Crowning the new king
Which of the chemo-immunotherapy combinations out there today is the undisputed “gold standard” for chemo-naïve CLL patients?
Several large scale studies at M. D. Anderson and elsewhere have established FCR (fludarabine, cyclophosphamide and Rituxan)as a very potent chemoimmunotherapy combination. Especially in chemo-naïve patients the response rates have been very impressive. Complete Response (“CR”) and better still, “PCR-negative remission” (really squeaky clean CR) are the holy grail that all patients hope to achieve as they go into therapy. FCR combination gives higher percentage of CRs and “PCR-negative remissions” than just about any other combination we have seen thus far. Of course, if you are not quite a ‘chemo virgin’ (even exposure to single agent Rituxan disqualifies you as being truly chemo-naïve), then FCR response statistics are significantly reduced.
But FCR therapy is not without its risks. Patients have to be aware of a non-trivial list of adverse effects, including neutropenia that can last for a significant length of time. During this period patients can be at risk of opportunistic infections – hence the need for carefully managed prophylactic therapy with broad spectrum antibiotics, anti-viral drugs and in some case anti-fungal drugs as well. The search goes on for combinations that give terrific response statistics but far fewer adverse effects, better bang for the buck.
Is PCR “kinder & gentler” than FCR?
Pentostatin is similar to fludarabine in the sense that it too is a purine analog and its mechanism of action in killing cancer cells is quite similar. Some researchers think pentostatin is a kindlier version of fludarabine and that it is therefore easier to tolerate and likely to have fewer adverse effects. Which leads us to the obvious question, would substituting pentostatin for fludarabine in the FCR combo give us the best of both worlds? Would PCR combo yield as good response statistics As FCR but with reduced risk of infections?
Most often it is very hard to answer questions like this with any degree of accuracy. That is because often we do not have results from strictly valid comparison trials between two competing therapy regimens. Apples to oranges comparisons are by definition imprecise and often mis-leading. For a change, we now have a well conducted and honest apples-to-apples comparison between FCR and PCR. The results were published at the recent ASH 2008 conference. Anyone who is considering therapy and trying to decide between PCR and FCR needs to read this article. Here is the link to the ASH abstract, followed by my cheat-sheet version that I hope is an easier to follow.
FCR versus PCR: straight up comparison
Until this latest study our understanding of FCR combo comes mostly from studies done at M. D. Anderson. Mayo Clinic has taken the lead in evaluating PCR. (Fludarabine was invented at M. D. Anderson, while pentostatin was invented at Mayo. I am sure you would agree, a certain amount of home court advantage and local pride is to be expected.) In these earlier, single arm trial PCR response statistics seen in the Mayo trial were similar to FCR statistics from M. D. Anderson. The hopeful news was that there were indications PCR may give rise to fewer infection complications and for that reason PCR may be easier to tolerate in elderly patients.
The present study was undertaken to see if indeed there is less risk of infections with PCR combination compared to FCR, whether the early indications can be confirmed in a head-to-head comparison. Thus, infection risk was the primary research objective of this latest study, followed by response statistics as a secondary objective.
Study design
The study was conducted at a number of community based oncology practices. Just that by itself is a good thing when considering the value of this latest clinical trial. Results obtained at expert centers like Mayo and MD Anderson may not be representative of what may be possible at local oncology practices. But majority of patients are treated by local practitioners and the results of this study are therefore more likely to be realistic indicators of what we can expect locally. In addition, this trial design is the most valid and head-to-head comparison we can hope for, with enough patients recruited to give the results good statistical credibility.
Well matched groups
Patients were randomly assigned to receive either FCR or PCR combinations. There were 92 patients in each group, a pretty hefty number. Random assignment takes care of biases. Here is how the two groups stacked up:
Pretty well matched groups I would say, and therefore the results give PCR a fair hearing. If anything, a few more of the patients in the PCR group were in earlier Rai Stages.
Therapy details
The table below gives the drug dosage information. The “FCR” combo is pretty much what we have come to expect from earlier work. In the PCR arm of the trial the “C” and “R” are exactly comparable to the doses in FCR. Don’t get excited about the lower milligram number for pentostatin in the PCR arm. This is very much a standard dose for pentostatin and compares well to the fludarabine dose in the FCR arm. In both the FCR and PCR arms of the trial Rituxan was given in a split dose in cycle 1, to reduce infusion related side effects.
Did PCR have the same ‘oomph’ as FCR?
Based on the response statistics shown in the chart below, it does not appear pentostatin did as well as fludarabine in combination with cyclophosphamide and Rituxan. The difference between FCR and PCR in terms of “CR” (complete remission) was statistically significant while in overall response rate (this includes all the folks that got any kind of a response: complete, partial and “nodal” partial responses) the difference was not statistically significant. A bunch more people had stable disease.
All in all, the results for both groups were less than thrilling and I will have more to say about that in the editorial section at the bottom of this article.
Adverse Effects
Surprise, surprise! The comparison of adverse effects between the two arms was not what I expected. PCR did not come across as kinder and gentler. Both arms had higher infection and hospitalization rates than I expected. Both regimens had significant toxicity, only about 50% of patients completed all the scheduled cycles. More than a third of the patients were hospitalized at some point while undergoing therapy, and the percentage of hospitalizations was higher in the PCR arm! Are you confused yet? You should be.
Editorial
I have to admit I am surprised by the comparison in the adverse effects profiles of the two arms. Here are some direct quotations from the abstract, highlighted for your convenience. My admittedly ‘snarky’ comments are in parenthesis.
- “Both regimens possess significant toxicity“. (Yeah, tell me about it. More than a third of our guys were hospitalized! I would call that significant toxicity.)
- “Response rates in this multi-institution, community-based randomized trial were lower than previous phase II trials of previously untreated patients“. (I wonder why? Are expert centers so much better than local oncology practices in treating patients?)
- “This trial did not demonstrate a lower infection rate with PCR using pentostatin at the 4 mg/m2 dose level“. (Hunh?? What gives? I thought PCR’s claim to fame is that it is going to be kinder and gentler than FCR?)
- “In early follow-up, no statistically significant differences with respect to overall response rate or survival were observed between FCR and PCR“.
- “CR rate was significantly higher with FCR“. (You telling me PCR has less bang and cost more buck? That does not sound like a winning proposition to me.)
- “We conclude that both PCR and FCR have significant activity in CLL and can be given safely in the community setting”. (Sure. Only half of the patients completed all six cycles of therapy in either arm, a whopping 27% dropped out due to adverse effects, and more than a third of patients were hospitalized. All in a days work, no problem mate, except if you happen to be the one facing the sharp end of the infusion needle.)
I am disappointed and baffled by these results. First and foremost, in this rigorous comparison PCR does not come off well. There was no advantage on the response side (in fact the CR rate was statistically worse), and there was no improvement on the adverse effect profile. This was both surprising and disappointing.
But what baffles me is why the response statistics for both FCR and PCR were so much worse in this study compared to earlier results reported by expert centers (M. D. Anderson and Mayo Clinic). Two possible explanations come to mind for this important discrepancy:
First, it may be that expert centers are trulyexpert at monitoring, protecting and treating patients, hence the better responses and less scary adverse effect profiles in the earlier studies. If this is true, then all of us have to think twice about getting treated at our friendly neighborhood oncology practice. However, not everyone has the choice of high-tailing it to Mayo or M. D. Anderson when therapy time rolls around. If this is the reason for the disparity in results, it further highlights the need for CME (continuing medical education) to bring local guys up to speed, we need to do everything we can to get the darn trickle-down of expert information to speed up. And, from my perspective as a patient advocate, it is all the more reason why you have to take an active role in your own health-care, get your ducks in a row before you make therapy decisions. What you and your local guy do not know may kill you!
The second explanation why the results of this study differ from the earlier study is more troubling. A randomized late stage study such as this with large patient cohorts and multiple centers is the gold standard for clinical trials. Randomization and use of multiple centers removes some of the bias built into single institution and single arm studies. Were the patients in the earlier studies recruited at earlier stages? Did researcher and/or instituional bias contribute to the more benign adverse effect profile and better response rates?
Randomized studies with sizable patient cohorts such as this clinical trial are expensive and time consuming. Neither drug companies nor research institutions are anxious to go the extra mile and more often than not we have to make-do with results published based on single arm and single institution studies. If there can be so much difference between single arm / single institution studies and well conducted “gold standard” randomized studies such as this one, how the heck are we to judge results? Is it all a case of beauty is in the eyes of the beholder?
Oy vey. If there is so much wiggle room in reported results from large scale but single arm and single institution studies such as the FCR and PCR trials at M. D. Anderson and Mayo, how much can we trust other study results obtained in early stage and often Phase -1 clinical trials with less than a couple of dozen or so recruits? And yet company press releases (with an eye on potential investors and stock price) present such early results as the next great thing and the lay press (with no clue as to the technical or statistical credibility of the results) dutifully echoes the glowing quotes from conflicted researchers. Sensational journalism sells.
There is always the third possibility that something is seriously wrong with the results reported in this trial. I am going to be doing some digging in the next little while to see if I can get a better reading of these tea leaves. If I hear anything that sheds light on this situation, on or off the record, I will let you know. For now, I suggest you stay skeptical about stuff you read in the lay press. And if you are trying to decide between FCR and PCR, based on these latest results you may want to stick with FCR. It has longer track record, seems to yield better response statistics (at least as far as percentage of CR responses are concerned and it sure as heck does not seem to be any worse than PCR when it comes to adverse effects. Who would have thunk it?
15 comments on "PCR versus FCR"
Chaya,
Can you comment on this abstract from ASH, from MD Anderson? It implies that PCR is less harmful than FCR (though it is not head-to-head, and reports a much higher ORR. Thanks, Helene
Pentostatin, Cyclophosphamide, and Rituximab (PCR) Achieve High Response Rates in Indolent B-Cell Lyphoma without Prolonged Myelosuppression
Felipe Samaniego, M.D., Michelle Fanale, M.D., Barbara Pro, M.D., F.B. Hagemeister, M.D., Peter McLaughlin, M.D.*, Jorge Romaguera, M.D., Sattva Neelapu, M.D., Maria Alma Rodriguez, M.D., Luis Fayad, M.D., Anas Younes, M.D. and Larry W. Kwak, M.D., Ph.D.
Lymphoma/Myeloma, University of Texas M. D. Anderson Cancer Center, Houston, TX
Background: The addition of rituximab to combination chemotherapy has improved treatment outcomes of indolent lymphomas. Combination therapy with purine analogs, akylating agents, and monoclonal antibodies is a promising approach for treating indolent B-cell lymphoma. Nucleoside analog-based regimens selectively target lymphoid cells, making them attractive drugs for lymphoid cancers. Pentostatin is a nucleoside analog that compared with other nucleoside analogs is reported to have less bone marrow cell toxicity. The combination of pentostatin, cyclophosphamide, and rituximab (PCR) is an effective regimen for relapsed chronic lymphocytic leukemia.
Methods:In this study, we examined the efficacy of pentostatin, cyclophosphamide, and rituximab for the treatment of B-cell lymphoma. Pentostatin (4 mg/m2), cyclophosphamide (600 mg/m2), and rituximab (375 mg/m2) were given on day 1 of a 21-day cycle with planned 6 or 9 cycles and restaging after every 3 cycles. Patients received prophylaxis with acyclovir 400 mg/po bid and trimethoprim-sulfamethoxazole 3 times per week. Small lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) tissues were stained for ZAP70 protein.Results: At the time of abstract submission, 80 patients with a median age was 60 years were treated, 43 patients with follicular lymphoma, 27 with SLL/CLL, and 9 with mucosa-associated lymphoid tissue. We observed an overall response of 77 out of 80 (96%), CR/CRu in 65 out of 80 (81%), PR in 12 out of 80 (15%), and mixed response or progression in 3 out of 80 (4%). Neutropenia (49% < 1000/uL), thrombocytopenia (2% < 100,000/uL), nausea (15% grade 3), fatigue (37% grade 3 and 4), and muscle pain (21% grade 3) was observed. ZAP70 staining and response will be reported. Two patients experienced prolonged pancytopenia that resolved and no cases of myelodysplasia were observed. Conclusions: PCR therapy is an effective regimen in indolent B cell lymphoma with tolerable toxicity.
Chaya
I was a part of the Mayo/OSU trial for PCR in 2004. At this point in time I am still in remission. According to my Doctor at OSU most participants came out of remission within 30-36 months, while I am going on 57 months.
There was an article about mcl-1 expression predicitng a longer remission time in CLL out of my trial. What is this? Can you please explain this in further detail. From what I read, it seemed to be something that the researchers just found out about.
Mcl-1 expression predicts progression-free survival in chronic lymph
Posted by: “Andrew Gach” unclewolf@olypen.com calebmishka
Fri Nov 14, 2008 10:22 am (PST)
Blood First Edition Paper, prepublished online November 13, 2008; DOI 10.1182/blood- 2008-08-173450.
Mcl-1 expression predicts progression- free survival in chronic lymphocytic leukemia patients treated with pentostatin, cyclophosphamide, and rituximab
Farrukh T Awan, Neil E Kay, Melanie E Davis, Wenting Wu, Susan M Geyer, Nelson Leung, Diane F Jelinek, Renee C Tschumper, Charla R Secreto, Thomas S Lin, Michael R Grever, Tait D Shanafelt, Clive S Zent, Timothy G Call, Nyla A Heerema, Gerard Lozanski, John C Byrd, and David M Lucas*
Ohio State University, Columbus, OH, United States
Mayo Clinic, Rochester , MN , United States
* Corresponding author; email: david.lucas@ osumc.edu .
Myeloid cell factor-1 (Mcl-1) is an anti-apoptotic member of the Bcl-2 protein family. Increased Mcl-1 expression is associated with failure to achieve remission after treatment with fludarabine and chlorambucil in patients withchronic lymphocytic leukemia (CLL). However, the influence of Mcl-1 expression has not been examined in CLL trials using chemoimmunotherapy. We investigated Mcl-1 protein expression prospectively as part of a Phase II study evaluating the efficacy of pentostatin, cyclophosphamide and rituximab in patients with untreated CLL. No significant difference by Mcl-1 expression was noted in pre-treatment or response parameters. However in patients with higher Mcl-1 expression, both minimal residual disease-negative status and progression- free survival was found to be significantly reduced (57% vs. 19%, p=0.01; 50.8 vs. 18.7 months; p=0.02; respectively) . Mcl-1 expression may therefore be useful in predicting poor response to chemoimmunotherapy. These findings further support pursuing treatment strategies targeting this important anti-apoptotic protein. Because the trials described were conducted before the requirement to register them was implemented, they are not registered in a clinical trial database.
Thank you,
Anne
Elmer:
The abstract you cited deals with a mixed bag of lymphoma patients – not CLL. (They do have a minority of SLL folks, a very nodal version of CLL). All of the authors are from the lymphoma section of MDA, further highlighting the difference in emphasis.
It is hard (impossible) to draw any accurate comparisons between this study and truly CLL focused studies. I did not see any statement to the effect that these authors saw less adverse effects using PCR versus FCR in lymphoma patients.
As you pointed out, their response statistics in this study are high, as are the single arm FCR work at MDA with CLL patients. I am at a loss to explain why these high response rates did not replicate in the double arm study I discussed in my article. It is worrisome.
Anne:
I am of course delighted by your long remission.
Mcl-1 has been known for quite a while. It is a gene that belongs to the Bcl-2 family and the protein that it encodes is involved in controlling the ease with which cancer cells can avoid signals encouraging them to commit suicide. Like several members of the Bcl-2 family, elevated levels of Mcl-1 are thought to make it easier for cancer cells to avoid apoptosis (programmed cell death) and therefore high levels of Mcl-1 gives a survival advantage to the cancer cells.
Bottom line, Mcl-1 is yet another of those prognostic indicators researchers are playing with, to see if it can do a better job of reading the tea leaves. They have been doing this for years.
But if indeed Mcl-1 is a dependable predictor and patients with low levels of Mcl-1 do well on PCR therapy, logic would suggest the same patients would do equally well (perhaps better?) on FCR too. If you take lucky patients with good prognostic indicators every therapy will work better for them – no great credit to the therapy itself, the good response statistics are more due to the nature of the patients chosen.
And that is what worries me in trying to understand the very good response statistics we see in single arm FCR and PCR studies done at expert centers. Was there some sort of (possibly unconscious) researcher / institutional bias where by patients with good prognostics were cherry picked for the studies? Is this a factor that was not present in the randomized study conducted at many different local oncology practices, and that is why the results do not seem anywhere as good in this study? I do not know, but I will ask around.
Morning, Chaya…
First, in response to this PCR thingy, I guess I have to say: NOW YOU TELL ME!
I feel like the coyote when the Roadrunner chases him off a cliff and he doesn’t know there is nothing under him until he looks down! You just told me there is nothing under me!
As you already know, I already had the PCR treatment starting in August of 2007.
I can honestly say that the only side effects (I wouldn’t even call them “adverse”) that I had was a cough and hiccups that developed a couple of days after the treatment. The hiccups lasted only for a couple of days and were easily handled by taking an omeprazole tablet (cheaper in the prescription form than Prilosec OTC! ) in the morning. The cough was very mild, and store brand cough drops from my local grocery store handled it very well.
I did receive 3 to 5 shots of neupogen between each cycle, but that was more as a precaution than that I really needed it. My neutrophils rarely got below 1,000 (only twice…with weekly blood tests) when we started the cycles, and were over 2,500 after the shots.
I suppose, like the coyote, my not knowing that it could be a poorer choice than fludarabine is what made it work so well with me! Both Dr. L and I are happy so far with the results. I hope I can eventually see results similar to Anne’s, above.
About that study you mention above…I notice that a large percentage of the patients were in stage 4. Could these be the ones that died? Could they be the ones who were hospitalized? There were more in stage 4 when the study started then eventually died in both groups.
And while on the topic, I’ve noticed this in other studies as well…they give total results, such as adverse effects, but don’t seem to break the results down (at least I can’t find the data) by age, stage, type of CLL (like the 11q that I have), etc.
Would be interesting in this case to see a breakdown of the results based on patient characteristics.
Harley
Harley:
You hit the nail on the head. There is little doubt that the response statistics are very much determined by the status of the patients recruited. If the earlier Mayo and MDA studies with single arm PCR and FCR trials respectively had fewer Stage 4 patients and a lot more Stage 1 and Stage 2 patients – compared to the double arm study we discussed in my article – then it is easy to see why the earlier trials had much better response statistics.
That is why it is so important to have these double arm studies done, so that we can weed out the effects of “cherry picking”, get a kosher apples to apples comparison between two therapy regimens.
The double arm study we discussed did not go into detail of how subsets of patients at different Rai stages performed in their trial. At least, the abstract I cited did not go into details, perhaps they did go into the nitty gritty stuff at the actual ASH presentation. I am sorry to have missed the 2008 ASH. Perhaps I will have the time, stamina and money to attend ASH 2009. It is amazing how much one can learn on and off the record at one of these annual galas.
The ongoing conundrum of how studies are set up and conducted will likely never change. Quite simply there are too many disparate interests involved and too much expense incurred in performing these types of studies to expect otherwise.
The very essence of “clinical research” necessitates that the clinical researcher wears no less than 2 hats; one as a researcher who advances his/her academic career via their research and at least a second as a physician who must care for people who have an illness and seek the best treatment available. At times a third hat (consultant to a pharmaceutical company) may also be worn. I believe that it takes a rare individual to keep the proper balance of things 100% of the time, human nature being what it is. I was especially impressed by two different physicians who I consulted during my journey who dissuaded me from entering studies in which they were engaged.
Having said that, there is also the issue of cost and practicality. These studies are often very expensive, so statisticians often seek to gain drug approval utilizing the smallest cohorts of patients and fewest number of studies possible. This, in turn, has led to many “surprises” after drugs are employed in the “real” world.
I expect that the same will be said when ofatumumab becomes available for use.
When new surgical techniques are developed within university settings and when new treatment protocols are used in similar settings, the original results are often better than those that can be achieved in the ‘real’ world in which most of us must work. Truly good techniques eventually succeed in the real world, and, at times the results are even improved upon as refinements and ‘real world comfort levels’ grow.
It isn’t too surprising to me that the results in community hospitals did not match those that might have been anticipated based on studies initially done in only 2 centers.
In my opinion, the message isn’t necessarily to “go to MDACC or Mayo Clinic for your therapy” so much as that PCR, indeed, is probably no better than FCR and MORE IMPORTANTLY” pay special attention to the level of care that you receive, wherever it is given.”
While great cooks sometime purposefully (or, perhaps, inadvertently) leave some small ingredient out of their published recipes, someone with talent and the temperment to “do it right” can still produce a great (or greater) dish in their own kitchen.
Something is very odd about the results. In this Mayo paper presented at ASH 2008, (Paper7303), an overall response rate of 91% is reported for PCR in contrast to the 45% rate reported above. Is this an apples and oranges effect?
I have been doing some digging around, and this is what I have found. The feedback comes from a couple of experts, provided I did not quote them.
1. The notion of PCR being a gentler and kinder version of FCR is gone for good. If enough pentostatin is used to get remission statistics to match FCR, then PCR is just as toxic as FCR. Even the earlier Mayo study did not see much by way of reduced toxicity – except in a subset of elderly patients. One expert pointed out this was scrambling to find some benefit after the fact, a subset analysis done after the study was complete – not considered statistically rigorous thing to do.
2. The response rate differences between this PCR versus FCR two arm study and the earlier single arm FCR and PCR studies at MDA and Mayo respectively is attributable to two things:
(a) Recruitment for the MDA and Mayo studies may have used more lenient criteria; the patients in these studies may have been in better shape than the patients recruited for the two arm study. And in any case, the two arm study had 80:20 mix of chemo naive and previously treated patients.
(b) The drug dosages were somewhat different. The two arm study used more purine analog (fludarabine and pentostatin for FCR and PCR arms) and less cyclophosphamide. Since there is a certain synergy to using (F + C) or (P + C), the two arm study may have less than optimum ratio of the purine analog and cyclophosphamide.
Bottom line, we can compare results only when the patient cohorts are well matched, and exactly the same drug dosages are used as well. Otherwise we end up with apples and oranges.
11qRick, I think you are right in your assessment of the experts wearing more than one hat. There is an inherent conflict of interest built into the situation. I do not know how to get rid of it, the best we can do is be cautious before signing on the dotted line and trying to do our own due diligence. It is hard to sort out all the pros and cons of clinical trials – I hope this is an area where CLL Topics can help the patient community.
Chaya:
Your last post, #1 at 7:49pm, raises a question. I was always under the impression that the dose equivalent between F and P was not know so how is that it is now known down to the exact remission rate?
Mickey:
Both pentostatin and fludarabine have been around for quite some time. Both have been used in CLL as well as other hematological cancers. Both have pretty well researched dose ranges (as well as maximum tolerated dose limits) over which their efficacy and potential adverse effects have been studied. My comment was intended to convey the fact that the difference in milligram numbers for the two drugs should not be taken to mean an automatic advantage for pentostatin.
I finished 6 rounds of PCR in October. I received treatment at a community oncology practice in Tucson, but my treatment was prescribed by a Mayo Clinic CLL expert. Interestingly, the Mayo doc recommended decreasing Pentostatin to 2mg/m2 instead of the “usual” 4mg/m2. He felt that the reduced dose was equally effective and resulted in fewer complications. Three months after completing treatment, my labs look stellar and my bone marrow showed just 0.12% CLL, (down from >90% before treatment.) I developed neutropenia 4-6 weeks after treatment concluded, but responded well to Neupogen. I had no infections or significant neutropenia during treatment. I guess I got lucky.
Steve
Having participated in a major single arm study in one of these centers, I pointed out to my Doc. that one of the phase II entry criteria, that of night sweats, had only occurred for me on one night five years prior to my treatment. That was good enough they said. I always felt “cherry picked” either due to my overall physical health but also because of my connections. To what extent major institutions select favorable candidates, subconsciously or not, I cannot tell, but from my own experience I believe it happens and that it would not take very many cherry picked recipients to make a difference in either response or complication rates in a small cohort.
Hi Chaya,
First of all let me thank you from the bottom of my heart for all the work you have been doing in helping me and many others have a better undertanding of the challenges of CLL.
I was rushed into fludarabine the first time the need arrived for treatment for my bulky nodes ( I looked like a bullfrog in full voice). Then I became aware of CLL topics and the world opened up to me in gaining a much needed understanding of what mt CLL/SLL was all about. My initial remission lasted about 11 months before the nodes started to grow again. What to do became my focus from thenon. The first thing I did was change my hematologist to one who would acutally talk to me and better still listen to what I had to say and actually answered my questions and worked with me from then on. I then, I live in Canada, jumped on a plane and visited the Mayo Clinic and had the full battery of diagnostic tests, which my original hematologist had told me I could spend my money on but would not change in nay way the manner in which he would treat me….unbeliveable but true. The results were not the best 11q, unmutated immuglobulin..high CD38 but at least I knew.
The team at the mayo wanted me to look at their clinical trial PCR, but as a resident of Canada it would mean paying the for it and travelling for the treatments. I then sat down with my new guy and in consultation with the Mayo and would you not beleive it a visitor from MD Anderson, who happened to be in town on a visit we decided on FCR.
So about 12 months after my remission I did the FCR bit. No real problems though as the treatments rolled by my neutropenia increased until the last of the six treatments was touch and go whether to delay it, but we ( yes I had a say in the matter) decided to go for it. Then came a long six months of feeling fine but ANC of 300 and white count around 1000 left me in a very risky situation. By this time I had yet another Hematologist when to my dismay number two had decided to retire before as he put it, my wife leaves with half my wealth???? He ate drank and slept his practise and was loved by one and all ans he took us through our challenges. The new Dr is young but very open minded and communicates and listens, I fell so lucky to have found two such Dr’s.
A bone marrow and bone biopsy showed me clean of CLL and confirmed our belief that the FCR was the culprit.
While I am still neutropenic I am well above the critical levels and able to get on with life and work hard at spending my kids inheritience. It’s been 18 months and I look forward to many more.
I continue to value your dedication to us all and devour all your communications as I realize the next step will be a real challenge to me and my Dr’s.
By the way did you ever listen to my song “Haemo Blues”?????
I finished six rounds of PCR November 08 and I was very pleased with results. Bloodwork improved dramatically and was left with only one small lymph node below the diaphram. Local and U of MI doctors pleased with outcome. I was given anti-viral, fungal, and bacterial drugs throughout the treatment and for ten weeks following treatment, and Neulasta following each round. I never went neutropenic. I had one medical event requiring a trip to ER, an intestinal issue, and the health department thinks I picked up a bug at an area resturant. Antibotics resolved. I’ve had CLL since ’97 and had six rounds of F in 01-02.
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