What is “Tumor Lysis Syndrome”?
“Tumor lysis syndrome” (TLS) is a potentially life-threatening complication. All too often I have heard from members whose local oncologists had not paid sufficient attention to this possible risk before starting chemotherapy. Once again, what you (and your doctor) do not know can kill you.
In simple terms, TLS is a risk if too many cancer cells are killed too quickly and the debris created by the dying cancer cells overwhelms your body’s garbage handling capability. As anyone who has lived through a garbage strike can tell you, things can get toxic and smelly pretty quickly once the garbage starts piling up in the streets.
One of the major components of the “garbage” created by dying cells is uric acid. Under normal circumstances your kidneys remove uric acid dissolved in your urine. Unfortunately, uric acid is only slightly soluble in water. Even when your kidneys are doing their best there is a limit to how much uric acid can be eliminated by this route. If the amount of uric acid that has to be processed overwhelms the capability of your kidneys, you are at risk of kidney damage or even kidney failure. Some of you may have had opportunity to worry about uric acid from other perspectives. “Kidney stones” are caused by precipitation of undissolved uric acid. Gout is a very painful disease associated with uric acid depositing in various joints.
Who is at risk of TLS?
Limiting our discussion to CLL patients and chemotherapy, generally speaking the folks most at risk are those with large number of tumor cells in their blood circulation, especially when they are treated with chemo drug cocktails with significant oomph. CLL cells are easiest to kill when they are easy targets out in open blood circulation, not tucked away and hard to reach in the protected environment of swollen lymph nodes and bone marrow. In other words, if your WBC (white blood cell count) is high and you are about to start treatment with common therapy options such as fludarabine or its various combinations with Rituxan, cyclophosphamide etc, you need to be extra aware of the risk of TLS. Killing CLL cells is a good thing. But you want to do it slow and easy so that your body can safely get rid of the uric acid created by dying cancer cells. What constitutes a high WBC? There are no hard and fast rules on that. In my book a WBC of 100K is high enough to worry about TLS. Your doctor may have a different cut-off point. In any case, best practices recommendation from experts is that patients should be protected against potential TLS by premedication ahead of getting therapy. Better safe than sorry, as they say.
Precautions
The simplest thing you can do to protect yourself is to make sure of you are well hydrated before, during and after each cycle of therapy. In other words, drink plenty of water (not coffee or caffeinated drinks) starting about a week ahead of therapy. The logic is pretty straightforward. The more water you drink the more you will pee and that improves your ability to get rid of uric acid. It is also important to empty your bladder at regular intervals and not just cross your legs and try to “hold it” because you are busy doing something else.
Allopurinol
Until recently the only drug available to help protect patients against TLS was allopurinol. Allopurinol is manufactured by Prometheus in the United States and marketed as “Zyloprim” by GlaxoSmithKline. In other countries other brand names are used: Allohexal, Allosig, Progout, and Zyloric.
Allopurinol is an enzyme inhibitor and in simple terms it slows down the production of uric acid. So, even if the CLL cells in your body are getting killed in record numbers in double quick time, one can hope that if you are loaded for bear with allopurinol this puts the brakes on how fast uric acid accumulates in your body. Allopurinol is taken orally and most doctors recommend that their patients start taking daily doses of it about a week ahead of start of chemotherapy. As you might guess, allopurinol is also used for treating gout and kidney stones – two diseases that are also caused by deposits of undissolved uric acid crystals in joints and kidneys, respectively.
One of the problems associated with allopurinol is that a significant percent of patients are allergic to it. My husband PC tried using allopurinol the very first time he was up for single agent Rituxan therapy. Three days after starting the drug he broke out in the most intense case of itching I have ever seen. Poor guy could not sit still even for a minute without needing to scratch! If you experience any rash or other skin discomfort, be sure to tell your doctor about it right away – and you may want to stop taking the drug while you are trying to reach the Man. “Murphy’s Law” dictates that most adverse effects seem to start on a Friday evening, when everyone has gone home for the weekend. Other and more serious adverse effects have also been reported for allopurinol. Further use of the drug was clearly a non-starter in PC’s case. The best we could do for all subsequent therapy sessions was to keep him very well hydrated, make sure he made the trip to the little boy’s room as frequently as possible and initiate therapy before his WBC reached dizzying heights. These are sensible precautions, especially if you have a history of kidney probles, or you have had kidney stones and/or gout.
Rasburicase
Now we have a new drug on the scene that has shown efficacy in preventing TLS. Unlike allopurinol which merely slows down the production of uric acid, Rasburicase catalyses the conversion of uric acid to allantoin. And this is important because allantoin is 5 to 10 times more soluble than uric acid, so you can piss it away more effectively.
At the recent ASH conference Sanofi-aventis reported the results of a study in adult patients with hematological malignancies at high or potential risk for tumor lysis syndrome (TLS). Rasburicase (brand name “Elitek”) significantly reduced uric acid levels in the blood compared to allopurinol. The study had three arms.
- First group of patients got rasburicase at a dosage of 0.20 mg/kg each day for five days
- Second group got rasburicase at the same dosage for three days, followed by allopurinol (300 mg/day) starting on the third day and continuing for another two days.
- The last group (the control group) got only allopurinol (300 mg/day) for five days.
There were roughly 90 patients in each group, quite a large number, and that increases the credibility of the comparison. The results of the study are summarized in the article below from Cancer Network:
December 8, 2008
Rasburicase reduces tumor lysis risk in hematologic malignancies
By Walter Alexander
SAN FRANCISCO — Rasburicase (RAS) is superior to allopurinol in adult patients with hematological malignancies whose treatment puts them at high risk for developing tumor lysis syndrome or who have hyperuricemia at baseline, according to a study out of Houston’s M.D. Anderson Cancer Center.
TLS is a potentially lethal metabolic complication of chemotherapy or cytolytic antibody therapy. The prevention and management of TLS includes hydration and reduction of serum uric acid levels (SUA). Although allopurinol (AL) has long been used for TLS prophylaxis, its efficacy in controlling SUA is limited, especially due of its lack of action on pre-existing hyperuricemia. Rasburicase, an injected recombinant urate oxidase, converts uric acid into readily excretable and soluble allantoin. RAS (Elitek) is currently indicated in the U.S. for TLS-associated acute hyperuricemia in children and adolescents.
Jorge Cortes, MD, and colleagues conducted a prospective, randomized, parallel group study with three arms (RAS 0.20 mg/kg/day; RAS 0.20 mg/kg/dose days 0, 1 with an overlap day of RAS and oral AL 300 mg/day, then AL 300 mg/day on days 3 and 4; AL 300 mg day). The aim was to compare the ability of the regimens to control serum uric acid (abstract 919).
The patients (275) had high TLS or potential TLS risk and had been diagnosed with acute myeloid leukemia, lymphoma, myelodysplastic syndrome, or multiple myeloma. Treatment success was defined as a plasma uric acid level of ≤7.5 mg/dL (day 3 through 7).
Dr. Cortes reported in a poster presentation that the plasma uric acid response rate (PUAR) was superior for RAS (87% versus AL 66%, p = 0.001) with a strong trend for improved PUAR for RAS+AL (78% versus 66%, P = 0.06). No patients in the RAS-containing groups failed to control PUA. Laboratory TLS was reported in 20.7% of RAS patients, 27.2% of RAS+AL patients and in 40.7% of AL patients. Clinical TLS was reported at rates of 1%/1% and 5.5%, in the respective groups.
Overall, RAS treatment was well tolerated with most adverse events attributed to chemotherapy or to underlying disease. RAS events were uncommon, with ≤2% of grade 3/4 events, ≤1% discontinuations and no related toxic deaths. Grade 3 or higher hypersensitivity or allergic reactions were ≤1%.
“Where AL prevents the formation of new uric acid, RAS destroys uric acid. AL can take a long time because you have to wait for the already made uric acid to be cleared. RAS gets uric acid down quickly, often to undetectable levels in a day. And it stays down,” Dr. Cortes commented in an interview with Oncology News International.
“RAS is superior to AL in normalization of serum uric acid, with a faster effect, in adult patients at risk for TLS. RAS alone or followed by AL are two valid options for this patient population,” he concluded.
Availability of rasburicase therapy
Rasburicase was approved by the US Food and Drug Administration (FDA) on July 16, 2002 for the initial management of plasma uric acid levels in pediatric patients with leukemia, lymphoma and solid tumour malignancies who are receiving chemotherapy that is expected to result in tumour lysis syndrome. We hope that based on the study discussed above rasburicase will soon be approved for adult patients as well. For folks like PC who are allergic to allopurinol rasburicase is a much needed second option.
What are your chances of sweet-talking your insurance company into covering rasburicase use ahead of the FDA ruling? The cost of five days of rasburicase therapy is calculated below:
Source: “Rasburicase (Elitek): a novel agent for tumor lysis syndrome”
If the company still has the same pricing policy, we are looking at a cool $14K or so for an adult weighing 70kg for use of rasburicase, compared to less than two bucks for allopurinol. Anyone thinks insurance companies will be thrilled with shelling out thousands of dollars versus chump change? Wanna buy a bridge in New York?
But hey, most of us know that in life you get what you can negotiate. No harm in trying to get this approved by your insurance company (or Medicare), but be aware you will probably need your doctor to certify you are indeed a patient at high risk of life threatening TLS and allopurinol is contra-indicated in your case because of known adverse effects (hypersensitivity). And be ready to support us when it is time to do a bit of squeaky wheel patient advocacy in front of the FDA. This is a pissing contest (ahem) where we have a stake in the results. It is expected that rasburicase will come up for FDA apporoval for use in adult patients some time this year.
23 comments on "Protecting Against Tumor Lysis Syndrome"
Chaya,
Thanks for reporting on this. You continue to be such a valuable asset to all of us with CLL. Your articles are well researched and written in very understandable terms. I can’t thank you enough.
Chris Randolph
Chaya,
Febuxostat is a new more potent allopurinol like drug that should be approved very soon for gout. On first blush, it does not seem to associated with the severe skin issues that limited allopurinol. It is so much more potent than allopurinol that it might more easily precipitate a gout attack in those at risk, and so must be taken with colchicine or a NSAI when a gout patient starts on it. The same caveat is true for allopurinol.
Its role in TLS is undefined, but I suspect it will find a place.
One last point. Starting a drug like Febuxostat or allopurinol months in advance of treatment can begin to lower total body uric acid load in those with pre-existing hyperuricemia though this is strictly an off label use.
Brian
The “catch 22” with a drug such as RAS is it’s high cost… this limits it’s use, which in turn keeps it’s cost elevated.
I digress, but once when I was caring for a young woman the only way that I could control her terrible nausea and vomiting was by using a drug called Kytril.
When she was able to leave the hospital the primary physicians caring for her asked me to write the prescriptions for the problems for which I attended her. Naturally I wrote her a prescription for Kytril, having absolutely no idea of it’s cost. Several hours later she tearfully called me from her pharmacy. Fortunatel, I was able to obtain several pills for her from the hospital ( a feat not likely possible today) and worked with her as an outpatient to keep things controlled without the Kytril.
I knew about RAS, but had no idea that it was that expensive!
For many people, careful attention to hydration, avoidane of certain diuretics prior to and during early therapy and dietary restrictions may work well when allopurinol cannot be tolerated.
I developed a diffuse rash within 6 days of starting allopurinol during my first course of treatment, prompting me to stop it (Stevens Johnson Syndrome is possible with allopurinol). Simple measures ( especially careful attention to hydration… taking care, of course, not to induce hyponatremia) worked well for me when therapy was repeated.
We need to work with the FDA and with drug companies and insurers to keep drugs such as RAS available for those people who really need it, such as those who begin with hyperiricemia, impaired Creatinine clearance and allergy to allopurinol.
Several good points are raised in the previous comments and I thank the authors. TLS concerns are obviously higher in patients with existing kidney problems – demonstrated by high creatinine counts and impaired creatinine clearance. Avoiding diuretics prior to therapy is a good one too. I understand gout patients have special dietary recommendations since some foods are prone to create greater amounts of uric acid and best avoided if you are concerned about TLS.
We as a community need to think about how best we can influence FDA and the drug industry when it comes to drug approvals and drug pricing.
I am not in favor of opening the flood gates and approving all drug candidates whole-sale. We NEED an FDA with teeth – otherwise we will be exposed to useless / harmful drugs with little protection. Remember all those glowing direct-to-consumer TV adds we saw for use of epoietin drugs (Procrit, Epogen etc) for boosting red blood cell counts during chemotherapy? CLL Topics blew the whistle on excessive use of epo drugs well before the lay press picked up the story – I refer to our article “The dark side of epo” on our flagship website)
I hope the new and improved FDA in the new administration actively solicits feedback from patients and their advocates. Anyone has contacts within the FDA? I understand they are supposed to have patient advocates as members on their approval committees, but most often they fill the positions with patients without the training or ability to make meaningful contributions. I get the feeling they do not really want anyone in there that is likely to have an independent opinion, rock the boat as it were. If that is the case, I am automatically disqualified since I do have strong opinions and I have taught myself to spot junk science a mile away.
Thank you Chaya for opening up this timely discussion as I am currently adding about 5,000 per week to my 242,000 WBC and preparing for 1st TX.
In my notes and not mentioned as yet is Hydroxyurea. I have yet to research this and wondered if this is a viable alternative to Allopurinol for my “tool kit” what problems or cost issues are associated?
Rasburicase sounded so good til you got to the cost. I was wondering if one were leaning toward a Rituxan monotherapy (hypothetically speaking) would the standard dosage of 375mg/m2 be more threatening than Low Dose R regarding TLS or can TLS be controlled via infusion rate alone? Setting aside the “CD20 Shaving” debate stemming from the work of Ron Taylor, he has demonstrated that Low Dose R administration rapidly clears peripheral blood of tumor. Is there a way of determining TLS risk between standard R infusion at 375mg/m2 and say R infused at 20mg/m2?
Wayne
Wayne…certainly be involved and share your concerns with your physicians, but I heartily suggest to you that you DESIST from being your own physician.
FYI, the reccommendation is generally to split the initial dose of rituximab into two parts (on separate days) when the peripheral WBC exceeds 40,000 or so.
Chaya can correct me, but the data re low dose rituximab have not yet been published. When SQ alemtuzumab has been given in conjunction with rituximab, it has generally been started in step up fashion prior to the rituximab and the ALC is generally markedly lowered befor the rituximab is given.
Whatever you do… I suggest that you dialog with, but listen to your physician. There are too many variables for non-physicians to try to manage their care.
Good luck,
11qRick
Thanks 11qRick but I still think my questions are within the appropriate purpose of this forum. I am not asking anyone to advise me how I should be treated.
I have been seen by Dr. Byrd, last June. He was unclear what to make from my “discordance” but said “you might make it another year” in the absence of “B” symptoms regarding tx. He prefers W&W until a 300,000 count is reached. His preferred tx is RF. Rationale being to hit it hard when first treating. Reserve Cyclophosphamide for 11q. He certainly has valid arguments that I must take seriously. Two other general Oncs had been pushing for me to enter tx much earlier. They were both ignorant of NCI-WG guidelines and were, I feel, reacting to my white count alone as my other critical blood markers are low but normal or “safe”. Even now I maintain high quality of life (just got back from Xcountry skiing 4 hrs in 5-10 degree weather) with an ALC of 211,000
The real question, which no expert can answer, is does my discordance play in favor for my marker profile warranting a standard RF or RFC first tx or do the clinical signs of progressive disease, large and profuse nodes and high B2M put me in a far riskier position for Fludarabine based protocols warranting a less toxic tx with little expectation of great or durable remission?
If I could be tested for chemo resistance it would be one hell of a lot easier to make decisions. I am not being my own physician but from what I have seen and witnessed in my 2yrs plus of this journey I would rather ask the questions probing the options than deliver myself trustingly into the hands of some of the Drs. I have encountered thus far. The latest Dr. who replaced my trusted oncologist who left my clinic for an R&D career did not even palpate my spleen yet was “huffy” with me for asking him why he thought I should be treated immediately. I want a reasoned approach and not the answer “because I have been at this for twenty years and you are inviting complications by waiting” Duh.. CLL is nothing but complications!
WWW
It is my impression that dividing the Rituxan dose over two days as well as slowing down the rate of infusion greatly the first few times patient is exposed to Rituxan is meant to reduce infusion related adverse effects (such as the infamous “shake & bake”, urticaria (hives), variations in blood pressure etc), and not an attempt to control TLS.
One approach that has been followed by some centers is to use fludarabine first, in an attempt to get the peripheral blood CLL count significantly reduced and out of the way, before initiating Rituxan therapy. The rapidity with which Rituxan kills CLL cells in open circulation is thought to add to the risk of TLS in patients with very high WBC.
Given the very wide variability in quality of medical care and the speed with which expert consensus is changing (and NOT always trickling down to the level of the local oncologist), I tend to agree with Wayne that the burden to be well informed falls on the shoulders of patients.
It has been my experience that true experts are rarely offended when a well informed patient initiates a two-way dialogue and takes an active role in the decision making. Even when the patient makes every effort to be reasonable and rational, sometimes the “huffy doctor syndrome” is evident (usually at the local level) and I think it is often a sign of insecurity or arrogance on the part of the doctor. Any physician who is too busy or too important to really listen to his/her patient is missing an important piece of the puzzle.
Bottom line, I am a pragmatist. Don’t burn any bridges that you might need later, but do remember you have a lot more skin in this game than anyone else. Negotiating with one’s doctor is no different from any other important negotiation. Being well informed and bringing a cordial and reasonable attitude to the negotiation is important – but so is a certain determination not to be intimidated or silenced into submission.
Chaya,
I can’t recall seeing a definition of what constitutes “well Hydrated”. Does being well hydrated mean something different depending on drugs used or body weight? How soon before treatment does one start lifting the mug?
We are all more focused on what goes in than what has to come out. Can you shed light on this issue?
WWW
Sorry, I took the easy way out and used an ill-defined term. I have not come across any credible definition of “well hydrated”. Perhaps commonsense definition is our best guide. The adage of a full glass of water with each meal, and a total of 6-8 full glasses per day is what my grandmom used to recommend. Sounds good to me! But I am sure this will vary depending on the climate, level of exercise, body mass etc. If anyone has a better fix on this issue, do speak up!
Wayne,
Good for you! We too have experienced at all 4 of the Oncologists that we have thus far encountered, Huffy Dr. Syndrome. We go in with our questions, charts, records etc and immediately feel the “vibes” in the room get defensive on both sides. We have been to 3 Cancer Clinics, not the run of the mill “local oncologist” and had such stereotypical encounters. Each having a “numbers” approach to why we need to start treatment SOON. Too bad they all seem to contradict each other! One went strictly by WBC, One by WBC and Platelet and the last mostly by platelets but that too would include a low HMG and HCT which both were in ok levels but when he got the blood work back he did a complete 360 and said that based on a drop in platelets only he changed his whole tune and said we need to look at starting therapy now??? We are so frustrated with all of it. It seems the more you know the worse it is…constant uphill battle to find a doctor that “gets it!” which brings me back to an early complaint/concern of mine…it seems to be all about the money and getting you into the “treatment system” asap. Even when you pin them down over what numbers exactly constitute a true health issue they don’t have any good answer and then they contradict themselves and each other….don’t let other well meaning people discourage you from being informed and making informed choices about your treatment because from what I have seen and experienced the past year or so is that it seems to be a big trial and (unfortunately at times) error guessing game. So the more info we can get (and this site is by far the best I have found in a year of daily, extensive research) the better your odds of winning this race.
PS
It would really help if more people could share their stories with all the info they feel comfortable sharing hearing other’s “numbers” in regard to counts and stuff really helps those of us struggling to know what is a high WBC, low RBC/HMG/HCT etc and like Wayne asked what is well hydrated etc… the TLS article helped us so much as my husband has a recently spiked WBC of over 100,000 so knowing how/what pre meds might be needed/helpful PRIOR to treatment we can discuss that we the oncologist ahead of time. More such “heads ups” are needed for the Control Freaks like me out here.
Maybe getting the total cost for emergency treatment of TLS patients vs the cost of Rasburicase might help convince the insurance companies of it’s worth. Anyone have any numbers to share?
In response to aengleid’s request that more members share their stories, I’m compelled to share my husband’s experience. Since he was diagnosed in June, 2005, I have been reading Chaya’s website and feel that I understand more about CLL, therapies and complications than I ever would have just googling around. Chaya is a true hero, especially in the wake of her recent loss. Her essay on grief on this site was as heart-wrenching a piece as I have ever read.
Once diagnosed, we were lucky to be close enough to a CLL Consortium Center and my husband is monitored there two or three times a year, as well as by his local hematologist. He has participated in a clinical trial there for untreated patients. His diagnosis came about as a result of his wbc count not returning to normal after his kidney was removed due to two malignant tumors, which had not metastasized. At diagnosis, his wbc counts were about 20,000. His FISH results at that time showed that he had the unmutated gene, positive Zap 70, but a 13q deletion and no p38–I know I’m not stating these numbers correctly, but our understanding was that he had two good markers and two bad ones, and that the unmutated gene trumped everything else and put him on a “moderate” or possibly more aggressive course.
He has been healthy and working for almost 4 years–he does have small lymph nodes in his neck, under his arms, and particularly around his aorta. A CT scan last week showed those nodes to be approximately 4 cm. His spleen is slightly enlarged.
Two weeks ago we visited the CLL Consortium hospital and he was examined by one of the most highly respected CLL doctors in the country. I would rather not use the actual names of doctors or hospitals. This doctor stated that the abdominal nodes and spleen were growing but not necessary for treatment yet, and because of my husband’s lack of fevers, night sweats, energy loss, etc. that treatment could be put off. However, the cbc showed that my husband’s lymphocytes had jumped to 342,000–a definite doubling within 6 months. This doctor recommended a beginning treatment of Rituxan for one day, then 3 or 4 days of fludarbine. He said he would confer with my husband’s local oncologist.
Surprisingly, just one week later, when we visited our local hematologist, the wbc count was at 243,000. There could be many explanations for the difference, apparently. At any rate, our CLL specialist feels that treatment should begin at about 250,000 because of, I think, thickening of the blood that could lead to complications.
My quandary now is whether to question this very esteemed doctor about why the first treatment should be FR and not FCR Lite, especially in light of the results that were just published on Feb. 1 in the Journal of Oncology. I think this doctor likes to begin with just FR and save the “C” for later. I am frustrated because I trust this doctor completely but have read so much about FCR Lite becoming the standard for first therapy. I know the first therapy is the most important and I don’t want to regret not discussing it in more detail. The other grave concern I have now is reading about TLS, which is new to me. Since my husband has only one kidney, will he be in even greater danger? The decisions need to be made very soon, and so much information is overwhelming me. I do plan to discuss the treatment with both doctors, however. I am given courage to “speak up” by Chaya’s earlier post that–“It has been my experience that true experts are rarely offended when a well informed patient initiates a two-way dialogue and takes an active role in the decision making.”
katmcgrat6
Thanks so much for sharing. I can relate more than you could know. We have seen some similar WBC issues and I feel your frustration. When a Dr tells you they need to start treatment because a certain number is elevated then a week later that number drops on it’s own you question what risks you might have taken unnessasarily. We have had over 4 different Dr’s and their opinions and they have all been different. I understand “frustration”. I am interested to see what answers you get to the TLS questions in light of the single kidney complication.
Please keep us updated.
April
katmcgrat6
The single kidney issue with reference to potential risk of tumor lysis is certainly worth bringing up with your expert. Let’s talk more on the phone about the specifics of your husband’s situation. But I do know well the expert you are talking with – he tends to be a bit busy and therefore it is possible to catch him on a bad day and it may be necessary to be aware of that – but by and large I still think most of our CLL experts are not offended by a well informed patient bringing credible concerns to the table for discussion.
The other side of the coin, a terrific CLL expert who is also a good friend tells me horror stories of patients who send him rambling multi-page emails and the most inane lay-press articles as the basis for medical discussion that wastes everyone’s time. How does one discuss the relative merits of FC versus FCR or FCR Lite in the same breath as ‘colon cleansing’ or ‘blood type diet’? Two different universes.
Hello,
I very much appreciate all of the comments from you all. I am scheduled to start FCR on February 25th. My local Doc is very good but he wanted to just do R. Since I had been to Mayo and did a EGCG phase I Clinical Trial, I suggested we call my Mayo Doc. The Mayo Doc felt like FCR was certainly the way to go so my local Doc
Cont.
So my local Doc agreed. I am at 191,000 WBC with HG 10.1 and platelets 90,000. Both Docs agree that Tx should be initiated. No Spleen or lymph problems or any other symptoms for that matter, as of yet. I have started Allopurinol, am drinking lots of water and have discontinued caffiene as of today, Feb. 19.
Called my Mayo Doc yesterday and he wants R to be given in each of the first 3 days with 100 mg day one, 450 in each of the next 2 days.
I have not really read much about CLL in the past and am getting a fast education. The course is set for 6 months of therapy.
I would very much like to talk to my Mayo doc about this expensive Rasburicase, it sounds good to me from what I have read………save the cost
Kind Regards,
Mark
Mark:
I will be keeping my fingers crosssed for you as you go through the six cycles of FCR.
As long as you do not develop hypersensitivity to allopurinol, it should be just fine to use it. You do not need Rasburicase in that case. I am glad you are also taking the other commonsense precautions to protect your kidneys.
Chaya,
Just spoke with my Mayo Doc this am and he wants me to have a bone marrow biopsy ASAP so we can be positive about the real cause of falling hemoglobin and platelets. He said with cases like mine that have no outward symptoms that 50% of the time other things can cause those numbers to drop.
Since FCR is a “ONE SHOT” deal it would be best to be sure before therapy is initiated.
Mayo Doc also wants me on sulfa 3X per week during therapy and for 6 months after treatment concludes.
Mark
Mark:
listen to your Mayo doc, you are getting good advice from him.
In addition to the sulfa during and after therapy, you might also want to ask about prophylactic antiviral protection (such as Valtrex) to protect against reactivation of HSV – shingles. Shingles can be excruciatingly painful, getting daily acyclovir or famcyclovir falls into the category of being safe rather than sorry. Both of these drugs are now readily available and have long track record of safety in daily administration over many years.
I have already started Acyclovir for the virus. For the past few years Valtrex has been a very good and consistent friend when various viruses appear.
Thanks,
Mark
Very good article and discussions.
My husband,Terry’s, local oncologist wants a new CT of his neck to pelvis to compare one from 6 mo before.
He said he would begin FCR. He downplays any side effects of the treatment.
Terry has bouncing #Lymps (or is it the lab?) that overall increase. Since dx in 2003 at 9,000 to 60,000 now and platelets hover around 100, spleen palpable, some nodes are palpable, recent MRSA, treated topically in nostrils.
He usually feels okay. One day recently he had a hard time walking up a steep Seattle hill to his office. He carries a heavy backpack. Some days he reports feeling more fatigued than others. He is a young 62.
I have some concerns.
One was in answer to my polite question, if he will order a bone marrow biopsy before initiating treatment. He said he saw no reason to do one. I had the idea it was standard to do a baseline before initiating treatment. Terry has a followup appt. for after the next CT in Feb. He has mutated gene and trisomy, is it 12 or 13? He’s had no admissions for infections and stays mostly well, active and working.
Another flag is discrepancies in the oncology office labs. Last month Terry’s internist noticed the WBC showed 20,000 higher at the oncology clinic results than from the nearby hospital draw 3 days before. Last summer Terry’s #Lymphs dropped in 6 weeks by over half, to 27,000, then went back up to more than double 6 weeks later, both at the oncology office lab. His immune numbers are low normal or slightly below.
Another concern is I don’t know if he’s been tested for causes for low platelets other than disease progression. He is not anemic.
I’m looking at 2nd opinions. Does anyone have contacts, experience, or confidence with a provider who sees a lot of CLL in the Seattle area? Terry is not inclined to travel in the fist weeks with a new employer. He knows them, having spent over 6 mo. working there for an agency. Now he is direct hire and enjoys his position.
I also appreciate your input. It is nice to not feel alone when facing decisions. Thanks,
Linda
Leave a Comment