In addition to CLL (still W&W for me), I have another chronic disease - hepatitis B (HBV).
I think I remember my parents talking about HBV when I was young - that I got it when I was born; and that I'm now immune to it, though I can't be a blood donor anymore. Then I forgot about me having HBV for a few decades. Ignorance is bliss until it wants to kill you.
So while HBV is in my body at some minimal levels, it can very likely activate itself once my immune system gets weaker, or when I start the CLL therapy.
Apparently most, if not all, of CLL drugs mention that they can reactivate HBV. Most CLL trials exclude patients with active hepatitis B (minimal, yet detectable HBV in my blood probably means I'm "active").
My hepatologist said I will need to take some hepatitis B antiviral once my W&W is over and I start taking some CLL medication.
Does anyone else here have both CLL and hepatitis B? Are some CLL therapies definitely forbidden for HBV patients? I had some high hopes for acalabrutinib with venetoclax one day when I need therapy; now I'm not sure anymore (both these drugs are not available in Japan where I currently live; my hematologist just does not know the answer).
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mantana
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Sorry to hear about your 2nd medical complication.
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I don't have Hep B, but because I have occassional spikes of ALT/SGPT levels, most doctors immediatly want to test me for Hepatitis. I do carry another semi active virus HHV-6a, for which there is no effective treatment.
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The good news is that there are USDA approved pallative treatments for Hep B (but no cure). Here is some useful information: hepb.org/treatment-and-mana...
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I hope some of those drugs are available in Japan (or Germany if you move there).
HEPCLUDEX® is a first-in-class entry inhibitor for treatment of chronic hepatitis B and D infections. The drug inhibits the HBV receptor (NTCP receptor) on the hepatocyte surface and prevents the infection of healthy cells and viral spread within the liver.
However, it was accepted as a treatment for hepatitis D, not B. What I can find, most of its trials were focused on hepatitis D treatment (hepatitis D needs hepatitis B to replicate), though it shows anti-HBV efficacy.
However, it is more difficult to foresee its efficacy in the context of well-established CHB (chronic hepatitis B), which is known to be a highly efficient infection; at the chronic stage, virtually all hepatocytes are infected.
Certainly, to be effective in CHB, this approach must rely on hepatocyte turnover, which, in turn, is dependent on the ability of the host immune response to clear the infected hepatocytes.
Considering the natural half-life of hepatocytes and the absence of a system to reinforce the immune-mediated turnover, a significant beneficial effect of this approach in CHB is not predictable, and important safety concerns must be considered.
I had hepatitis b 40 years ago, I developed immunity, by sero converting. My understanding is when you develop antibodies you have immunity,and are no longer infectious and are not classified as active.
If you have antigen and no antibodies you are active and positive,
And infectious unless you receive drug therapy and are undetectable which I presume is your situation
There are treatments available I believe,and presume you are on one?
I'm not on any HBV treatment, never was. Except self-administered 500 mg aspirin a day started a month ago or so - there are some studies showing that it can lower liver cancer likelihood in HBV patients:
It also lowers inflammation in general (and more inflammations - more cancer risk; CLL - more other cancer risk).
I know aspirin may not go well with lower platelet count we have with CLL. But it's liver cancer which is THE bad cancer here.
Anyway - these may be the questions more suited for my hematologist. However, here in Japan, the doctors almost never tell you what's wrong with you - except "you have hepatitis B; treatment is not necessary"... and are sometimes reluctant to answer questions (though I realize doctors are humans, every patient is different, hematologists are not hepatologists and so on).
Just to answer myself, or anyone who finds this thread in the future: there have been cases of people dying once they've started their CLL therapy and their HBV reactivated/flared.
Therefore it's utterly important to test yourself for hepatitis B virus (you may not know!) prior to CLL treatment, and use an antiviral and proper monitoring if you have an active or prior HBV infection.
Apparently having hepatitis B does not prevent from using Acalabrutinib, provided the patient uses an antiviral and is monitored carefully:
Consider antiviral prophylaxis (entecavir and tenofovir are preferred agents) and monitor for infections due to hepatitis B virus (HBV) reactivation in high-risk patients.
Hepatitis B surface antigen (HBsAg)-positive
Prior HBV infection
Increasing HBV viral load in patients planned for allogeneic hematopoietic cell transplant or anti-CD20 or anti-CD52 monoclonal antibody therapy
If patient is HBsAg-positive or hepatitis B core antibody (HBcAb)-positive:
Use baseline quantitative polymerase chain reaction (PCR) for HBV DNA to determine viral load.
Administer prophylactic antiviral therapy or preemptive antivirals upon detection of increasing viral load.
With venetoclax, it's not so clear if it can cause HBV reactivation, but antiviral is also recommended:
Venetoclax, a small molecule inhibitor of BCL-2 used in refractory cases of CLL may have a potential risk of HBV reactivation, but no case has been signaled to date. The same consideration also applies to azacitidine and decitabine, hypomethylating agents used to treat acute myeloid leukemia.
It has also been suggested that treatment of cancer with antibody immune checkpoint inhibitors (anti-CTLA4 tremelumab and ipilimumab; anti-PD-L1: Nivolumab and pembrolizumab; PD-L1: durvalumab, atezolizumab and avelumab) is a risk factor for HBV reactivation, to be prevented by anti-HBV prophylaxis
For what its worth, my husband had a liver transplant. His blood type was rare so he took the first liver offered to him which tested positive for HBV. They were able to successfully keep the HBV to barely detectable levels with Epivir so his lowered immunity from the anti rejection immunosuppressants couldn't cause a flare up. It was never an issue since the Epivir kept it stable.
I tested positive for HBV antibodies and whilst I’ve had nearly every virus going - this was one I was pretty sure I’d missed.
It was decided that one of my donors through IVIG had probably had hep b and I’d got the antibodies that way. Why was it significant - if I’d come back positive for having had HBV - I’d not have been able to go on FLAIR trial.
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