How To Treat High Thrombocyte Count (JAK2-V617F Mutation) ?

Discussion in 'Blood Work, Labs' started by marteagal, Aug 4, 2016.

  1. marteagal

    marteagal Member

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    Hi everybody, I would like to know your opinion on how to bring an elevated thrombocyte level under control (Peat-approved). A colleague's father was to undergo a knee surgery but during the routine examination prior to surgery, they assessed several blood parameters and found a high thrombocyte count (722 Gpt/l; reference range: 150 - 360). The doctors therefore refused to perform the operation and, instead, did some further blood testing, suspecting that he might have iron issues. By the way, he is 83 years old.

    Results (sorry, I forgot to note the units):
    Transferrin: 1.9 (reference range: 2.0 - 3,6)
    Iron: 20.4 (reference range: 7.2. - 21.5)
    Ferritin: 176 (reference range: 22 - 322)
    Iron saturation: 43 (reference range: 16 - 45)

    From my understanding, if anything, he has too much iron but the doctors think iron is too low.

    However, they also tested for the presence of the JAK2-V617F mutation, which was confirmed. Wikipedia has the following to say about this: "Mutations in JAK2 have been implicated in polycythemia vera, essential thrombocythemia, and myelofibrosis as well as other myeloproliferative disorders.[11] This mutation (V617F), a change of valine to phenylalanine at the 617 position, appears to render hematopoietic cells more sensitive to growth factors such as erythropoietin and thrombopoietin, because the receptors for these growth factors require JAK2 for signal transduction." Pubmed lists 1,218 publications on that matter.

    Since the majority of studies found via pubmed are not Peat friendly or contrary to Peat's views, I would like to ask whether this condition can be combated using Peatish methods at all?
    If I've it grasped correctly, the doctors consider giving him substances cytotoxic against bone marrow.

    From my limited understanding, the thrombocyte numbers should be tried to be brought down in order to prevent blood clotting etc.. But given the mutation, is there any chance to achieve this?? Would, e.g., aspirin even help? (I think, its mechanism of blood thinning is different.)

    Or, is it perhaps wrong to interrupt the system? My colleague's father is 83 and I suppose the mutation has been there his whole life without complications that I know of, so why trouble at all? His body seems to have arranged with the situation. I don't know if this view is legitimate!?

    It would be great to hear your opinions, thank you very much for reading and, hopefully, helping.

    --
    Here some additional blood parameters:

    Erythrocytes: 4.3 Gpt/l (reference range: 4.5 - 5.9)
    Hemoglobin: 8.5 mmol/l (reference range: 8.7 - 10.9)

    [The unit "Gpt/l" likely means "gigaparticles per liter"]
     
  2. OP
    marteagal

    marteagal Member

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  3. PakPik

    PakPik Member

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    Hi marteagal :)

    I'm not sure why they're considering he has iron deficiency? Do you happen to know why they say that? Maybe there are some special considerations for people with that mutation, i.e, they don't process iron well or something like that?
    The parameters you shared don't seem to point to low iron, at least according to the sources I have checked they might even point to high stores.
    It would be good to further inquire with doctors.

    I did a quick search on pubmed and found (it's a 2007 study, so there may be more recent considerations nowadays)
    The treatment of polycythaemia vera: an update in the JAK2 era
    "Major predictors of vascular events are increasing age and previous thrombosis. Myelosuppressive drugs can reduce the rate of thrombosis, but there is concern that their use raises the risk of transformation into acute leukaemia. To tackle this dilemma, a risk-oriented management strategy is recommended. Low-risk patients should be treated with phlebotomy and low-dose aspirin. Cytotoxic therapy is indicated in high-risk patients, with the drug of choice being hydroxyurea because its leukaemogenicity is low."​

    So it may be worth checking all of the options and discussing them with the doctors, and hopefully take the more beneficial / less risky route.
    Iron overload also predisposes to vascular events so hopefully they'll verify his true iron status before -maybe erroneously- embarking on iron supplementation.
     
  4. OP
    marteagal

    marteagal Member

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    @PakPik, thank you very much for your reply and the reference!

    I like the suggestion of phlebotomy. Although her father is pretty old and age is a risk factor, he has not yet experienced any vascular events which would classify him as "high-risk" patient.

    With regard to iron: I confused it: The doctors' suspicion of low iron was BEFORE they found out that he bears the YAK2 mutation. I got that wrong.
     
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