“Must Have” Information: Couple of CLL Experts Speak Out
One of our members brought to my attention a very nicely done overview of the CLL scene today. (Thanks “grifj”!) The paper is authored by Dr. Tom Kipps of UCSD and Dr. Kanti Rai of LIJH – you cannot find two better qualified or more highly regarded CLL experts in this country. Here is the link to the article; all you have to do is click on it to read it. Trust me, it is a lot less painful to learn about this disease and your options when you are not facing urgent situations requiring your immediate decisions.
The paper is meant for the continuing education of medical professionals (“CME”). But it is surprisingly easy to read and well written. What I liked most was the brief case histories presented, followed by interesting multiple choice questions. If you are a type A personality like me, taking this pop quiz about CLL is almost irresistible. (Not to brag, but I aced the quiz – smirk.)
Even if you do not know all the answers, the good thing is that the paper gives the “correct” answers and then goes on to explain why the authors felt that was the correct answer. Here is a quotation of the sort of things discussed
An Older Patient With High-Risk Features
MR is a 70-year-old man with CLL diagnosed 3 years ago. He had been doing well until about 4 months ago when he began experiencing progressive fatigue, night sweats, and abdominal fullness with early satiety after eating. He otherwise maintains an excellent performance status of 0/5 by the ECOG criteria and lacks significant medical co-morbidities. On exam he is noted to have significant palpable cervical lymphadenopathy and a spleen palpable 7 cm below the left costal margin. His white blood cell count (WBC) was noted to be 125,000 with 97% well differentiated lymphocytes, which was significantly increased from that of his WBC of 13,000 noted at diagnosis. His hemoglobin was 10.1 gm% and his platelet count 98,000. His leukemia cells were noted to express high levels of ZAP-70 and to use unmutated IgHV. Cytogenetic analyses demonstrated the cells to have deletions at 11q22.3.
1. This patient is:
a. high risk
b. low risk
Correct Answer (a) The patient is at high risk (Stage IV), as the patient’s platelet count is below 100,000. He also has anemia, most likely reflecting disease-related marrow suppression. In addition, his prognosticmarkers are unfavorable—unmutated IgV(H) gene, and ZAP-70 positive—and he is symptomatic.
2. This patient should:
a. be placed on wait-and-watch status
b. have treatment started immediately
Correct Answer: (b) This patient is in need of therapy. He has symptomatic disease and evidence for compromised marrow function. Left untreated he probably would develop worsening cytopenia and increasingly symptomatic disease. Studies have shown that patients with high-risk stage disease benefit from therapy.
3. High risk patients without significant symptoms should:
a. be placed under observation
b. given a therapeutic regimen that will stop progression
c. treated with the goal of achieving a complete response
Correct Answer: (c) Even if prognostic markers are favorable, symptomatic high-risk patients should be placed on a therapeutic regimen with the goal of a complete, or maximally achievable response.
4. A preferred therapy for this patient would be:
a. Fludarabine + cyclophosphamide + rituximab (FCR)
b. Fludarabine + rituximab (FR)
c. Bendamustine-rituximab
Correct Answer: (a) In view of his adverse leukemia-cell cytogenetics, namely the deletion at 11q, he should be considered for combination chemoimmunotherapy. Clinical studies comparing the outcome of treatment with fludarabine versus fludarabine and cyclophosphosphamide have demonstrated the combination of the purine analog with an alkylating agent to yield higher complete response rates and longer progression free survival times after therapy than treatment with fludarabine alone. The difference in outcome is particularly apparent for patients with CLL cells that have the 11q deletion.
A worthwhile discussion
Let’s talk about this and the other questions raised and answered in this interesting article. Not all the answers are obvious and you may not agree with the authors’ justifications for their choices. Some of the information in the article is downright scary, such as the survival statistics quoted in their Table 4. I am not sure I agree with these statistics, there are lot more details to be considered before I will buy these bleak statistics. So, read the article carefully, take the quiz, then post your thoughtful comments here. I will do my best to moderate the discussion.
In a way this article came to my attention at just the right time. I am getting ready for our second workshop on August 14th. We will be discussing FCR therapy protocol in great detail and this article helped me formulate my thoughts. I am looking forward to seeing some of you at our workshop. Radha (our webmaster) will be sending out the venue and driving directions over this weekend. For those that are not able to attend the workshop, I will post the PowerPoint slides and my talk on this website.
RSS Feed
37 comments on "Your Continuing CLL Education"
Thank you, Chaya. Very helpful.
Dear Chaya,
When you say you aced the quiz, does this mean that you agree with the answers? In particular, the correct answer to question #2 of Case #3 is that the patient should be placed on therapy. I thought that the watch and wait would have been more appropriate until the onset of symptoms or evidence of spleen or liver enlargement.
Chris:
I aced the quiz in the sense that I could guess what the authors thought were the right answers – not necessarily that I agreed with all of them.
The particular one you point out (Question #2 of Case history # 3) is one of those ambiguous ones. The authors point out this is a young patient (53 years old) with poor prognostics (unmutated, ZAP-70 positive) with ALC almost doubling in one year. They are silent on the subject of FISH abnormalities – which is a pity.
The case made by the experts is that this patient has rapidly growing tumor load. There is reasonable chance that over time the patient may gather more chromosomal abnormalities and possibly other complications such as autoimmune disease. By treating now, chances are good the patient will get a good remission and possibly set him up in good shape to consider a mini-allo stem cell transplant. The young age of the patient seems to be the driver here. Waiting much longer may make it harder to get a really clean remission and therefore compromise successful outcome of a transplant. Remember, clonal evolution to more aggressive variety happens a lot more often in IgVH unmutated cases.
I would have felt a lot more comfortable with the chosen “correct” answer if the authors also gave FISH status. For example, if this was a 17p deleted case – or even a 11q deleted case – the need for immediate therapy would be that much clearer.
But you are right, this one was a little close to call.
Chaya,
Thanks for the quick response! Case #3 mirrors our current status, except a little younger and one year further along (No bad deletions by FISH).
Dear Chaya, My signficant other is 58 years old. He is high risk.(bucket C}. I know this because I got the test results. He says that he doesn’t want to know the results. His oncologist has never discussed his results with him. He told him to think of this disease as arthritis, and to live his life. He has his cbc with differencial done every three months. His last wbc was 19,000, hgb was 12. hct. was slightly low as well as his platelets. What should I do? Thanks, Lynda
I noticed that many of the citations were 3 to 7 years old. In my view, it is encouraging to see the rapid advances in the field, and to realize that the people on the cutting edge are changing the survival rates significantly. For instance, Kay’s chart in the article was 2002 when Stage I diagnosis was on average 8 years. What would a chart written today, 2010 look like?
Thanks for the article. Great reading.
Tom
As usual thanks for this article Chaya – however my adobe reader keeps on throwing errors when I try to read it, and all I can see is the exotic cover. Any chance of a “save as text” version?
Apart from that I am particularly interested, being 2 years into a good remission after FCR. But in the UK, FCR is available for firstline treatment BUT NOT afterwards. I would be very interested in your Maryland conference but unfortunately I can’t make it due to the Atlantic Ocean, so I’d be very grateful for any information which comes out of it.
Thanks!
Lawrence,
Cornwall, UK
I agree this case 3 is a tricky one, and I am sure Kanti and Tom meant it to be so, but here I would agree with that some treatment would be best. Reading between the lines, that they say the other 2 options are good indicates the ideal treatment is not clear in their minds. I think we can guess that if this patient appeared to Kanti 5 years ago he could have gotten Alemtuzumab. It is also encouraging to hear them pushing non-myeloablative sten cell transplants. No one should have to face the choice of a 50-50 cure or die gamble in their 50s.
Two other points were more interesting to me. The cutoff of cd38 being 20-30% seems to show clinicians like to trust their instincts sometimes. The lion’s share of data on cd38, and the seminal work by Damle in the Chiorazzi lab has used 30% as the cutoff.
Finally, the 1st case deals with a high risk patient with significant symptoms: anemia and palpable cervical lymphadenopathy and a spleen palpable 7 cm below the left costal margin but question 2 deals with a high risk patient without significant symptoms. They did not give the age of this theoretical patient, which is very critical to me.
I think most clinicians would wait and watch, which is what happened to patient 1. Maybe they would be steered into a trial such as FCR lite or lenalidomide but breaking out the big guns on someone without significant symptoms does not seem justified. If the correct answer is really give FCR, then why did patient 1 wait 3 years with no treatment? I am not aware of any new (or old) clinical data that shows an advantage to treating someone just because they are unmutated or have high Zap70. In fact I think the germans have shown the opposite. Please correct me if I am wrong but they have real trial data to back up the other decisions and give none for this question. Patient 1 has one of the worst chromosome deletions but was still not treated while asymptomatic. Either patient 1 was treated incorrectly or the answer to question 2 is wait and watch. There is no way out of that box.
As I said, age might be the real question. I can not believe any of the top CLL clinicians would treat a 75 or 80 yr old with no symptoms when fludarabine could really kill them by infection, but someone 55-65 maybe then they should be treated.
Also the WBC would be critical for the theoretical asymptomatic patient in case 1, question 2. If they have a 20,000 WBC no one would treat them with FCR but if they are clinically astmptomatic with 100,000 WBC, then I think most would start them on something. Also I would bet a person with just one of unmutated, high cd38, high zap 70 or a del 11q would be treated differently than someone with all 4. They did not say the CD38 of patient 1, but he has the other 3 and was not treated while asymptomatic.
Dear Chaya
Thank you so much for share this helpfull article that contibutes for our learning about this disease.
Jorge/Ana
Dear Chaya,
Thank you for all the articles you write. Recently, the article about our livers was especially wonderful.
I think the confusion over a “quiz” question could be the different wording between the question and the reply. The question refers to a patient without symptoms and the answer that has confused some of us refers to the patient having symptoms. Could it be that the question and answer aren’t in sync?
Greetings from Ann Arbor. I know you lived here a long time ago. I thought of you when I donated extra to the Humane Society of Huron Valley, but I didn’t notify you. They have opened a new, improved, and larger facility next to their former “digs” and they are doing a wonderful job placing animals in new homes.
Chaya,
My wife, age 55, is newly diagnosed “very early CLL.” Slightly enlarged nodes in neck only. FISH showed Trisomy 12; ZAP 70 +; CD38+; High LDH; still waiting for results to see if she is mutated vs unmutated.
Looks pretty grim, according to the paper you refer to.
However, when I read “FISHing for the Genetic Answers” by Michael Keating at M.D. Anderson, her outlook may not be as grim as it appears, specificaly because of her Trisomy 12 status.
Have things changed that much?
Thank you for helping us stay abreast of this mystery. It really is a complicated with uncertain treatment protocols and outcomes. This article got me worrying. I also now think I should learn more about treatment “induced” secondary malignancies.
My partner is a young patient (51 years old) with “poor prognostics”(?) (IvGH unknown, ZAP-70 positive) with ALC NOT doubling in one year, and NO FISH abnormalities. FISH; CD5,Present; CD19 was not addressed; CD20, present but dim; CD23 present; CD38 subset present; Surface lambda expression-Dim; % abnormal cells – 60% – small to med. WBC’s 27,300 after 7 years (or more – seems slow?).
He is on “watch and wait” status, but this article makes his condition sound much worse (other than the RAI, which is 0). Is he high risk because of the ZAP-70, and should possibly be treated right away?
ramo01:
I am not sure what to tell you. If your significant other does not want to get engaged in the process and his doctor is not pro-active in taking better care of him, you have a tough situation. Perhaps you can suggest he see a psychologist for counseling first? Many cancer patients go through a time of denial as a way of coping with the news.
tcb700:
Survival statistics reports are by their very nature a few years behind the times. But I think there is little doubt our guys a living longer – thanks to monoclonal antibodies such as Rituxan and better understanding of how to protect, when to treat and who to treat. Stem cell transplants (min-allo) continue to become safer. This cancer is by no means cured. Improvements come in small increments and often it is two steps forward and one step back. But progress is being made, of that I have no doubt.
Lawrence Hanney:
I am not a techno savvy enough to answer your question. Please write to Radha, our webmaster (address on the contact page) and she might be able to help you.
Tex:
FISH is part of the prognostic picture. You will know a lot more about her status after you get the IgVH gene mutation status. Unmutated IgVH along with positive ZAP70 and CD38 does point to a high risk CLL. But do remember these are general statistics, and there is always a chance that the individual patient’s disease follows a different path.
Waterflows:
Perhaps you should get that IgVH gene status test done? But the slow progression over 7 years is a huge indicator of indolent disease. Proof the pudding is in the eating. That fact alone trumps all the rest, in my opinion. I doubt very much that treatment decision will be based on positive ZAP70 alone. Rai stage 0 patient with no symptoms and slowly progressing disease is correctly placed in watch & wait. Hope that helps.
Michigan, good point, a typo with/without would explain everything.
Chaya,
I didn’t think so but maybe I’m in a crappy mood. I read the paper and it is good. My problem is the answers were F/R and FCR only.
Why was B/R praised as the best thing since sliced bread? and not too long ago.
Are we again back to who is paying for this, etc?
My last chemo was rough. I had 6 months of B/R. I had refused anything with F as I had miserable reactions, esp. Shingles. Also I am 77 years old and didn’t think I could handle it again. Believe me, B/R was no walk in the park.
Why do “they” praise a drug and then it’s not even on the list? Why do we have these new drugs and then two years later, they are not recommended.
Please no one tell me this is what we find out in clinical trials.
I guess I am in a crappy mood.
Take care and Blessings. I’m out of the mood already.
Rita
Rita:
Every new drug on the horizon is hailed as the greatest thing sliced bread. That is a given. If you rememeber, I had a couple of not so flattering reviews of bendamustine. (“Face lift for bendamustine” in http://www.clltopics.org ).
While we have to be careful not to buy into over-the-top hype put out there by marketing geniuses and savvy enough to read between the lines of less than objective “professional” papers influenced by large grants of money, it is important also not to throw out the baby with the bathwater. Bendamustine is a powerful drug, there are early indications that it may be effective in patients who have already burned through other drug options (such as fludarabine refractory patients. It is always valuable to have more options.
By the way, the authors of this paper are not saying bendamustine is no good. They are merely pointing out that given the much longer track record of FCR and FR, it makes sense to use these combinations (unless they are contraindicated for some reason) rather than go for a less well understood drug such as bendamustine. Once again, it is a matter of weighing risks and rewards. Why take on the risk of unknown or less well understood bendamustine based protocols if FCR will do the job as well or better, but with lower risk of nasty “surprises” by way of toxicity?
And I am sorry you don’t feel like hearing it just now, but that is what clinical trials are all about. Learn stuff we do not know, yet. Last but not least, not every expert would agree with Rai and Kipps on each and every one of their ‘correct’ answers. It will be a while before CLL therapy decisions can be made with absolute certainty and with eyes closed. For now, the increased number of options goes hand in hand with increased uncertainty.
I know you too well Rita. It will be hard for you to stay in a crappy mood for too long! You are too sunny and generous for that.
Did anyone else have trouble reading this file. 1st page picture came up for me…no text…adobe reader complained about text being not readable.
Regarding the survival charts, do they differentiate between low platelets from ITP versus bone marrow infiltration by tumor ?
Thanks
Thanks for alerting us to this article. I have never had symptoms other than some black & blues…and very low platelet counts. I have energy etc. They gave me the 6 part CRP but no Fludarabine . This article seems to prescribe it for all cases. PS…after 6 months, my platelets are dropping again.
Dear Chaya and others,
I apologize for my crappy mood letter. I could use the excuse of my health. Or my eye. Had to go as an emergency to get my eye injected with avistin. But that wasn’t it.
It’s when my computer acts up.
I promise to control myself more.
Blessings,
Rita
bmalkiel:
You have aced my quiz, spotting the single biggest weakness in the suvival chart they had in this article.
Low platelets due to autoimmune disease is distinctly different than low platelets due to bone marrow dysfunction. The same thing goes for low red blood cells (and therefore anemia) due to AIHA versus bone marrow dysfuntion. I discussed this distinction in a couple of reviews of Mayo articles, as far back as 2003, titled “Staging does not predict survival”. Here is the link if you would like to read my review:
http://www.clltopics.org/DC/SurvivalStaging.htm
Basically, Dr. Zent of Mayo points out “Among patients with anemia or thrombocytopenia, mortality was significantly higher in those with bone marrow failure compared to an autoimmune etiology.” So, it is important to know why the platelets (or red blood cells) are low. Rai Staging (which seems to be the basis of the survival chart in this article we are discussing) does not take the “why” into considertion. Please note one of the two authors of this article is none other than Dr. Rai, after whom the staging system is named.
Hello Chaya and all,
Regarding the case of the 70 year old male, FCR may be better than FR or BR. But what about other therapies? In June of 2005 Dr. Keating of MD Anderson wrote that while FCR yields the best response in patients, the survival of patients >70 years is not improved because of increased infections and secondary cancers. Reason: FCR is bad news for bone marrow in elderly. In the brief article Keating stated that MD Anderson would not use FCR on patients older than 70 years. Rather they would use Rituxan and Leukine (GMCSF). And in the body of this article the authors give passing reference to high-dose methylprednisolone and rituximab as a treatment which does not do so much harm to the marrow.
Chaya, I hope you can address this issue on Saturday.
Ed
monag764:
You have been given one of the present day standard therapies for treating autoimmune distruction of platelets (“ITP”). Unfortunately, it is hard to fix autoimmune disease once and for all. This is true of ITP as well as AIHA. Since your platelet counts are dropping again, chances are you will need therapy again. I have written about ITP in some detail earlier on. You can find the articles by going to the CLL Topics website ( http://www.clltopics.org ) and searching for the key word ITP in the search box at the top right hand side of the home page.
A certain percentage of ITP cases seem to be influenced by H. Pylori infection and it may be possible to help the patient by eradication of this common bacteria by means of powerful antibiotic therapy. I do not know if you fall into that category or if the process of H. Pylori eradication will work for patients who have entrenched disease. But it may be something to discuss with your doctors.
Chaya,
I have not read any abstracts that state putting the “C” in FCR will give an 11q deleted patient an “equivalent” remission. I have read that “C” is helpful for the mix when treating 11q patients.
I recall Hamblin expects to see about a year’s remission (FCR/11q) and Byrd posted an abstract several years ago about this deletion strongly pushing for “risk adapted” therapy. That’s a lot of toxity for a year’s remission.
I’m wondering what’s up with these two guys – although well known and revered in the CLL community – I haven’t read peer reviewed abstracts supporting their claim of an “equivalent” remission, have you? Perhaps you will be discussing it in the meeting.
Ann
In response to Lawrence Hanney’s point about FCR only being available in the UK for first time CLL treatment, I wonder where he heard this? Barts Hospital has offered me FCR as a second time treatment, if/when I need to go again. I’m 18 months into a CR with a first time round treatment of FC only.
Molly
Ann:
A 2009 paper from M. D. Anderson has the remission and survival rates of 11q patients treated with FCR at significantly higher than the one year you report. ” The median follow-up was 17 months. At 1 and 3 years, the survival rates were 97% and 91%, respectively, and the relapse-free survival rates were 100% and 77%, respectively.” http://www.ncbi.nlm.nih.gov/pubmed/19117034
While there have been no head-to-head comparisons of FCR versus FR, we do have very well conducted F versus FC clinical trials which show FC is clerly superior to single agent F, especially in high risk cases. So, since addition of “R” seems to help in all chemotherapy, by inference FC + R is likely to be superior to F + R. I realize this is not quite as clear as it would be if we had a two arm trial comparing FCR versus FR in well matched group of patients.
ED71:
Kipps and Rai specifically discuss the point you raise, namely older patients with reduced bone marrow reserve may not do as well with profoundly myelosuppressive therapy options such as FCR. Please read the article carefully.
The authors further point out that patients with cardiovascular disease, diabetes and similar comorbidities (all of which become more prevalent as people age) may not be good candidates for FCR.
Yes, we will be discussing points such as this at the workshop.
Thank you, Chaya.
Without you and your wonderfull helpers, a lot of us would remain in the dark about this disease.
Stay well,
Monique
Hi everyone,
I sent out the location and directions for next Saturday’s Workshop this weekend, so if you registered for the workshop but didn’t get the email, please write to me (radha@clltopics.org) and I will make sure you do get it!
Thanks,
Radha
Dear Chaya,
Once again, information we need, masterfully summarized and critiqued. I’m one of the “lucky” ones (a mixed bucket but still w&w after almost 6 years) so I especially appreciate your articles about handling the early stages. As a retired chemist, I also appreciate the straightforward way you share technical information. Thank you from the bottom of my heart!
Whalewatcher Ellen
Hi
UK members:
For the members in N Ireland England (remember Scotland and Wales have their own guidance)I suggest you read the latest NICE guidance on use of FCR for patients needing second line treatment, on their website. It is not great news for those who have received Rituximab during first line treatment, although there are certain exceptions where this can be waived, eg if you received R in a clinical trial. You will receive R for second line if you have had other chemo combinations, unless you relapse within 6 months of treatment and/or are refractory to fludarabine.
This decision has already come out of an appeal stage (the guidance was even worse beforehand) so there is no further appeal available. The good news on the horizon is that there will be a review of the evidence in Dec 10. NICE were not convinced by the German trial evidence of FC vs FCR.
PCT’s who fund the drugs are now using virtually all NICE guidance that goes against a particular drug or treatment as a means of not funding that treatment.
J
I didn’t ace the quiz so I can’t brag about that, but I sure have aced the survival chart! I was diagnosed 5 1/2 years ago at stage 4 ( due to the 7 platelets they could find to count), began FCR immediately, and 4 years later learned that I have 17P deletion. That puts me in the box in the bottom right corner with a ONE year survival rate. If my hem/onc had told me 5 1/2 years ago that I had one year life expectancy I would have gone home to die without any treatment at all. The 5+ years haven’t been a picnic (I’ve tried almost everything out there) and I can barely walk now due to steroid myopathy, but I’ve done some fun things and continue to stay as busy as my fatigue allows. This article was written before Arzerra was approved by the FDA so it’s not listed as an alternative for Fludara and Campath resistance (that’s me) and at Arzerra dose 10 of 12 coming up tomorrow I’m thinking I’ve flunked that TX as well, but I’m expecting to live through the whole course and then try radiation on my nodes. This disease is worth fighting till the last possible TX has been tried or CMV or pneumonia catches up with me.
Betty
Betty:
My problem with that chart was exactly what you noticed: the one year survival expectation listed in the bottom right corner. That is plain WRONG – based on thousands of patient case histories I have come across over the last seven years.
You keep on fighting Betty. Damn the statistics! You have more zest for life than many perfectly healthy folks I know.
My son who is 42 years old was diagnoised last week with CLL. He was told he is in the early stage. He had some swollen lymph nodes about a month ago in his armpits and one side of his neck. They have gone away. He does have ulcers and acid reflux disease and I found out he has not been taking the meds for that. He quit taking them about 3 yrs ago. He also suffers from bad night sweats but not all the time and weight loss , then he gains weight and loses it. He is 5 feet 11 inches and is down to 144 pounds though a couple weeks ago he only weighed 138 pounds. He works hard. He works building commericial trucks and has been working the past 5 years or so on his home and not getting enough sleep. I am at a loss. I want to be strong and encouraging for him but my heart is breaking. He is my first born and only son. Is there anything else that could mimic CLL? He had blood work done and that flow cytometry test. He went to his regular Dr. and a week ago the Dr called him while he was driving to a school conference for his daughter. The Dr told him to pull over and proceded to tell him he had leukemia and had 1-3 years to live. My son was devasted, and me, when he told me I was so damn mad at that DR. I didn’t know what to do.I felt it could have been handled differently. He could have asked him to come in the next day to discuss his lab report. What A BIG JERK . I can’t even tell you what I thought or said. The next day my son went to a hemo/ongologist and he put my son in a watch and wait mode. If he was in the early stages would he have the night sweats or weight loss???? My husband also has some bad night sweats at times but does not have CLL he is 70 yrs of age. My son has had cysts many years ago behind his ears and I had them in my armpits but it was called something else that I can’t pronounce. Like hydrametria/supperativa. We both had surgery to remove them. Me 20 years ago and my son about 12 yrs ago. Supposedly that was heriditary I know I am grasping at straws here. I have been reading as much information as I can on CLL in order to help my son. Does anyone have any idea what our next step should be? We have discussed going down to the Mayo Clinic and perhaps they could run more tests. We live in MN.Our local Drs. don’t seem to have a handle on this disease. A ZAP 70 was not done on him. He did have a high white blood cell count and the flow cytometry done and that was it. Please help me. Thank you. And no I am not in denial I just need to know what is going on and what to expect. Jan
ione44
I am only a cll patient and not a doctor. But, I want to share a few things with you that I have learned through this process. First a little background. I was diagnosed May 2006. I had just turned 45, five days ealier. I was on watch and wait until August of this year and have started treatment at NIH. YES! There is treatment.
You have to know that doctors are like any other people, some of them are smarter than others, some of them have egos while others don’t, some of them have tact while (obviously) other don’t. Do not keep a doctor that you are not comfortable with. There are too many out there and you don’t have to put up with this kind of treatment.
It is your money (or your sons money)spend it wisely. I fired my oncology radiologist because he kept ignoring my concerns and talked to me like I was an idiot. There is definately a lot of this I don’t understand, but I am fully capable of understanding if/when explained.
You need to drown yourself in the knowledge of this website because it will offer you a wealth of information and help calm you a bit. Chaya is a scientist and has a gift if disseminating the information to us in a more understandable way. Don’t get me wrong – it is still a lot of information and if it is not your profession, it is complicated.
I have also learned that it would be impossible for your local oncologist to keep up on every change/new drug/new treatment on every kind of cancer they are treating in their practice. They deal with many kinds of cancers on a monthly basis. I have actually given my local oncologist the most recent information regarding cll.
Once you arm yourself with this information, you should see that it is unlikely (again – I am not a doctor nor do I know his prognostics) you will lose your son to cll in three years. There are many statistics on this website that will back that up. Especially if they put him on watch and wait right now and the cll is in early stages.
This site also helps to put things into perspective. You said you son’s wbc was high… what is high? Mine got to 315,000 before treatment – that is high! Plus, you will also learn on this website that the wbc isn’t the only prognostic that will determine when to start treatment.
He needs to check to see if there are any spots open at NIH (National Institutes of Health) in Bethesda, MD. The team of Dr’s there are specialists in CLL and are on the cutting edge of the disease. It is FREE (thanks to all of our tax dollars) if he gets in the study. Most of us could not afford this kind of expertise offered there.
One of the specialist at NIH reassured me that CLL is a “managable” disease and their goal for me is to “manage” it until I am 90 and get hit by a bus. I personally, am hoping for a cure in the next few years (additionally a stem cell transplant can be a cure). I am quite the optimist.
I hope hearing from a fellow patient helps. There is no doubt that this is serious and I am doing everything I know to do to fight this disease, but also live my life as fully as possible. Quite frankly, I have lived my life almost without interuption from cll. And expect to live many many more happy, healthy years.
I would be more than happy to talk to you if you would like.
The very best to you!
Dear Karen, Thank you for posting your comment. I really appreciate it. I did get a letter from Chaya and was also grateful to her for her comments and help. I think I overwhelmed myself by going on the computer to many websites and accomplished nothing except to confuse myself. This is the only site I will be going on now. I believe I need to know what actual people are going though and how they are dealing with CLL that is why I posted my comment in the first place. It is nice to have people to talk with and to get encouragement from. We live in Duluth, Minnesota and are going to try get an appointment with the Mayo Clinic. I guess I don’t understand that if Dale is in the early stages of Cll why he has night sweats and loss of weight. I did buy him Ensure and multi vitamins plus Vitamin D3 and Calcium. I didn’t know what else to do at this point. He has managed to gain some weight back. The night sweats have been going on for quite awhile but not every night.Yes I would like very much to be in touch with you. How would be accomplish that? Thanks so much. Jan
Leave a Comment