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"]
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"]