Hi Paul,
I know what you are going through. I have been there and you will come through it!
In some sense, what is happening to you is "normal". I will explain and then offer a suggested path.
By the time we are diagnosed with CML, the cancer has had years to grow, expand throughout our blood system and displace normal blood formation. Unfortunately, we do not feel any symptoms of disease until just about all of our blood system has been replaced by a leukemic one. This is why at diagnosis, under the microscope, all a pathologist sees are leukemic white blood cells. We are sick because these cells are crowding out red blood cells.
When you start treatment (imatinib), there is a massive leukemic cell death. In addition, TKI drugs suppress normal blood formation. All TKI's do this. This creates a huge drop in cell counts leading to a hole in our blood, sort of speak. This is normal. It happens to everyone - but severity of myelosupression is an issue.
Once leukemic cells are killed, the body senses a need to build new blood and triggers normal (and leukemic) hematopoietic stem cell division and differentiation. The presence of imatinib keeps killing leukemic cells, but it takes time for normal blood cells to replace your leukemic ones. This is the problem. Speed of recovery is slower than leukemic cell death. But it can be managed and you will get through it.
The trick is to "coax" your body into replacing your leukemic blood with normal blood gradually. This will take a year (on average). The process involves step wise drug holidays (no drug) while your blood system recovers. Granted, your leukemic system is also recovering, but after you achieve a near normal blood count, you whack the leukemic system again. Normal blood keeps recovering and leukemic blood is in a stalemate. Eventually enough normal blood cells are dividing to compete with the leukemic ones getting killed and your normal blood takes over.
I do suggest you consider talking with your doctor about switching from imatinib to dasatinib (aka sprycel) low dose (20 mg) which is very effective at doing this. This is what my doctor did and he is one of 4 top experts in CML research.
Your blood counts will crater again after re-starting therapy and when it does, you stop therapy once more. You monitor your blood counts weekly for recovery and then resume therapy (again low dose). You may have to do this several times. I had to do this 4 times. I had a blood system crash (neutrophils fell to 0.1 - dangerous level), stopped therapy, blood system restored, low dose started, blood system crashed again (but not as bad) and so forth.
Eventually, your normal blood system will have recovered sufficiently so that when you restart therapy, your myelosuppression is not severe and you can live with it and stay on drug. At this point, your leukemic system continues to degrade and your normal system is back up and running.
Read the paper linked below which describes the protocol.
As it turns out - patients who suffer the most with myelosuppression tend to be the ones who respond the best once they overcome it. And with less drug (i.e. less toxicity and adverse events).
I was switched off imatinib to dasatinib (20 mg) to manage my crashing counts using the procedure above (dose interruption, low dose restart). It took me several months to achieve equilibrium and then my CML counts crashed - all while on low dose. I eventually became "undetected" and have now been without any drug and staying undetected for over a year. This can be your future.
Be vigilant. Have your blood counts measured weekly - and as soon as they are high enough restart therapy. Test, monitor, stop, restart as your normal blood system takes over and you keep whacking CML with each restart. Talk to your doctor using Dr. Cortes' research about switching to low dose dasatinib upon restart. You can always increase drug dose if it proves insufficient as well as change to other drigs. But I have a suspicion your will respond well.
