Grounds for re-staging to Rai Stage – IV?
The other day I heard from a good friend whose local oncologist had just changed his Rai Stage from a reassuring Stage – I to a scary Stage – IV. The reason for the change? His latest CBC (complete blood test) done a couple of days earlier showed his platelet count was 96K. This is just shy of the 100K lower limit many labs use for healthy platelet counts. All other counts were doing fine and there were no other symptoms – unless you count being a tad tired after putting in long hours planting trees.
True, definition for Rai Stage – IV is based on thrombocytopenia (reduced platelets). Going by the book (and brain not engaged!) the doctor promptly declared my friend had now graduated to Stage – IV and should start treatment (FCR) right away. Which brings us to the important question: are there other reasons besides late stage CLL that can cause platelet counts to drop? Are some possible reasons for dropping platelet counts more serious than others?
Let me count the ways ..
There are many different reasons why my friend’s platelet counts came in below the “magic” threshold of 100K. Some are trivial, some need attention, some can be downright alarming. It is foolish to put all these causes in the same basket! Call me picky, but I have serious problems with this shoot first and ask questions later approach to medicine.
Reliability of blood tests
Let’s get started with some of the more trivial reasons. How accurate do you think the platelet count number is on your latest CBC? What if it was 115K last month and this month it is “only” 96K? Should you get ready to write out your last will and testament because you are now at Rai Stage-4?
Not on your life, not without a bit more digging to understand the result. For starters, platelet count measurements are notoriously poor at accuracy and reproducibility. If you gave two samples of blood on the same day and CBC was run twice on the two samples, same lab tech, same machine, same phase of the moon or whatever, the two platelet count results can still differ by as much as +/- 10 or more. You see, platelets have a tendency to clump (which is why they are so important in proper clotting of blood). They may clump a tad more in one sample and less in the other. The machine counts a clump of, say, 4 platelets as 1. You can see how that can be a problem right there.
How about tests done in two different labs, using different machines? The variation can be even more pronounced, depending on how well the machine is maintained and calibrated. That is why we encourage our members to try and get their blood work done by the same lab each time, as far as possible. For women who are still menstruating, it is also important to get the test done during the same part of the cycle each month, in order not to bias red blood cell counts.
Now for a really trivial reason why platelet (and other cell) counts may drop in a given test: try drinking a couple of glasses of water just before you drive over to the lab for your blood test. Your blood is “diluted” pretty much as you would expect with all that water sloshing inside of you, and all your counts would be lower!
How then do we make sense of CBC reports?
For starters, do not get fixated on any single number in one lab report. That is why we encourage our members to plot their lab data on a graph and look for overall trends. You can download a nifty spreadsheet template that you might find useful in monitoring your charts from our flagship website www.clltopics.net
The platelet counts for the past year are plotted below for a generic patinet, with a computer generated best-fit straight line (blue) through all the data points. Looking at the blue trend line it is clear there is a slow decline in the platelet counts, not unexpected in a patient with CLL.
While it is true that the latest point in February fell just a tad below 100K, looking at the scatter of the data points from the blue line, it might as well have been 110 and not 96. The scatter of the points represents the errors inherent in the lab equipment and other such stuff we discussed above. A reasonable assessment of this data is that there is a gradual decline in platelet counts and it would be a good idea to keep an eye on it and not let it get a whole lot lower before considering therapy.
But tell me, do you still think the last platelet count number in February is a big red flag needing urgent action with the biggest gun available to you, no questions asked? You will be happy to know in my friend’s case, a second blood test done a couple of weeks later put his platelet count back where it normally is, in the low hundreds. No drama here, nothing to see, move on folks.
There are also some non-trivial reasons for drop in platelet counts that may still have nothing to do with CLL. Certain medications can confuse the immune system and cause platelet destruction. Examples include heparin, quinidine, quinine, sulfa-containing antibiotics, as well as some oral diabetes drugs
CLL related causes for low platelet counts
The definition of the high risk group in both the Binet and the Rai systems of staging depend upon anemia and thrombocytopenia. But most experts now agree, it is important to consider the why of low red blood cells and platelets, not just the how low.
Bone marrow packed to the hilt with CLL cells
As your CLL progresses, there is a gradual accumulation of CLL cells in your body. These useless cancer cells accumulate in your blood (you will see it as an increase in WBC and ALC), but many more will accumulate in swollen lymph nodes, spleen, liver and most importantly – your bone marrow. Over time it is possible for the bone marrow to get infiltrated by so many CLL cells that there is little room left. A bone marrow biopsy can reveal the exact status. I have seen bone marrow biopsy results showing as much as 90-95% infiltration of the bone marrow.
Why is this important? Well, your bone marrow provides a very unique function. It is the only place in your body where new blood cells (red blood cells and platelets, for example) can be created. Millions upon millions of these cells die each and every day due to normal wear and tear and a healthy bone marrow replaces these lost troops with fresh new cells. But if the bone marrow is thoroughly infiltrated with CLL cells it cannot perform its proper function and make new cells. The result is a gradual dropping off of red blood cell and platelet counts (the drop off can be precipitously steep as the level of infiltration gets higher and higher). Think of it as a factory with perfectly good machinery, but one that is packed to the rafters with garbage. Until the garbage is cleaned out there is no way for production to start up again. In CLL terms, this means start of appropriate therapy to clean out the bone marrow, kill as many of the CLL cells festering there and free up some space so that normal cell production can begin again.
Dead or dying bone marrow with damaged hematopoietic stem cells
A more dangerous reason for low counts across the board could be that the bone marrow is completely shot, either because of the cancer itself and/or the effect of prior harsh chemotherapy treatments. For these or other reasons, the stem cells have given up. No more production; crucial machinery is busted beyond repair and the factory is burned to the ground. A bone marrow biopsy would reveal a graveyard type of scenario, no new baby cells being produced, nothing happening. No new red blood cells or platelets or neutrophils being made.
There is no way to fix dead stem cells, except to replace them with healthy new stem cells from some one else, new stem cells to take over the job of producing all the vital cell lines. We are talking mini-allo stem cell transplant from a willing and healthy donor who matches the patient. Bone marrow aplasia – when the bone marrow is no longer able to produce necessary cell lines – is serious business. Without a stem cell transplant the patient would become dependent on frequent transfusions for all the necessary cell lines – just to stay alive. This is not a good place to be, long term.
Role of the spleen
The other reason for low red blood cells and low platelets could be that although they are being produced normally back at the “factory”, (bone marrow), they are not being allowed to do their job properly and in fact they are getting destroyed before their time.
The destruction could be due to improper functioning of the spleen, for example. Your spleen acts as a filter of sorts. If it is clogged (enlarged) with lots of CLL cells, it does what any clogged filter would do, it does not let stuff get through that is supposed to get through. People with large swollen spleens due to CLL infiltration could have good, perfectly normal platelets sequestered and destroyed by their spleens. In such cases, splenectomy (surgical removal of the spleen) is often recommended.
While this is major surgery, and no one wants to leave behind a piece of their original equipment in the operating room, splenectomy has surprisingly excellent results and few complications if done early enough. Surgeons have perfected laparoscopic methods where only tiny incisions are made and this speeds up the healing process. Many patients live just fine without a spleen; but be aware that patients without a spleen have to be a lot more careful about infections. You are advised to go the nearest emergency room at the first sign of a fever.
Autoimmune disease
Another reason for low platelets (or red blood cells) could be autoimmune disease. Even though CLL is a B-cell cancer, when your system is choke full of these malignant cells, they manage to corrupt a lot of other parts of the immune system as well. Under normal circumstances, the body depends on antibodies and killer cells such as T-cells and macrophages to protect itself from foreign invaders. When things go wrong, as in advanced stages of CLL, everything gets subverted to some degree.
Autoimmune disease is one face of this subtle corruption from within. Antibodies may be produced that attack red blood cells and platelets, tagging them unfairly as “foreign and dangerous”. Killer cells then home-in on these unfortunate cells and kill them. In autoimmune disease the careful distinction between “self” and “non-self” breaks down, and the very defenses that should keep us safe start attacking various parts of the body. When platelets are the hapless targets, it is called ITP (idiopathic thrombocytopenic purpura). When red blood cells are the targets, it is called AIHA (autoimmune hemolytic anemia). Patients with either ITP or AIHA can see sudden and frighteningly steep drop in platelet counts and red blood cells respectively. Diagnosis of autoimmune disease as the root of the problem is confirmed by identifying the antibodies that are tagging the poor innocent cells and getting them killed. Autoimmune diseases is often treated with steroids (prednisone) with or without Rituxan. When steroids are no longer enough to control autoimmune disease, it may be necessary to treat the underlying CLL as the root cause of the problem.
Refractory AIHA and ITP can be very dangerous and not something to be taken lightly.
Putting it all together
Once we have eliminated the trivial reasons (such as variability in the lab test results) it becomes important to rule out the most dangerous reason for dropping counts – a dead or dying bone marrow. If this is the reason for dropping counts (red blood cells or platelets), that is bad news indeed.
If platelet counts are dropping due to untimely destruction of platelets in a clogged spleen, even though they are being produced OK in the bone marrow, this can be corrected by splenectomy, or CLL therapy to clean out the spleen. Similarly, bone marrow infiltration can be decreased by suitable therapay. Growth factors such as Procrit (which give the bone marrow marching orders to make more red blood cells) are often used to correct anemia in cancer patients. Use of growth factors to correct low platelets is not quite as common. At a pinch, patients can be stabilized by means of transfusions of red blood cells or packed platelets. Be aware most hospitals do not transfuse unless the patient has hemoglobin less than 10, and platelets are rarely transfused until the patient’s counts drop below 10-20K!
If the problem lies in autoimmune destruction of platelets (or red blood cells), the usual approach is to use steroidal drugs such as prednisone or dexamethasone to calm down the immune system and tamp down the berserk killer cells. It is a very effective approach. The downside is that long term use of steroids is very immune suppressive and can leave the patient more vulnerable to infections and the like. Also, most patients become resistant to steroid therapy sooner or later. Rituxan is often used in combination with steroids and this seems to give better results. AIHA and ITP are complex beasts. Please refer to our flagship website www.clltopics.net for full length articles on both of these conditions – we go into a lot more detail there.
Getting back to the Rai staging issue
Below are the criteria used in staging patients into the various Rai stages. The Binet system of staging used in Europe and else where is not all that different.
Rai Staging System
Stage 0: Your CBC shows absolute lymphocyte count is too high, more than 5.0 K. You probably have no other symptoms, and the CLL was most likely diagnosed as a result of a routine blood test. Patients in Stage – 0 do not have swollen lymph nodes, spleen or liver. And you have hemoglobin, red blood cells and platelet numbers that are all in the normal ranges. Neutrophils are also “in the pink”, and you have not noticed any higher frequency in getting infections.
Stage I: By this stage, some of your lymph nodes are swollen (lymphadenopathy), but that is the only thing that has changed from Stage – 0. Everything else is still within the normal limits, and the spleen and liver are doing fine too.
Stage II: Besides the swollen lymph nodes of Stage – 1, you have now graduated to where either your liver is swollen (hepatomegaly) or the spleen is swollen (splenomegaly). The CLL has now started impacting other organs of the body, in addition to the peripheral blood, lymph nodes and most likely the bone marrow as well.
Stage III: The pivotal indication of Stage – 3 in the Rai classification system is anemia, there are too few red blood cells and too little hemoglobin. Since red blood cells are the only carriers of oxygen, not having enough red blood cells is pretty hard to miss. You will start to feel out of breath, tired after exertion, and generally not up to your old feisty self. This is considered such an important criteria that a patient is defined as Stage – 3 if he/she has significant anemia, even if the lymph nodes are hardly swollen, and the liver and spleen are doing OK too.
Stage IV: Like Stage – 3 discussed above, the crucial criteria for putting patients in Stage – 4 is not having enough platelets (thrombocytopenia). The lymph nodes, liver, or spleen may be swollen, and there may be too few red blood cells (anemia). Typically, patients in Stage – 4 have all the bells and whistles, swollen lymph nodes, high WBC, swollen spleen and liver, anemia and thrombocytopenia.
Details missed by the Rai staging
As you can see from the definitions of the Stages III and IV above, the pivotal issues are anemia and thrombocytopenia. Rai staging does not ask why red blood cells or platelets are low in order to make the call. It is sufficient if the counts are below established norms. But as we have discussed above, the why of the matter is very important indeed!
The abstract below reports on 132 patients with CLL/SLL. Careful analysis showed that if the anemia and thrombocytopenia were due to autoimmune disease, as in AIHA (autoimmune hemolytic anemia) and ITP (immune thrombocytopenia), there was no significant penalty in terms of overall survival. If these patients had been put in the high risk category based strictly on anemia and thrombocytopenia as per the Rai and Binet staging systems, they would have been miscast in the role. On the other hand, if the anemia and thrombocytopenia were due to bone marrow failure, then the risk of death was significantly higher and the “high risk” classification is justified.
Am J Hematol. 2003 Sep;74(1):1-8.
Autoimmune cytopenia does not predict poor prognosis in chronic lymphocytic leukemia/small lymphocytic lymphoma
Kyasa MJ, Parrish RS, Schichman SA, Zent CS.
Division of Hematology/Oncology, Department of Medicine, Central Arkansas Veterans Healthcare System (CAVHS) and University of Arkansas for Medical Sciences (UAMS), Little Rock, AR
Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is characterized by an acquired immune defect that can cause autoimmune complications, including anemia and thrombocytopenia. We conducted an observational study of the epidemiology, clinical presentation and significance of autoimmune complications of CLL/SLL in 132 patients from a large population (>45,000 veterans), in which at least 90% of patients with CLL/SLL have been previously identified. Over a period of 12.5 years, 12 patients (9.1%) had autoimmune complications; of these, 6 (4.5%) had autoimmune hemolytic anemia (AIHA), 5 (3.8%) had immune thrombocytopenia (ITP), and 1 (0.8%) had pure red blood cell aplasia (PRBA). All 6 cases of AIHA had a positive direct immunoglobulin test for IgG and C3d. In 6 patients, CLL/SLL was an incidental finding at the time of presentation with autoimmune cytopenia. Nine out of 10 patients responded to immunosuppressive therapy, which was complicated by serious infection in 7 cases, one of which was fatal. The major cause of mortality in patients with autoimmune complications of CLL/SLL was secondary malignancy. Survival of patients with immune cytopenia was not significantly different from CLL/SLL patients without immune cytopenia. Among patients with anemia or thrombocytopenia, mortality was significantly higher in those with bone marrow failure compared to an autoimmune etiology. We show that in a non-referred population with a high incidence of CLL/SLL, autoimmune cytopenia can occur early in the natural history of the disease. These data suggest that the Rai and Binet classifications for CLL need to be modified for patients with autoimmune cytopenia.
PMID: 12949883
60 comments on "When platelet counts start dropping"
very interesting article Chaya. I had never read any of this before.
Thanks
Once again a completely thorough yet simplified presentation of another critical topic. Thanks so much Chaya. This is so valuable. Regarding your spread sheet, I am one who has benefited greatly over the last five years using it religiously. Thankyou PC. My platelets have often followed that scattered pattern along the blue line, and in the 100k zone. It’s a comforting guide really, to help steer a more thoughtful and calmer course.
Having said that, my platelets now have tanked in the last couple of months along with other key markers going in the wrong direction. Consequently, on Monday I started back on SubQ Campath. Today (Wed) was my second dose. I’ll be adding rituxan for my Monday sessions starting next week.
Thanks again for all you do, and for doing it SO well.
Bob Larkin
Dear Chhaya,
I was told there is some drug now for low platlets but is still not approved for CLL. Can you throw some light on that?
Regards
Hiten Jhaveri, Mumbai-India
Excellent elucidation of thrombocytopenia.
Best,
Lloyd Shane
Chaya,
I have been struggling with ITP for over a year now following PCR treatment followed by Campath consolidation. None of the conventional treatments (IVIG, WinRho, steroids, platelet transfusion) worked and they were reluctant to give me more monoclonals following recent Rituxamib and Campath. Platelet counts are usually below 10,000 which are a very scary place to be and, due to the driving restrictions, seriously impact on the quality of your life. I did get a transient response to Prednisone + Danazol + Vincristine but this had to be stopped due to neuropathy. I recently started on one of the new thrombopoietin agents, N-Plate injections. I chose this over the “pill” (Promacta) because I was concerned about the recommended need for biweekly liver funtion tests and drug interactions. At first I had little response to 6 weeks of escalating doses, with counts remaining below 10000, but now I am happy to report, with the reintroduction of Prednisone, my platelets went from 24000 to 240000 in just one week ! Of course, now we will have to readjust my doses and nobody can predict what next weeks’ number will be but that seems to be the lottery of life with CLL. My take on this is that the platelet stimulating drugs alone do not work and require concurrent blocking of the immune system for a combined effect. Anectdotally, my oncologist has 3 patients with ITP who do not have CLL who had huge responses to NPlate alone. We’ll see where this road leads because every week things change.
Ben Malkiel
Terrific info, thanks.
Now how come I can’t find a humble note of encouragement like: “If you found this article helpful and you would like to make a financial contribution to the health of this under-resourced site moving forward, please follow this link. Thank you.”
I would not be offended to see such a message in all your postings. People need to be reminded to help! And we will not feel pressured to give when we cannot.
Closed mouths don’t get fed. We’re behind you all the way Chaya.
All the best, Jim
This brings up a good reason to keep an accurate chart of one’s blood results. I use Quattro Pro and started my own database in 1999 when we first started getting weird lymph counts and swollen nodes. I update it with the results of each blood test (my doctor emails the complete test results the same day she receives them)!
Since ALL the data is present in one place and can be charted and analyzed for trending with just the click of a mouse, I often printed out trend analysis charts or graphs to take with me with the data that we may have an interest in during that visit. She has kept a couple of my complete listings, as that shows more on one page than the method the hospital uses.
Now I don’t have to print them anymore! With the new building at the Wilmot cancer Center at the U of R, they have computers in each exam room. I put my updated chart, graphs or data on my website, in a folder for the hospital, and we can access anything of interest right there in the exam room. This helps as we often have questions about data I had not charted, and we can access the entire database unlike the hospital’s database which only goes back for the last 5 tests without having to access another database. And their’s are not able to be easily charted or graphed.
They have a shortcut to my website on the desktop of the computers now!
In summary, for those who have not started yet, do indeed use a database to keep track of everything. It helps everyone out.
This article clarifies the mystery of blood counts very nicely. Thank you very much! There is one thing that I haven’t been able to understand about the staging process. If the (grossly enlarged – 10 x normal size) spleen is removed because chemotherapy didn’t correct the low platelet count or improve the condition of the spleen, and, after the spleen is removed, the blood counts return to normal, is that patient then staged lower? Or are they still considered to be in stage iv because their system is “incomplete”?
My husband basically wants no information about his condition. This question is something I haven’t been able to find information on leading me to believe that the stage would still be considered IV. I would appreciate any help. Thank you!
Maryann
Chaya
The information you provide has allowed me to be a better informed patient. I was diagnosed with CLL in 2004 and AIHA last fall and was treated with predisone with great results. I am receiving monthly IVIG transfusions and last month the blood work showed an alarming drop in the platelet count. Fortunately after retesting it was determined to be a lab error. This article was very helpful in understanding the key areas that I need to be watching for.
Thanks for all you do!
Jimeluiz, I love your comments. This is probably one of the best if not the best information Cll education site on the web. Chaya and her team have been absorbing all the cost and time associated with this nasty condition. How about the community helping out so we can continue to receive this information not easily available on the web. Chaya even writes at a level we can all understand. There is a “Donate” link on the site which I use and is very easy to set up a payment schedule. Think about helping to keep this site up to date and very informstive. Chaya, your a great American.
Chaya,
All CLL patients should feel so fortunate to have you on our side. This article explains clearly and concisely the issues involved in platelet loss and what to keep in mind as a patient. I for one, have been a somewhat atypical stage 0 patient and was thrown for a loop when my onc began talking about treatment with my wbc below 20k—but my platelets were continuing to drop.
I can’t thank you enough for the wonderful work that you do—-oh, yes I can and will make a contribution today to keep the site alive and the information we need coming.
Thanks again Chaya—(incidentally your name means life in Hebrew)
lynn
My spleen was the size of a partially inflated basketball (literally). My platelet count had dropped to 60, and I was very anemic. They were going to remove my spleen, but a BMBx showed 70% bone marrow involvement, so they rushed me into FCR instead.
After 4 cycles (with slightly reduced fludarabine) completed almost 2 years ago at age 65, my spleen is not palpable. My platelets hang around 200, although I drink fluids like a fish. My other counts are great. I am in what my doc says is an MRD negative CR using either a 5 or 6 color flow (he didn’t know which).
A recent ASH report states that CR’s via FCR today carry a progression free median of 7 years. Dr Hamblin says that those stats are for the old 1996 CR guidelines, not for those of us with better CR’s. He also says that since I have already survived for 2 years, my expected median today should be more than 7 years even under the old guidelines.
If a doc advises you to have a spenectomy, you may want to discuss with him the possibility of having FCR instead.
For me, so far, FCR has been a tremendous success story. Of course, we all know….
Chaya,
Again you have shared your knowledge and information with us. I greatly appreciate your thoughtfulness.
Knowledge is Power.
I finished with Rituxan in February and am currently on Chorambucil and experiencing the ups and downs of my platelets. This is the first time my rbc and platelets are envolved. Your information is valuable to me.
Sincerely,
Rita
Thanks everyone for the kind words. Bob, your comment about PC brought tears to my eyes. My Sweetie lives on in the memories of all who truly value what I try to do on this site.
As for donations, yes, I can use some. People have been registering for membership in droves, but the number that hit the donate button is distressingly small. The money is obviously needed and welcome, but even more than that I can use the sense of validation that comes with people putting their money where there heart lies. Talk is cheap, as they say. I confess there are days when I second guess myself and it is hard to get out of bed for yet another day of CLL advocacy / education. Mothere Theresa I am not!
As I said when we started “Updates”, this is an experiment to see if the patient community will support my work with their hard earned cash. I am afraid the jury is still out on that question. It may be that the time has not yet come for my brand of advocacy / education, not when it comes to grassroots support. If that is the answer to the experiment, I will accept your verdict and move on. You decide.
Getting back to the subject of ITP, I came across a terrific Mayo Clinic review of the options open to patients with refractory ITP. If any of you want to read it send me a personal email. I must warn you, it is pretty grim reading.
I will dig a little more into the new drugs that may help as platelet growth factors and write about them in a future article.
I think that the definitions in the Rai staging are unfortunate. My platelets dropped below 100 in 1998, four years after diagnosis. For four years they ranged from 70 to100. No one talked about treatment until my spleen got seriously enlarged and I was having fevers. I was in the RFC trial in 2002; during treatment my platelet count was between 40 and 60 and they stayed there for almost a year.. Since then they have consistently been in the 70’s and 80″s. When I had sinus surgery in 2003 they were at 58 and my oncologist ordered a platelet transfusion ahead of time. My remission continues, my counts are steady, and I haven’t had bleeding or bruising problems–except that I need to maintain pressure on the site of a blood draw if I don’t want a spurt!
Still, it’s nice to hear about new drugs that are working.
Cathie Nicholl
Chaya, shame on anyone who uses your site without giving what they can to support it. As you said, it is more a matter of validation. Some of us may not be able to send a lot, but every person should be sending what they can. Over the years my husband has had low platelets, I do not see exactly an explanation for this that I can understand. All other counts are great, but platelets have hovered in the 100K range for years. Then again, maybe the Rituxan is keeping things from getting worse, and maybe it is actually ITP keeping the platelets from getting better. Beth
Chaya
After my 2nd chemo (Chlorambucil), my platelets tanked to 10 and remained at this low level until I had FR Jan./08 when it went to 31, then down to 8. I required 3 platelet transfusions and 13 blood transfusions. They have been in the 40 to 60 range ever since. Today, after 2 rounds of Chlorambucil and 3 rounds of FR + Dexamethasone, they have climbed to 73. My oncologist intends to give me about 4 more cycles of FR. He told me that if I can complete these chemos, I could expect a remission of about 2 years.
Any comments that you might have would be gratefully appreciated.
Irv Noble, 75
Canada
Maryann:
Yes, it is quite proper to change your husband’s Rai staging down from the scary Stage – IV if his counts are now stable. But one of the points I was trying to make in this article is that Rai staging is not as important as it used to be, in fact it has become a bit of an outdated thing. In my layperson opinion it is more important to get a handle on the patient’s prognostics based on modern, molecular level tests such as IgVH gene mutations status, FISH, CD38, ZAP70 and B2M. “What kind of CLL do you have” is probably the most widely read article on our flagship website clltopics.org. The “Bucket classification” we defined there is used by most patients now and even a few oncologists have started using it!
EBW:
Some people have consistently low platelet counts all through their lives. There seems to be an ethnic component to it and some groups of people have low platelets without any negative consequences. Basically, the proof of the pudding is in the eating. If low platelets are not causing any problems such as excessive gum bleeding, then there is nothing to worry about.
Irv:
I am glad FR + dexamethasone is doing a good job of bringing back your platelets. That your oncologist has added dexamethasone suggests to me that perhaps he thinks you have an autoimmune component to your low platelet problem. Is that the case? Also, I would like you to read the recent full length article on ITP we have on CLL Topics website. It has some information regarding ITP and H.Pylori that might be interesting to you. In some cases eradication of the very common stomach bug H.pylori has been effective in helping with ITP and low platelet counts.
Chaya, I can’t tell you how much I appreciate your answer to my question about staging. You made my day! :)My husband initially had a poor prognosis, being diagnosed with “very advanced” cll. Therefore, even though it is almost meaningless, I am grateful to mentally be able to take him out of the stage iv bucket. He has had two courses of chemo, FCR (which didn’t hold very long), and PCR (@ 80% strength)prior to his splenectomy. The chemo was supposed to hold him 1- 2 years,and it was two years in January. Now that I know he isn’t necessarily in stage IV anymore, I feel relieved, like I can stop waiting for the other shoe to drop because his blood counts are still good.
Thank you so much! Maryann
Chaya, Thanks for all that you do for us—your work is valued!
If a swollen spleen and low platelet counts are the only problems a patient has, they may want to consider a laproscopic spleenectomy. I happily had my 8 pounder removed (by a very experianced doc)—after two consults. I have been able to avoid drugs for almost three years! This option is probably not for most people, but it is one worth considering if they fit in those narrow parameters. You get to save the big chemo guns for later, get rid of a “potential-probable” future problem while you are healthy and some future treatments are more effective.
Everyone should consider giving what they can for a subscription to the most up-to-date and important “periodical” available to the CLL community! This site is worth more to me than a few throw-away magazines and a couple of movies. Imagine how much this site would be missed and how much harder your research would be if it were to go away.
Chaya,
Again thank you for this very timely article on low platelets. I have been charting my condition since day 1 with a system that has worked for me, Not so much a graph but I can do that as well to see where the pattern is going.
I have been very fortunate so far without treatment, the concern has always been the low platelets though. This had helped me understand the clumping of cells. Last month my platelets were 99, this month they are 88. So it is confusing at times, to still feel fine but looking at the counts say something else. I will see my oncologist tomorrow to discuss all of this. Thank you for your help. And now that I just found you I would hate to see this site go away. I would if I could support , but am not working at present. Thankfully we are still insured and my husband is employed. This has been invaluable information and the first I have seen that explains it in such detail.
Chaya,
As a computer software challenged person I must say that your & P.C.’s charts are a wonderful tool that many health care clinics and oncologists do not have access to. I found this depressing because I have had to use your charts to argue with oncologists who have only looked at one or two current lab reports by which they were recommending treatment.
Initially, I was put off by thinking I would need to purchase MicroSoft Excel to use your charts but in your article you mentioned free shareware called Open Office which is easy to use and I hope more patients get the message to chart their bloodwork and look for trends connected to reasons as you have pointed out in this article.
On three occasions from one year ago I have had Doctor panic caused by spiking away from median values. Your charts have provided a rational way to prolong Wait & Watch with a measure of safety.
with much gratitude & a donation,
WWW
Chaya,
One tip: ask the heme-onc to personally review the slide. Platelet clumping can be seen by the human eye under the microscope, but not by the automated counters.
More recent reassurance from the article:The prognostic significance of cytopenia in chronic lymphocytic leukaemia/small lymphocytic lymphoma by Zent et al in BHJ 2008
“Although cytopenia caused by BM failure predicted a poorer prognosis in CLL, cytopenia caused by AID was not an adverse prognostic factor. These findings suggest that patients with cytopenia due to AID (auto-immune disease) cannot be meaningfully classified by the current clinical staging systems.”
That said, I have seen other articles that suggest the opposite. Moreover, the treatment for ITP is usually immunosuppressive, the last thing we CLLers need. Also ITP can force the need for treatment sooner, and can rarely be the cause of death itself (brain hemorrhage or bleeding from an otherwise non-fatal trauma). It is always scary to be walking around with single digit platelets, knowing a bump on the head could be catastrophic. Fortunately, spontaneous bleeding is rare in ITP, as the platelets are younger and stickier-super platelets, so lower counts can be better tolerated than in bone marrow failure.
Splenectomies may work for ITP as well hypersplenism (enlarged spleen)
The TPO mimetics are a new exciting (and expensive) option. Much to learn.
Brian
Brian:
No argument from me, I agree completely with you autoimmune disease is not something you would wish on anyone, and refractory ITP or AIHA can be life threatening.
That said, I think the point Dr. Zent makes is very important and I want to make sure there is no confusion on that front. Autoimmune disease can be treated in the majority of patients, with relatively safe drugs such as Rituxan and prednisone. Notice the operative phrase is “relatively safe”. As most of you know, I am not a big fan of prednisone but it does have its role and it is an important part of controlling out-of-control immune system cells. I know of hundreds of CLL patients with AIHA and ITP who are alive years after diagnosis of their autoimmune disease. If nothing else, they get time in which to get their ducks in a row, perhaps plan for a stem cell transplant. Both of us know how much planning goes into that process!
A dead or dying bone marrow (ie., dead or dying stem cells) leaves no therapeutic options other than an allogeneic stem cell transplant. That is about as bad as the news can get, and that is the basis of the Rai Stage -IV classification, the last stage of a five stage classification. It is not logical to put some one in this last stage if all that is required to stabilize their counts is, for example, a splenectomy. This is a major shortcoming of the Rai staging system, in that it does not distinguish between the various reasons why the platelets or red blood cell counts may be tanking.
Transplants are not for sissies. I know, I was there on the frontline with PC as he fought for his life last summer. Moreover, as we all know, not everyone has the ability to take the mini-allo transplant option, either because of age and general health, lack of a matched donor, or lack of insurance. For these people a dead bone marrow is pretty close to a death sentence. Trying to stay alive with transfused blood products is just not practical as a long term solution.
Bottom line, I will take autoimmune disease any day of the week if the other option is bone marrow aplasia, where stem cells that have given up the ghost.
Chaya,
Thank you as always for sharing your wealth of information w your straightforward & practical approach. I agree that the Rai system is outdated, I actually had a consultation w him several years ago & was not so impressed. That said, the splenectomy that I had 4 yrs ago to remove a 15 inch spleen & which promised that my platelets would increase by a large percentage even before I was out of the OR, didn’t live up to it’s promise. All my other counts increased but my platelets have consistantly remained @ around 30K. Since I have no other options now(having LGL T cell leukemia)I will put up w the bruising & bleeding gums for as long as I can & hope that someone will find a better way than the toxic drugs they are offering now. And when they do,I know you’ll be the first to report on them in a straightforward, honest & compassionate way.
Thank you for all you do,
Lorraine
Dear Chaya,
I think that the role of asprin, stanback, B C powders, and the likes should be discussed along with the warning to all cllers who have platelett problems. Also I think vitiman k should be discussed, as i dont think any of these have been mentioned above. Also the Institute for Traditional Medicine in Portland Oregon, has some interesting information and data on ITp and treatment with chinese herbs.
With Best Regards To all,
Raymond Parker
Chaya,
Thank you again so very much for your time invested to this web site. May it continue and may all who benefit from it donate with a greatful heart.
After my platelets dropped to 80 last month and Hg to 10.4 my local Doc wanted FRC right away but it was actually Dr. Zent that advised me to get a bone marrow biopsy first so that I would be certain of the reasons of these drops. Wise advise I say.
Well, the numbers were found to be considerably better after bone marrow biopsy only 4 days after my last “alarming” CBC the numbers came back up rather drastically and so FRC was postponed for at least another month.
That sure supports what you have said here. Numbers can sure vary and change. From 10.4 to 11.7 Hg in 4 days and from 80 to 96 platelets in 4 days. Enough to put off FRC.
Thanks again,
Mark………..gong to donate NOW
Dear Chaya,
Thank you for this excellent commentary which is one
more of hundreds of informed materials and analyses of great value
you have provided to the CLL community.
Over five years I have been blessed and rewarded in having you
as an unmatched resource. I am sure other people have benefited from
your research and willingness to educate us. There just is no better way for our CLL Community to understand this disease and its many
ramifications. If we look at your “Table of Contents” as well as all the
”Recently Published Articles” the font of information is invaluable.
There is solid and medically based information presented in terms
we can understand. There are proven and informative solutions enhanced
by your sound suggestions, expertise and insights.
Chaya, you have expressed a need for ongoing financial support.
I feel an URGENCY to address this. You are willing to dedicate
your LIFE to our cause. It seems only fair for our CLL Community
to reciprocate. You are deserving of this support.
We can not just read these excellent messages and take them for granted.
Hours and hours of research and writing goes into them.
You would be a devastating loss to all of us. It just can’t happen. I urge others to join with me giving you our ongoing financial support and to pass this message on. You have my permission to put this message on every new” Updates.”
PC’s “giving spirit” is with us always.
Gratefully,
Jean Hartigan
Chaya,
great article, as usual. My one other comment is that I think it also should be mentioned that platelets decline, and I mean by a lot more than what could be explain by normal variability in CBC tests and what not, may be the first sign (announcement) of the bone marrow having been pushed to the limit by invading/proliferating CLL lymphocytes, and enlarged spleen kicking in to do its part. Red cells and hemoglobin could remain normal for another month, more or less, before it all comes crushing down and requiring transfusions.
Arnold
yeah, and one other comment. I totally agree with other people who commented on this already. Come on people, show your appreciation, kick in a few $$ (or whatever your favorite currency is.) Not everything on the internet is/can be free.
Arnold
Thanks, Chaya for your helpful advice on my platelet problem. Yes, I do have an autoimmune problem connected to my low platelets. I will discuss the possible H.Pylori connection with my oncologist.
Irv Noble
Thank you, Chaya. CLL Topics is the best online support I have found for reliable information since my diagnosis last February. I will send monetary support as often as I can. Bless you for what you are doing.
Margaret
Thanks Chaya for your comments on ‘measurement errors’ and the importance of ‘looking for trends’. Speaking as a retired analytical chemist and CLLer, this is an aspect of science (medical and otherwise) that never gets enough exposure within the general public. Keep preaching!
Al
After having one physician press for treatment based on only one data point only to reverse the recommendation after another, more favorable, data point, I learned long ago to never ever decide on anything unless the test result is reproduced at least once. I have seen factors of three variation in test results over 48 hours so I am well aware of the variability in automated systems. As for bringing humans back into the test as Brian suggests, we have this situation with those that read x-rays, CT scans, echo cardiograms etc and even there one finds disagreements. Perhaps counting cells may be easier than these examples but I would still stick with my reproducibility requirement before submitting to any procedure.
This is a little off base to this post but… My wife was diagonised with cll in Mar 04 after 2 yrs of trying to figure out why she had a non itchy, under the skin rash and on going cough with a lot of mucus. Finally saw an onc whho gave us the “good news” about this lucky cancer to have. 5 rounds of chemo later, fludara refactory & rutuxan allergic, we are sort of in a waiting period. The question I have is who else has on going coughs and musus & how do you control? The good docs tell us they have nothing to do with cll but her father had a regular cough & cll, her uncle, non blood the same & my father ditto. (Piety my kids & grand kids) Any help on this one tcd111
TCD,
Your wife may need a work up of chest xrays and maybe even a CT scan of her lungs but aside from a full workup from her personal doc I will tell you about my chronic cough.
I was diagnosed in 04 and have yet to have any direct treatment other than removal of some skin lesions and treatment for a very persistant cough.
The cough started in Winter(Feb) 2007 and I was put on 3 different kinds of antibiotics, I think keflex, z-pac and clindamycin. The cough kept persisting and I finally got releif in May of 2007 by using a steroidal inhalent called Advair. As long as I used Advair the cough would be controlled. I needed to use Advair all through that summer until the cough finally went away in the fall. I hope this helps. Make sure you have someone follow up on her cough.
Chaya, I am not sure if this is where this part of the website is the place to discuss this or not so give us some advice if you want this type of discussion to be held somewhere else.
Regards,
Mark
Hi Chaya
I live in Australia, and tried to do an electronic donation a while ago, but it didn’t seem to work. I am now posting a cheque, although not a huge amount, I hope it manages to make a small difference. Your research and comments have been invaluable and I am indeed grateful to be able to learn so much about this insidious disease. My husband Doug has had CLL/SLL for 13 years now, and was 53 when diagnosed, with initial treatment of Cyclophosphamide & Rituxan in 2003. We are more anxious now as he is requiring treatment more frequently, with more complications cropping up such as infections, splenic infarct, DVT and excessive bouts of fatigue. For the past twelve months he has had monthly infusions of IVIg to alleviate the infections, and every six months one infusion of Rituxan. His counts have increased more rapidly in this past six months. Platelets have been as low as 81, but currently sitting on 145. Thank you again for all your valuable work.
kind regards
Gwen Russell
Mark
Thanks for the info. She has had a recent CT, has seen an ENT doc for tubes in ear and all types of blood work, possible auto immune so we are well covered in that department. Advair is something she used several years ago and unfortunetly I don’t remember if it helped but will be worth discussing with doc tomorrow.
Also I wasn’t sure if this was the best place for this discussion but with all the patient knowledge available here, How else?
PS Chaya, I forgot to say “your welcome and thank you for all you do” I sometimes get too focused and forget my social skills.
tcd111
THIS IS A MESSAGE THAT IS NOT FOR CHAYA
This site is an incredibly important resource for people who have entered into an area of the unknown. Since I was diagnosed 3+ years ago, I can’t tell you how many times the information that Chaya and PC have made available to us has made a difference in my life and given me comfort when my blood has taken some new and unexpected turn. Just the charts give me an opportunity to keep the various counts in perspective as mentioned in the article above.
THIS IS A LABOR OF LOVE FOR ALL OF US THAT NEEDS AND DESERVES TO BE SUPPORTED AND CONTINUED!
It is very easy to set up a simple monthly deduction through Pay Pal to help keep this site viable. If everyone who reads this message had a $10.00 per month donation sent to CLL Topics, I think it would go a long way to keeping the site up and running- and the fact is most of us could afford more than $10.00 a month.
Come on people, if you are able to navigate this site, you are able to set up an automatic donation.
THE WONDERFUL WORK THAT CHAYA AND PC HAVE DONE DESERVE IT -AND WE DESERVE IT.
Chaya – please do forward the (grim) full report. My partner had a spenectomy in February and has been in full cll remission post campath May of 2007. The ride since then has not been scott free and the platelet drops added ITP to the journey. We are lucky to have healthy bone marrow but dropping platelets. We expect to begin Nplate a NEXUS clinical trial next week. Before joining this program, however, we are searching for more information on the “not for people with blood cancers” comment in the Nplate data. Please let our community know if you come across information on NPlate and CLL/ITP patients. We are in year 17 or so of this journey and we keep on keepin on. Bless you for all your efforts and as our unappointed advocate! Jennifer musiclover@cfl.rr.com
Dear Chaya, Clinical Care Options published an expert opinion on advances in treating ITP, including Nplate and Promacta, in Jan 2009. The article also reviews and compares traditional ITP treatments. The “Qualifying Statement” at article’s end may be helpful specifically to Jennifer. Access to the website is at http://clinicalcareoptions.com/Oncology/Login.aspx . Access requires a free, simple login, and the aticle is at http://www.clinicaloptions.com/Oncology/Resources/News%20and%20Comment/Expert%20Viewpoints/January%202009%20Liebman.aspx . CCO is a useful site that often reports on CLL-related topics and meetings such as the annual ASH and ASCO conferences. Content is often provided by researchers and clinicians familiar to CLLers, including Drs. Keating, Byrd, Rai, O’Brien, Furman, Wierda and many others of similar high reputation and accomplishment in CLL research, treatment, and complicating conditions.
Warm regards,
Tim K.
Dear CLL friends
I had CLL from 1998 to 2007 with severe low platelet counts (0..30K).
In july 2007 I was lucky to get a minitransplant and it seems like I’m 100% cured.
I have had very severe low platelets during most of my CLL period and have developed my own theory based on many articles (http://www.pdsa.org/) and carefully study of all my blodtest (more than 200) during that period.
My CLL disapeared after the initial fludarabine chemo (1999). But my platelets remained very low (0..30K). I was diagnosed “ITP” and my spleen was removed. It didn’t help at all.
What helped a little was rituxan, but only short term (2-6 months). My CLL remained not visible at all from 1999 to end 2005. The doctors didn’t know what to do they even doubted that I got CLL.
In order to supress my immune system and allow the platelets to stay in my blood, I got mabcampath in febr. 2005. It helped! within some month my platelets normalized, but then came my CLL !
My theory is:
My immunesystem did fight the CLL so hard that all my platelet was destroied (a normal reaction, your platelets go low when yor immunesystem fights an infection, virus etc ) My Immunesystem was able to keep the CLL at a very low level (invisible), but when I got mabcampath (known for its massive immune-supression) the immunesystem could not fight the CLL any more, My platelets was normalized, but my CLL soon showed its ugly face.
12 month after the mabcampath I was diagnosed with non-mutated CLL and bulky nodes all over.
Luckily I got a steemcell transplant and it went OK.
The doctors doesn’t seem to care, they treat and don’t really care about what the reason is.
hope you can read my english….
Fred (Denmark)
Chaya
As you may remember from an E-mail I sent to you, i am a patient who has been on w and w for 9 years, but now am troubled by falling platelet counts (now down to 74). The above article and comments are both very relevant to me and extremely helpful. The cause of my low platelets has yet to be determined. Apparently, there is no infallible test for determining someone has ITP.
I hope you don’t mind if i make a few comments about your article. They are not meant to detract from it at all.
My understanding (and I am happy to be corrected-I am not a medic.!) is that bone marrow failure and bone marrow infiltration are not one and the same thing. My belief is that a patient is more likely to get into stage 4/C through bone marrow inflitration by the lekaemic cells. If this was the case, I think there would be a reasonable possibility that the infiltration could be reversed (probably only tempoarily) by treatment such as FCR. Bone marrow failure would be another matter
My gut feelling is that ITP would probably be a better scenario than bone marrow infiltration (and, of course, bone marrow failure). However there does seem a fairly acute shortage of available data. The article you referred to above covers an extremely small number of patients with ITP. In the CLL Topics article in which you covered ITP, you referred to an article in Blood, November 2007. This article indicated that ITP was a significantly adverse prognostic factor, However, the article seemed (to me) set extremely stringent parameters for what constituted ITP-the ITP within these parameters seems very severe. I would speculate that ITP could present in milder forms.
I am going to be tested for H. Pylori! Thank you for pointing out the link in your CLL Topics article!
Regards
Antony
Anthony:
You are absolutely right; there is an important distinction between bone marrow infiltration and bone marrow failure. I have written often before on the subject of bone marrow infiltration but I probably should have made that point here as well. In fact, I will edit my article accordingly as soon as I publish this response.
In simple terms, if a patient’s bone marrow is infiltrated so heavily by CLL cells that there is no room left for proper functioning of the marrow, it cannot produce all the other cell lines needed for living. The bone marrow is the single location where brand new platelets and red blood cells can be made. If the factory is filled to the rafters with CLL cells, the machinery cannot work right and make the necessary products. The obvious way of fixing this problem is to treat the underlying CLL. Once the CLL cells cluttering up the bone marrow are killed and flushed out, the marrow can start working again.
Bone marrow failure is a very different beast. Here we are not talking about a congested factory; we are now talking of a factory where all the machinery is broken beyond repair. Giving it a good spring cleaning is not going to do much to solve the problem. Once the precious stem cells in the bone marrow are dead or dying, the only way to fix the problem is through replacing them with brand new stem cells from a willing donor – namely, a stem cell transplant.
I do disagree with your assessment that a CLL infiltrated bone marrow is more dangerous than ITP. A packed marrow can be cleaned out, by an appropriately chosen chemo-immunotherapy. ITP on the other hand is an autoimmune disease that is very hard to control. A well respected physician told me that once the body learns bad habits (as in autoimmune pathways) it is very hard to break the habit. There is good reason why thrombocytopenia gets the attention of most clinicians – even though I agree the Rai Stage -4 associated with thrombocytopenia needs to be modified a little.
Thank you for your thoughtful comment.
Chaya
Thank you very much for your full reply.
I just wanted to say that my comment that it was better to have ITP compared with bone marrow infiltration may indeed have lacked adequate justification.
Antony
Chaya
I haven’t seen mention of Neumega on this update page on platelet count. (Neumega: Treatment for Thrombocytopenia; Date: October 16, 2003 on clltopics.org)
Is this not used for low platelets any longer? Is there something better?
Is there dietary things one should avoid or add to help with a low platelet count?
Thank you and all who offer input.
maka
Maka:
You raise a good point about Neumega. I do not know much about it. I will try and come up on the learning curve and then report. In the meanwhile, if any of you have experience with this drug, do tell.
Chaya,
Wonder if there is any correlation between more vigourous exercise and holding platelet counts. Was diagnosed 6 months ago (age 48) with a supposedly more “indolent” form of the disease but counts have gone from 276 to 200 in that time. At this rate I’ll be in platelet no man’s land in 9 months.
Just wondering if there are any natural remedies for slowing platelet decline. I guess were all on the train….some trains are faster some slower but all aboard. None including your brave husband deserved this lot I can tell you that.
Sorry for venting…you and your work here are a God send.
David
Chaya
I am a patient who has been on w and w for 3.5 years and face this exact situation: falling platelet counts for the last three months(now down to 84-88. Actually when platelets fell from 110 to 90 three months ago, so did my ALC and Hgb. I was completely asymptomatic until then; a few weeks later I had nodes swelling on both sides of my neck ; it was slightly painful and then poof it was gone. Recent blood test shows ALC at 30 and platelets around 88. My doctor wants to do FCR. I am mutated IgVh with no deletions but high CD38, an unusual combination but would be considered an excellent candidate for remission with FCR, according to a very reliable CLL expert.
I do not believe I have ITP. It is a very difficult decision to start FCR as I have no symptoms but that option is definitely in the cards at some point and I have almost decided to go with that based on an opinion of the CLL expert and my doctor. I mentioned BMB, campath and splenectomy and my doctor said they are not required.
I will have another test done in a month and may go with FCR in 2 months.
As far as I can tell, one other option is FR as I would like to avoid Cyclophosphamide due to its toxicity.
Are there other options than FCR, FR or splenectomy. Platelets only last 10 days so transfusion is out of the question.
Paul:
From what you have said, it seems your dropping platelets are due to an impacted bone marrow (you have ruled out spleen sequestering and ITP). If indeed that is the root cause of the thrombocytopenia, then the therapy of choice should be one that works well in bone marrow clearance. Neither Rituxan nor Campath (as single agents) can do a good job on this front. I have not seen enough data from Treanda or Revlimid trials to get a good sense of how they perform in bone marrow clearance. so, unless you are willing to go down a path less trodden, your choices are what your doctors have recommended, FR or FRC. Possibly PCR, which is just FCR with Pentostatin replacing fludarabine.
In your shoes I would insist on a BMB and new FISH test (if the previous one was more than a year ago) and spleen evaluation.
Dear Chaya,
Thank you for your prompt response. My doctor ruled out ITP as I have no symptoms, however spleen sequestering is not. He said it was a ‘classical’ pattern: platelets dropping while ALC shot up.
Are you aware of treatment options for platelet spleen sequestering other than spleen removal ?
I am a bit puzzled by him not needing BMB. A friend of mine who sees same Dr has had a couple already so he really sees no need for this.
I am also considering getting a second ‘treatment’ opinion only at Mayo – as I Canadian I could not afford treatment there, just the consultation portion …
Any suggestions along those lines ?
Paul:
Has your doctor said your spleen is enlarged? it is one of the things determined by physical palpitation at your medical consult. It is also possible to do a CT scan to get a more precise answer.
An enlarged spleen (swollen because it is sequestering healthy cells and / or choke full of CLL cells) can be treated two ways. First, by therapy of choice to treat the underlying CLL, which should also help the spleen shrink back to size; and second by surgical removal of the spleen. Splenectomy is remarkably easy procedure, usually done laparoscopically (so called keyhole surgery requiring very small incisions) and people recover quickly. The downside is that people without spleens have to be a lot more careful about avoiding infections.
Chaya, last month my husbands wbc’s zeroed out causing a 3 week delay in chemo round 4, this month his platelets have been 40,000 for the second week delaying chemo again. Ct last month said spleen is normal (it almost ruptured from 5 neupogen shots while preparing for round 1 chemo leaving him in ICU for 4 days) size and all nodes previously enlarged are now gone. Should we be concerned now with the platelets at 40,000? What should we be asking the doctor this wednesday and what should our major concern be at this point. My head feels so overwhelmed with info. Do you or any others have pearls of wisdom to share? Thank you, Eileen
My husban has cll/sll. large b cell with richerts transformation. we have been fighting for ten years. first in 2000 with chop, 2005 with fcr, 2008 with treanda. rituxan. Now we are at a halt. He received oxiplatin, fludara, cyctoxan, rituxan 2 treatments in ohio. He is itp. pneuomina platlets keep dropping today below 5000 and rbc 9.6 we are getting platlets for the next 4 days. the doctor said the cll is taking over. he has enlarged spleen. We are now on dextamsone.which helps but when he is offit for 4 days he gets worse. the doctor said not to go off it he takes 4mg of 10 pills a day. THe doctor said the steroids arekeeping him alive . He should have passed 4 weeks ago after being in the hospital for 13 days. he developed staph infection from his port so that was removed. I need help. What can we do to get these platlets up. if we can get them to stay over 20000 there may be some help. he has been getting pain in his left side. The clinical trial of oxiplatin nearly brought him to death. the bone marrow is not producing. He ivig. What can we do to stay alive. Please help someone
Hi Chaya,
I have had CLL for over 10 years. Had CHOP-R 2 years ago and just finished 8 weeks of Rituxan to help with ITP. My bone marrow is 35% infiltrated and my spleen is not enlarged and I feel fine.
BUT…..my platelets won’t stay up.
I just read this article and came across you saying:
” Getting back to the subject of ITP, I came across a terrific Mayo Clinic review of the options open to patients with refractory ITP. If any of you want to read it send me a personal email. I must warn you, it is pretty grim reading. I will dig a little more into the new drugs that may help as platelet growth factors and write about them in a future article.”
I’d be interested in reading the Mayo Clinic report about reviewing options. Thank you
Vinetta:
I wish there was something I can say or do that will make a difference in your husband’s situation. It is awful to feel so helpless. I do not want to make things worse by pretending to know more than I do. This is a very complex situation and you are not going to find answers in such a situation from a layperson patient advocate like me.
All I can tell you is that I have walked in your shoes, I know what you must be feeling. You are doing the best you can – no one can do more. I hope that brings you some solace. Best wishes to you and your husband.
Dear people,
my father was diagnosed with CLL about 7 years ago. He was treated with Leukeran, small dose and not to long. He came out very well but now after seven years his platelets are dropping again and he is now at 54. His doctor is thinking about radiotherapy in small doses and a few times to see if his platelets will increase again (as well as his HB). Anybody with advise for me? His criterium is that another round of Leukeran will go through his whole body and also destroys the good things and radiotherapy will only be local. I guess his believe is that the decrease in platelets is caused by the enlarged spleen and not the bonemarrow. Is there anybody with advise for me? Sorry for my language, I am from the Netherlands, Thanks so much, Aly
Sorry, forgot to mention that the radiotherapy will only be for his spleen!
My platelet count dropped from 145 to 98 in last two months, different
labs. Can this be an anomoly? The first at NIH in late July and second
in late Sept. with my oncolgist. No noticble difference in spleen, or
other symptoms.
I am schedule to be retested in two months. Thoughts?
PROTON PUMP INHIBITORS and DECLINING PLATELET COUNTS. Over the past year following my stage I diagnosis, my platelets steadily dropped, eventually falling below the UCSD lab normal range. Since I had favorable cytogenetics with early testing, I asked my oncologist to review the meds I was taking for conditions unrelated to CLL, to see if there might be pharmaceutical culprit. She suggested I d/c my Prilosec, a proton pump inhibitor (PPI)for several weeks, saying I’d see a fairly quick rebound if it was the cause. Within 2 weeks my platelets had shot back up to 180. Subsequently I tried another PPI, Protonix, and platelets went down to 136. Stopped it and again within 2 weeks they were 176. A Blue Shield pharmacist that I then spoke with confirmed an association between depressed platelet counts and PPIs in some patients. Am now taking Pepcid AC twice a day, which functions differently to mimimize duodenal ulcer potential. My platelets remain in normal range. This is an anecdotal report, then confirmed by a pharmacist who seemed aware of relevant medical literature.
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