBsAb level over 50 mIU/ml. He was treated for 27 months with entecavir before achieving this endpoint. Ten months later, this patient was found to have a viral load of 13,737 IU/ml (79,949 copies/ml). His HBsAg was detectable, and he was started on tenofovir (TDF) at the time of this abstract submission.
Conclusions: Our experience shows it is possible for HBeAg negative Asian-American patients to seroconvert to anti-HBs while on oral CHB therapy. Using a quantitative HBsAb level of >50 mIU/ml as an endpoint to discontinue therapy was difficult to achieve, and did not prevent relapse in the one patient who achieved it, despite a persistently detectable HBsAb level. Further studies are needed in larger patient populations to determine the best endpoint for stopping oral CHB therapy, to maximize durable seroconversion and viral suppression.
HBsAb of 10mIU/mL is considered to be protective!. This one patient had 50 mIU/mL and he still relapsed. Sure would like to understand why.
Have a read of this paper:
HBV Treatment Induced HBsAg Seroconversion to Anti-HBs in 9 Asian-American Patients: Experience in a Community Clinic
H. Lee1; K. Hu1; S. Tonthat1
1. GI/Hepatology, U.C. Irvine, Irvine, CA, United States.
Background: Although HBeAg seroconversion to anti-HBe has been a standard treatment endpoint for HBeAg+ patients, patients who achieve this endpoint have a 20-40% relapse rate over a 5 year period. HBsAg seroconversion appears to be a more durable endpoint of HBV treatment than HBeAg seroconversion, but it is difficult to achieve. Several natural history cohorts of HBV patients have shown a low incidence of spontaneous HBsAg seroconversion, approximately 0.5-1.0% per year. Registration trials of HBeAg+ patients on tenofovir DF have shown 10.8% of patients achieve HBsAg loss and 7.7% of patients seroconvert to anti-HBs over 4 years. However, HBsAg loss was not seen in Asian patients or in HBeAg-negative patients.
Aim: To assess the probability and durability of HBsAg seroconversion in Asian-American patients treated with standard of care (SOC) nucleos(t)ide analogue oral agents in a community clinic.
Methods: A retrospective chart review of patients with CHB, who received nucleos(t)ide therapy from a single Irvine, CA clinic from 2008-2010.
Results: We identified nine Asian-American patients on treatment with nucleos(t)ide analogs who achieved HBsAg seroconversion. 4/9 (44%) were male, 8/9 (89%) were HBeAg negative at baseline, and the median age was 48 y.o. 4/9 patients were started on therapy by their primary physician, and their baseline viral load and ALT were not available. For the five patients with complete data, the median starting HBV DNA level was 69,392 IU/ml, and median ALT level was 53 U/L. 6/9 patients were treated with tenofovir (one of whom had lamivudine + TDF), 2 were treated with entecavir (ETV), and 1 was treated with adefovir (ADV). All nine patients achieved a normal ALT and undetectable HBV DNA on treatment. Treatment was discontinued in one patient when he achieved a HBsAb level over 50 mIU/ml. He was treated for 27 months with entecavir before achieving this endpoint. Ten months later, this patient was found to have a viral load of 13,737 IU/ml (79,949 copies/ml). His HBsAg was detectable, and he was started on tenofovir (TDF) at the time of this abstract submission.
Conclusions: Our experience shows it is possible for HBeAg negative Asian-American patients to seroconvert to anti-HBs while on oral CHB therapy. Using a quantitative HBsAb level of >50 mIU/ml as an endpoint to discontinue therapy was difficult to achieve, and did not prevent relapse in the one patient who achieved it, despite a persistently detectable HBsAb level. Further studies are needed in larger patient populations to determine the best endpoint for stopping oral CHB therapy, to maximize durable seroconversion and viral suppression.
HBsAb of 10mIU/mL is considered to be protective!. This one patient had 50 mIU/mL and he still relapsed. Sure would like to understand why.
usually these are available on scientific journals or pubmed, but not sure f this is a study or just clinical case reports
we should have a look on the france universities where they doing it and in italy but i think this is nothing new, i heard they are doing about the same in pisa but they have problems because healthcare and insurance dont want to pay for tnf and interferon together because too expensive.......the blocks on hbv combo treatments are just a matter of costs, that's why in india you can find even triple or more combos they have the cheap generics
anyway tenofovir should have little time left and interferon too, cn you check when their patents expire in europe?
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