Avatar_universal
hbvdna
my mother(59 years old)has been detected with HbsAg +ve(250IU/mL) in 2012
at that time her HBVDNA (Quantitative was 37 IU/mL) and her LFT is normal since then.also she is HBeAg -ve ,
HB core antibody, Igm -ve ,
but now on 27th april 2013 her HBVDNA is 2500IU/mL,LFT NORMAL..
PLEASE TELL ME WHAT TO DO..AM VERY TENSE. WE r from india .
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Avatar_universal
You should check her on fibroscan and ultrasound. Also retake hbsag quantitive test yoir result means >250 iu/ml. In fact it is nuch higher.
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wat abt her latest HBVDNA (2500IU/ml) last year it was only 37IU/ml.
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wat abt her latest HBVDNA (2500IU/ml) last year it was only 37IU/ml..is treatment needed.plz reply
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Hbv dna can go up and down ant 2500 is not too bad. The main test is fibroscan and hbsAg quantitative in IU/ml.
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does she need medication
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You need to do above tests to understand. What is her ALT?
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her ALT is normal..we check it every 2months
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What is normal, post the figure!
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her ALT IS 22 u/l  its normal range on report is mentioned to be upto 31u/l
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no so important but fully normal alt for women is 19 and 30 for men
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When it comes to older patients, my personal view is to choose treatment with Entecavir or Tenofovir. A pill a day eliminates unnecessary worries.

I agree with others that whether you should start treatment depends on a Fibroscan to assess the state of her liver. Hbvdna do fluctuate, but if persistently above 2000 iu/ml, treatment should be considered.

Just my opinion.
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when should we retest her for HBVDNA ..what should we do or her that will be best for her.plz tell me am really worried
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I think re-test in 3 month time her hbvdna should be reasonable.
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thanks God bless
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Recent abstract of Replicor in EASL


Abstract 776
    
ESTABLISHMENT OF A POTENT ANTI-HBSAG RESPONSE AND DURABLE IMMUNOLOGICAL CONTROL OF VIREMIA WITH SHORT TERM IMMUNOTHERAPY AFTER REP 9AC'- INDUCED HBSAG SEROCLEARANCE IN CHRONIC HBV INFECTION    
    
M. Al-Mahtab1, M. Bazinet2, A. Vaillant2*
1Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh, 2REPLICor Inc., Montreal, QC, Canada. ****@****

Background: HBsAg is known to block cytokine responses and its persistent circulation during immunotherapy may block immune stimulation in patients with chronic HBV. REP 9AC' is a nucleic acid-based polymer (NAP) that clears serum HBsAg by blocking HBV subviral particle formation and release. The ability of add-on immunotherapy after REP 9AC'- induced HBsAg seroclearance to establish a permanent immunological control of chronic HBV infection was examined.
Methods: Add on immunotherapy to existing REP 9AC' therapy was initiated in patients experiencing HBsAg seroclearance with persistent serum HBV DNA. Immmunotherapy consisted of thymosin α1 (Zadaxin™) or pegylated interferon α-2a (Pegasys™). Virologic responses were monitored by measuring serum HBV DNA (Roche Cobas™), serum HBsAg and serum anti-HBs (Abbott Architect™).
Results: REP 9AC'- induced HBsAg seroclearance was achieved in most patients with 8-16 weeks of treatment and was accompanied by the appearance of moderate free anti-HBs titers (50-60 mIU/ml) and reductions in serum HBV DNA (to 1000-3000 CPM). Addition of Zadaxin™ or Pegasys™ to REP 9AC' therapy resulted in rapid and profound increases in anti-HBs titers after as little as 6 weeks of immunotherapy to titers comparable to or greater than those observed in healthy patients with a strong vaccine response. In 8 of 9 patients, all treatment was halted after 13 - 27 weeks of immunotherapy exposure. In these patients, anti HBs titers off-treatment are currently comparable to or exceed those observed in uninfected subjects with a strong HBV vaccine response up to 4 months off treatment. Additionally, serum HBV DNA is also supressed or is declining in all of these patients off-treatment. Currently, serum HBV DNA levels have reached < 500 cpm (2 patients), < 150 cpm (1 patient) or < 116 cpm (LLOQ) in the remaining 5 patients.
Conclusions: REP 9AC'-induced HBsAg seroclearance appears to potentiate the immunostimulatory effects of either Zadaxin™ or Pegasys ™ in all patients, suggesting that circulating HBsAg may play a direct role in blocking the stimulation of immune function by immunotherapy. Short term exposure to immunotherapy in the absence of HBsAg may induce permanent immunological control of HBV infection in most patients.
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