Has anyone else struggled with low blood counts (red, white, and platelets) after starting treatment? My son was diagnosed with CML most likely chronic, possibly accelerated, mid December 2020. He had very high white counts and anemia with normal platelets at diagnosis and spent a week in the hospital. Went on hydroxyurea and Imatinib (600) initially, came off hydroxyurea after two weeks and had normal white counts, anemia (though had been moving toward normal) and normal platelets at that time. However, a week after that was diagnosed with pancytopenia and taken off the Imatinib to let bone marrow rest as I understand it. However, while off Imatinib, his counts continued to drop even lower. He is back in the hospital getting blood and platelets again and will have a bone marrow biopsy again later today. He received blood last week too as well as initially after diagnosis (but was also bleeding for days after the first bone marrow biopsy hit a small artery branch so the blood was likely for the bleeding rather than not producing blood cells). I think he is up to his 8th bag of blood plus 3 platelets. Initially, we were more hopeful about the diagnosis, but I have not been able to find out much about low red, white and platelet counts and am really worried. Doctors at this point seem very unsure and are waiting for results of next biopsy. Has anyone else been diagnosed with Pancytopenia? Does this usually resolve with time or could his marrow be permanently damaged from the hydroxyurea and Imatinib or something else?
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New CML with question about Pancytopenia after treatment
I reacted the same way when I first started treatment with imatinib and developed pancytopenia. I had to stop imatinib to enable my blood counts to recover. I was switched from imatinib to a low dose dasatnib and developed pancytopenia again with neutrophils severely affected, red blood and platelets less so. My doctor at the time, who is a researcher in the field, mentioned he has seen this many times and suggested that we keep pursuing on again, off again with low dose dasatinib in order to stabilize my blood system. He told me as long as my blast cell count is very low (zero ideal), we have time to stay off drug and "pulse" treatment. It was successful.
What may be happening is a conversion from leukemic blood (CML) to normal blood as our TKI starts to work. When most of the blood making system is leukemic (as many of us are at diagnosis), there is not much normal blood making cells to pick up the deficit caused by relative sudden death of leukemic cells.and pancytopenia can set it. What has to happen is for normal blood stem cells to replenish bone marrow as leukemic stem and progeny cells are killed off. For many patients this replacement is not simultaneous depending on bone marrow health as one system replaces the other. For your son, it is likely that his bone marrow does not have enough normal cells to recover his normal blood system quickly enough - but it will. It takes time. For me it took two months (on / off TKI) and then over the next six months a slow steady rise toward normal. To this day, my red blood is still slightly below the normal range, but I am undetected for CML.
Tyrosine Kinase inhibitors (imatinib, dasatinib, etc.) halt CML cell division leading to CML cell death. This sudden drop in "blood" cells triggers specialized kidney cells to release erythropoietin hormone which stimulates the bone marrow to make more blood (red blood, in particular). Both leukemic cells and normal cells divide in response to this stimulation. As your son's blood counts recover and he begins treatment again, the newly created leukemic cells get killed off and the new normal cells continue. Over time, a systemic replacement of his diseased leukemic system is replaced back to normal.
It all depends on how severely damaged his bone marrow is from the leukemia. The bone marrow biopsy is being done to look at the blood cell genetics more closely to see if some other chromosomal abnormalities are at work. I had several. Hopefully he will get passed this early pancytopenia phase. One emerging protocol is to re-start pancytopenia patients on a much lower dose of a second TKI (in my case it was dasatinib 20 mg), to keep CML somewhat in check as the normal blood system builds back. What was a surprise (to my doctors) was not only did my blood system recover, but my CML system collapsed while on 20 mg dasatnib. Several of the chromosomal abnormalities disappeared as well. Dose is important in how TKI induced pancytopenia is managed.
Let us know how it goes.