Just wondering if we should be expecting WBC Morphology to become "normal" once the O+V treatment is complete. I'm not sure what UMRD means concerning these tests, but as a newcomer to this treatment, I was expecting all bloodwork to appear within normal ranges and parameters if and when remission is achieved. I'm certain additional bloodwork and tests will be done once the treatment is near completion this summer. Since we are not even halfway through the V treatment, I'm not surprised that his WBC morphology is still "abnormal" just wondering if this result will change as his treatment progresses.
Many thanks in advance to everyone in this community for all of your valuable education and support! Happy holidays to all, and looking forward to a happy and healthy 2023!
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lisakc1
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Maybe, maybe not. This disease isn't like an infection, where once the bug is gone things return to normal. This isn't defective lymphocytes in the blood, replicating themselves.This is a fundamental change in basic stem cells residing inside the bone marrow. These stem cells, even though only certain ones may lead to lymphocytes, may affect the others inside the bone marrow that are also being formed. They are right there next to each other, in that microenvironment, and since they "are different" their interactions with these other early cells all crowded inside, is also different. These defective cells causing the CLL take over the bone marrow, such that the stem cells making the other cells are either permanently affected or temporarily crowded out. Using me as an example, ever since I got this disease, my platelets have hovered around 100K even when in a clinical remission. Maybe they get up to 125K which is still abnormally low. They just don't get back up to normal range anymore. But I don't bleed excessively when cut, my gums don't bleed, and my easy bruising isn't really "deep" (light colors, not a deep blue-black) and clears up fairly quickly without being painful. So my docs aren't too worried, and I don't think I need to treat it.
Some people have red blood cells affected permanently and struggle with anemia, others may have neutrophils or other cells that technically aren't from the "lymphocyte line" affected. Our immunity is changed, with defective lymphocytes and possibly other problems. Still others seem to have zero effects once in remission. No way to know ahead of time if everything returns to normal, or not. This picture shows all the different cell types that originate from the parent stem cell in bone marrow.
Thank you! Your explanation makes a ton of sense, however, this risk is not explained when the patient is in the "watch and wait" stage. It appears that other healthy stem cells can be permanently damaged while waiting for treatment. This was surely never explained to us. Thank you so much again!
I am not sure that the healthy cells might be damaged (even permanently) when crowded out by CLL unless/until there is a high level of infiltration. Otherwise we would see anemias, neutropenias, etc. earlier on in the process. We know there is potential damage from the treatments. The targeted ones do less damage. We don't see the high rates of neutropenia, anemia, etc. like with standard chemotherapy. And since the treatment itself can also cause some problems, there are guidelines of "when to treat". A slow moving disease may not need treating in what, 1/3 of people? Why risk damage to the marrow cells if the disease turns out to be indolent? So there is a Watch and Wait, and guidelines for absolute treatment. This "crowding" potential is why some docs want a BMB, to see how crowded the marrow is. Mine was almost pure white with CLL cells, healthy marrow is red. I had yet to reach anemia, neutropenia, etc. But I knew what would happen if I didn't treat soon, my variant became really active and my white cell count jumped up to 50K within 6 months of previous blood tests. I started looking at treatments and got into a trial before I "technically" needed it. My cell lines were normal except lymphs, but my doubling time was less than 6 months so I met the criteria to treat.
IMO the risk isn't going to be explained much up front because docs don't generally explain the risks in every judgement call they do. Cuts & scratches aren't automatically given antibiotics, yet the risk of sepsis is real but it's so low unless the symptoms warrant it, docs aren't going to go into "worst case possible" scenarios and the treatments that might be needed. They wait to see what happens, and watch the symptoms. Same with early diagnosis CLL in Watch & Wait. However, the impact of hearing the word "leukemia" in the diagnosis warrants a bit more explaination, which they do. They just typically don't spend a lot of time up front going into all the possible details/outcomes. This is oversimplification, of course, but I think the analogy is valid. And our docs are generally not educators, it's on us as patients to learn everything about our disease. Large educational institutions have "patient education" as part of their mission, so patients choosing this type of provider gets more than smaller practices. Major diseases have educational programs offered at large institutions, but we have a rare disease, and there aren't funds allocated to educate us at the clinician-treatment level. We look to the disease organizations, and now places like this website.
My husband was anemic for a couple of years before treatment, was told not to worry about it since it was caused by his CLL.... RBC and Neutrophils are now in the the "normal" range ever since he started treatment. We were told at diagnosis not to worry, some people never need treatment and if he did, the condition was very treatable... totally downplayed to alleviate worry I'm sure. I prefer having ALL the information, good and bad so that we can make informed decisions, but I'm sure everyone is not like this. Thank you so much again for your thorough explanation!
Great explanation!! Thank you from a third person. Takes away some of my “disappointment” at my numbers not being normal after 2 years on Acalabrutinib (especially neutrophils which ranged from 0.2 to 0.5 prior to treatment and now are in the 1.25-1.5 range). I haven’t had an infection since treatment so maybe that’s “the proof in the pudding”😀
This is a common mistake, one which I made when I reached remission:- "I was expecting all bloodwork to appear within normal ranges and parameters if and when remission is achieved."
I knew that my absolute lymphocyte count would be low, and hence my WBC would be low, because unfortunately, we don't yet have approved treatments that only kill CLL cells. The collateral damage of killing healthy B cells lowers both, plus venetoclax can also kill off some T cells. My ALC and WBC have bounced around below to just in normal for the 2 years since finishing my treatment.
Per the iwCLL guidelines, section, Definition of response, relapse, and refractory disease,ashpublications.org/blood/a... a complete response, Table 4, a complete response only requires, for blood counts:-
- Platelets ≥100 × 10^9/L
- Haemoglobin ≥11.0 g/dL (untransfused and without erythropoietin)
Usually these will improve over time, particularly if this is his first treatment.
Its not the count that I question, but the morphology of the WBC, the size and shape of the WBC, shouldn't they be in the "normal" range after treatment is finished? As always, you teach me a great deal, don't know how I would get through this without your knowledge and expertise!
Morphology refers to "the form and structure of organisms without consideration of function". So you really can't talk about WBC morphology per se, because your WBC is comprised of neutrophils, lymphocytes, basophils, eosinophils and monocytes. Within just the lymphocyte category, you've got B cells (healthy and some CLL), helper and cytotoxic T cells and NK cells. I think SofiaDeo 's answer is what you are after, then you need to consider how long the disruption to the typical balance in those white blood cells will take to normalise after (a) the long term effect of CLL on the mix of white blood cells, both from infiltration in the bone marrow, plus cytokine signalling, which influences the balance and degree of T cell exhaustion, then (b) the impact of treatment. This can take years to rebalance, if it ever does.
Thank you.. My naive thinking was that ALL B cells would get wiped out, including those pesky CLL stem cells and that they would be replaced with healthy B cell stem cells.. guess this is why there is no cure. My guess is, that once again, it's a journey and everyone is different. Thank you again for your patience and thorough explanation! I will keep you all updated with ours!
It's a little more complicated. Look back at the chart. The same stem cells can make either myeloid line or lymph line precursors, depending on what the body needs. It's not that we have X number of stem cells that make only myeloid cell lines, and Y number that make only lymph lines. From what I am reading, changes in the balance of chemicals surrounding these cells determines what cell line is made. So if we are bleeding and need platelets and RBC's, our stem cells are stimulated to make those. When we are fighting an infection, the exact same cells may switch to making lymph line T and B cell precursors. The problem is, some of these stem cells turn out cell lines where the lymphocytes have parts of the DNA missing, or extra pieces (trisomy). And over time, these defective CLL lymphocyte cells don't even leave the marrow, they crowd out the other stem cells from functioning properly and people start to have problems making RBC's and neutrophils and platelets. The drugs we use, try to affect the lymph line more, but since at least some of these chemical signals causing cell differentiation are related to *ratios* or concentrations of existing chemical messengers, it's extremely difficult. We may not be able to completely block a protein used in multiple cell processes without causing problems in the other cells. And research is looking at how further mutations, such as NOTCH, affect this complex juggling act. So we are somewhat affecting the stem cells, that's why we see problems with RBC and neuts and platelets. When we suppress stem cells "too much", all cell lines can be affected.
The current way to wipe out all the B cell progenitors and start fresh, is with a transplant. CAR-T is more promising IMO since it is using our own DNA, so fewer problems than even a sibling match, for a stem cell transplant. Traditional chemotherapy can work for wiping out stem cells in CLL, but only in certain patients where the lymphocytes carry specific defects. But since traditional chemotherapy can also severly affect other marrow cells, docs should not use it unless it will work, hence the "Test Before Treat" push, to make sure folk have variants that can be affected. Other defects (notably del 17p) aren't really affected by the older agents, and shouldn't be used in these patients. And these new "multiple gene testing panels" are trying to find out the correlations between any missing proteins (like a NOTCH mutation) that modulates these stem cells activity/function, and how the disease is further affected.
Thank you so much for your explanation. I am in awe of your knowledge and expertise! For me, understanding the science gives me a sense of control which I often times lack when trying to cope and manage the treatment for this condition. Even though I’m not the one affected, my job is advocate, home nurse and cheerleader. I can’t do my job without this understanding, so I am in your debt! Thank you so much again and wishing you a happy holiday and a worry free 2023!
uMRD means undetectable cancer cells (remission) - I completed my 1 year regimen of O+V 10 months ago and have been told it could take years for my blood to return to "normal". I have my oncologist appointment later this month (December 2022) and should have more to say about my remission status and blood status. That being said, I feel great!
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First appointment since ending V+O treatment 
dental work while on V + O
Since being on Imbruvica 425....WBC has climbed to greater number....
Ibrutinib VS V&O
