Lenalidomide lets loose

In a word, brutal. That's how I would describe my first ten days of lenalidomide, aka Revlimid.

I took my first 10 mg dose on Thursday, March 4. For the next two days the main symptom was fatigue, which is common among those starting the drug. It was nothing insurmountable, but it did require an extra hour or two of sleep at night and a nap during the day. (I took the pill at bedtime, which is recommended.) Waking hours were accompanied by a certain amount of cat-like lethargy, but I was still able to work at my home business. I would not want to be starting Revlimid while holding a high-pressure job or managing a busy household. This drug is the enemy of multitasking.  

By Saturday I was starting to feel noticeable effects of tumor flare, which is where the brutality comes in. It seemed as if my lymph nodes (and probably spleen) were growing by the hour. My abdomen became so distended that I looked at least eight months pregnant. A baseball was developing under my right arm. By sometime Sunday my neck was wider than my head. I could barely button my largest pair of pants. I was eating less because I was feeling full faster -- my spleen was probably pressing on my stomach and the abdominal bloat was pushing up from the other direction. I would say that in a matter of just a few days my lymph node bulk increased by at least 50%, and that's just a rough guess. It could have been upwards of 100% in some areas.

Each nightly pill added fuel to the fire. It seemed as if the nodes were intent on growing whether there was space for them to do so or not. While I knew that tumor flare is a normal side effect of lenalidomide, it was still scary. It provided me with a snapshot of how much worse my chronic lymphocytic leukemia could get if things got that much more out of control.

By Sunday evening I was experiencing a new symptom: trouble getting a deep breath. Up until then I was willing to tough it out, despite the discomfort. Bloated, distended, ready to give birth to an alien baby, that I could handle. Shallow breathing, not so much.

The shortness of breath was not constant, nor was I feeling like I was going to pass out. I was getting enough oxygen. But it was disconcerting, to say the least, and it was becoming more frequent the longer I stayed on the drug. Perhaps a mass of nodes was pressing on my diaphragm, or perhaps nodes were interfering somewhere else with the breathing process, or perhaps both. I couldn't help but wonder how much worse it might get.

I should interject here that, according to studies, tumor flare can crop up anywhere from 0 to 56 days after starting Revlimid. Median time to resolution is 14 days. I was just four days in.

By Monday night I had the intuitive sense that taking more Revlimid had the potential to push me into the realm of unintended consequences. I considered using steroids to dampen the inflammation since ibuprofen had proven worthless -- both ibuprofen and steroids are  accepted methods of managing tumor flare -- but steroids also interfere with the ability of Revlimid to prod an immune response to the CLL. So it seemed somewhat counterproductive to start down that road, and I had no idea how long it might take for steroids to begin to work effectively.

Ultimately, I decided not to take the drug. I checked with my doctor on Tuesday, and on her advice I didn't take it that night, either. The shallow breathing actually worsened on Tuesday, to the point that I curtailed most physical activity. I didn't feel an improvement of symptoms until Wednesday, especially later in the day, a few hours after I had my weekly 1000 mg dose of oftatumumab.

I met with my doctor that day -- try holding an intelligent conversation a half hour after you have gotten 50 mg of intravenous benadryl -- and we decided to temporarily scale my Revlimid dosage back to 5 mg. Since then, the tumor flare has continued to abate.

There is some debate about whether tumor flare presages a better response to the drug. A report issued by Celgene, the drug's maker, summarizing the findings of various studies, put it this way:

"There have been conflicting reports regarding the association of response to therapy with the occurrence of tumor flare (TFR) symptoms. Padmanabban et al. reported (2006) that TFR may be associated with clinical response and Coleman et al. reported (2008) that [in] four CLL patients, symptoms of TFR signaled a response. Sher et al. also stated that the occurrence and severity of TFR appeared to correlate with clinical response (2009). However, Ferrajoli et al. reported that, in their 2008 study, TFR did not predict for a higher response rate, but did develop more frequently in patients with lymph nodes >5 cm compared to other patients (53% vs. 15%)."

So, ultimately, there is no way of knowing for sure whether my lymph node explosion was a good thing. There's also no way of knowing whether cutting it short was a good or bad decision CLL-wise, although it certainly was the right call breathing-wise. If you can't breathe, CLL is a moot point.

Uneventful ofatumumab

The start of treatment was delayed two weeks because of a cold. Colds, as some of you know, can be a particular challenge to CLLers since we have degraded immune systems with few functional B lymphocytes, lowered immunoglobulins, and too many CLL clones gumming up the finely-tuned works. 

Sure enough, my lymph nodes grew as the clones reproduced in a frenzy, trying vainly to fulfill their intended function. Somehow I managed to get over the worst of the cold in a couple of days, after which it dragged on at a low level, but not quite low enough to safely begin treatment. 

Once I had recovered, things got underway last Wednesday with the opening dose of ofatumumab, aka Arzerra. GlaxoSmithKline starts you out with a baby dose of the stuff, 300 mg over six hours, just to make sure you don't have any serious reactions. The infusion rate begins at 12 mg an hour and is gradually increased every half hour to 200 mg. Premeds consisted of two Tylenol, 50 mg of IV Benadryl, and 100 mg of IV hydrocortisone, aka Solu-Cortef. 

Absolutely nothing happened, other than the Benadryl putting me into a rather comatose state. Being a fully-humanized monoclonal antibody, ofatumumab may cause less of an allergic reaction than its cousin, the mouse juice rituximab. I have often had mild infusion reactions to the latter -- flushed face, tightening of the throat, and the like -- usually during the first infusion of a cycle. With the ofatumumab they may as well have been giving me water. That doesn't mean no one ever gets a reaction; it can and does happen, it just didn't happen to me.

The one thing I did notice is some mild redness on my neck (below the ears) where the lymph nodes are inflamed. Back when Rituxan was working pretty well on me, I used to get the same thing. This seems to me to be more a consequence of the drug working than an infusion reaction, especially since I have only noticed it toward the end of an infusion or after it is done. Other than that, I can't report any noticeable effects of the Arzerra, but at 300 mg, I wouldn't expect to see much progress.

Next week I'll be given the customary 1000 mg dose, along with more of the dreaded Benadryl. The day after I start the lenalidomide (Revlimid), 10 mg daily. In other words, Houston, we will have lift off. 

My little OL protocol: ofatumumab and lenalidomide

Yes, that little ol' lab rat, me, is about to undertake a cutting-edge protocol to fight chronic lymphocytic leukemia: ofatumumab and lenalidomide.

I call it the OL protocol, and there’s a trial at MD Anderson in Houston that’s just starting to accrue patients for a two-year study of this new drug combination.

Thanks to a forward-thinking oncologist who is willing to fight like hell for her patients, and thanks to two drug companies that are willing to help those who can’t afford to pay the enormous costs of the treatment, I am going to be following that protocol from the comfort of home, or at least from a comfortable chair two hours away.  I start next week.

Because I will be one of the first CLLers to try what could become an important  therapy for our community, I will blog about my experience on a somewhat regular basis.

To briefly review, ofatumumab is the fully-humanized anti-CD20 monoclonal antibody that was approved for CLL in October by the FDA. It goes by the trade name Arzerra but old CLL hands (Man, I guess I am one of those!) may better know it as HuMax-CD20. It was developed by Genmab and licensed to GlaxoSmithKline.

Lenalidomide, which I wrote about in my last post, goes by the name Revlimid, and was developed by Celgene. It has been approved by the FDA for Myelodysplastic Syndrome and Multiple Myeloma and has had some interesting results in CLL.

December’s American Society of Hematology meeting included a report from MD Anderson on a trial of rituximab and lenalidomide in 37 relapsed and refractory patients, all of whom had used Rituxan in the past. The new OL trial appears to be based, in terms of timing and dosages, on their experience with RL.

Dr. Alessandra Ferrajoli and the team o' Texans reported an overall response rate of 68%, of which 51% received a Partial Remission and 16% a Nodular Partial Remission. Sixteen percent had stable disease and 16% failed the protocol.

Other studies have shown an overall response rate of 32%-47% among relapsed CLLers given single-agent lenalidomide, so MDA considered the combination with the monoclonal antibody to be “superior to single agent lenalidomide, despite all our patients having received prior rituximab.

“Additionally," the authors wrote, "there was no increase in toxicity and lenalidomide-associated tumor flare reaction was less frequent and less severe with this combination compared to single agent lenalidomide.”

For the record, a 2008 MDA study of single-agent lenalidomide in relapsed patients showed an Overall Response of 32%, which includes a Complete Response of 7%. An additional 25% achieved stable disease. A 2006 study by Dr. Asher Chanan-Khan’s group at the Roswell Park Cancer Institute in New York reported an Overall Response rate of 47%, with 9% achieving a CR. Another 18% had stable disease. 

My prospects

Clearly, my response can fall anywhere on that rather large map, landing from CR to CRap. And just as clearly, this protocol is not going to be a cure for CLL nor an avenue to a molecular remission. But it may serve as a welcome and effective control, and I have reason to be optimistic as I begin.

I have always responded well to whatever new drugs I have been given and there is no change in my FISH profile that would indicate a loss of that ability. Of course, having had several treatments over the years, some disease resistance has developed in response. Indeed, the CLL cells have created a rather secure suburban community in my abdominal lymph nodes. The ability of lenalidomide to disrupt that micro-environment, including the nurse-like cells that help CLL remain comfortable, is a definite plus.

I am also younger and in better shape, both in terms of my health and disease state, than many of the participants in these trials. I can weather the side effects -- notably fatigue, tumor flare, and possibly low neutrophils and low platelets -- that may come my way.

Ofatumumab will assuredly be more effective on me than rituximab, to which I no longer respond well after many, many uses. Indeed, ofatumumab has given a new lease on life to any number of people who have tried it before me, some of whom I have known personally, and many of whom had stopped responding to Rituxan.

Readers may recall in my last post that I said I did not wish to use ofatumumab as a single agent, that it was too important a weapon to use gratuitously. That remains the case, and I don’t see the OL protocol as a wasteful extravagance.

I have a lot of abdominal lymph node bulk, enough that a year’s worth of steroids, Rituxan, and even cyclophosphamide were unable to make much of a dent in it. Ofatumumab is a new drug for me; with some luck, my nodes might respond the way they did to Rituxan when I first used it six years ago. In other words, they may undergo a noticeable reduction that can then be hammered home by the lenalidomide.

Can I completely clear the abdominal nodes? It would be quite a feat, but all things are possible in life and combination immunotherapy. Even if I can’t, can I reduce the bulk by a meaningful amount -- say 50% -- and throw my disease level back to where it was in 2005 or 2006? I think even hardened realists would say that is possible. The 2008 MDA study of single-agent lenalidomide reported a greater than 50% improvement in lymphadenopathy in 41% of patients. I'm probably starting from a worse position than most patients in that trial, but remember that we are also adding the ofatumumab.

Such a reduction in disease –- along with hopefully enhanced immunity, including a cessation of autoimmune hemolytic anemia, with its endless threat of hemolysis –- makes this an especially intriguing protocol.

Nothing else out there holds the prospect of doing all these things for me, especially with minimal toxicity, and these are all things that need to get done. For what it’s worth, some of the experts find this drug combination to be full of potential. I am told, for example, that MDA's Dr. Michael Keating is “very keen” on it. 

Perspective: Playing for time vs. transplant

It’s the right thing at the right time, as far as I’m concerned, which brings up an interesting point. When I was diagnosed in 2003, neither of these agents existed for CLL. Despite the feeling among us patients that progress can never come fast enough, here is a case where two new drugs may make a significant impact on my disease. So there is indeed some wisdom in playing for time if you have the stomach for it.

Playing for time is something that you have to finesse as you go, since the disease is not static. Much depends upon your biological markers -- IgVH mutational status, chromosomal deletions per FISH, ZAP-70, and CD38. But the bottom line, which I think is sometimes given short shrift in patient discussions, is your actual disease progression, clinical history, and ability to respond to treatment. 

To my mind, it's the practical stuff that counts. Which brings us to the stem cell or cord blood transplant, sometimes seen as the CLL end game. For many of us, and maybe even yet for me, that will be the case. But I think it is a little premature to be swept along on some kind of bandwagon, thinking that transplant is inevitable and maybe even desirable. Perhaps, if meaningful control of CLL can be obtained by means of OL and other agents in the pipeline, some of us will have a realistic alternative.

Frankly, transplant results are virtually impossible to predict. Talk about arbitrary and capricious: You can die. You can be cured, or at least disease free for a long, long time. You can also relapse and have to wake up to fight the whole messy, draining battle all over again. You can struggle along for years with debilitating graft vs. host conditions, from skin reactions to gastrointestinal problems to seizures.  Many patients are grateful to be alive despite the side effects; others have regrets. 

One wrote to me off the blog: "Do not underestimate the effects of chronic GVHD. When you read about them, they might not sound too bad; however, the collective experience of multiple GVHD effects can make life after a transplant quite miserable.  And chronic, in this sense, must be seen as a permanent condition."

I will never forget Dr. Terry Hamblin's comment that he knew of two patients who were so beset by post-transplant graft v. host problems that they killed themselves.

There is a yin and yang to this, of course, and I am not discounting the success stories, those who write that they are "recovering nicely" after two years, and those who are a few years in with only minor problems, nothing to get too excited about, and with no regrets about having taken the big step. 

I keep a list of blogs on the right side of this page. Scroll down and click on those of the transplant patients: Brian Koffman, Jackie Sue, Ron Gottula, Dan O’Mara, and Harvey's Journal. Take a look at Tom McCune’s website; Tom was once the CLL cure “poster child,” now in relapse. Check the posts at CLL Forum and ACOR from patients like Chonette and JursyGurl, both of whom are having success with minimal trouble so far (you go, girls!). Read Raywood's Great Stem Cell Transplant Caper, and then read all the nice comments about him on CLL Forum's "In Loving Memory" page; Ray was a character, an irrepressible optimist and guitar picker who put CLL to Country music. But all the sunshine in the world doesn't guarantee success. Neither, for that matter, does a Vulcan-like level of meticulous preparation.

Gather all this –- and more -– into your head and you may conclude, as I have, that the transplant is unpredictable at best, freakishly difficult much of the time, and, obviously, fatal at worst. You may as well go into the hospital singing "Luck Be a Lady."

"They call you lady luck
But there is room for doubt
At times you have a very un-ladylike way
Of running out . . ."

I think the outcome is well out of your hands despite however many statistics you arrange in your favor (the optimistic configuration of published data can indicate an element of wishful thinking that creeps into even the most rational of minds.) When the chips are down, you're putting all your chips on the table. A transplant, to my mind, is something you do when you HAVE to do it and no sooner.

It is not a battle that I am afraid of, but it is not one I am jumping to fight if there is a wiser way to conduct the war. 

I am hoping that OL will be an effective weapon, something of a game-changer, at least for a reasonably long time. I’m 53, healthy other than the CLL -– my blood pressure tests out these days at around 120 over 70 and my primary care doctor wants to frame my lipid profile.  My quality of life is good (when I’m not hemolysing).

Beyond the medical facts, CLL has taught me that I am mortal, and so it has ironically given me the gift of being able to live life fully today, to let go of old regrets and unhealthy patterns, and I am happier than I have ever been.

So why not still play for time? 

There is a fine line in CLL between being too proactive and too reactive. Much of my CLL journey has been spent trying to find and stay close to that line. At times I have been more successful than others. I think -- I hope -- that I have found it with the OL protocol.

It's the line of scrimmage between me and the disease. It’s first-and-ten and I will move the ball down the field as best as I am able, however many yards at a time. I’ll report on it as I go.

Treatment update: My new friend len

I suppose an update is in order. No news is good news when you have CLL, and I’ve had no news for awhile. Now I’m gearing up for treatment again, this time with lenalidomide, better known as Revlimid, also known as "len" for short.

All of last year’s treatments basically bought me stable disease. A CT scan comparison from January to September showed only marginal improvement in abdominal lymph nodes, which is where most of my 11q-deleted disease lives these days. Over time my CLL has become less leukemic, more nodal, and my blood lymphocyte count is practically normal.

I remain at Stage 2, for what it’s worth. When I’m not hemolysing due to autoimmune hemolytic anemia (AIHA), my red blood count, hemoglobin and hematocrit remain well in the normal range for a man. I’ve not seen the slow decline in those counts that follow with progressing disease. Over six years my platelets have gradually dipped, settling now in the 120s. That’s just below what’s considered normal, absolutely high enough for full clotting function, something to note but not to worry over.

My latest FISH test -- I get one every year, and the results have a huge say in how I approach treatment -– still shows the 11q deletion only, on 31 out of 200 chromosomes. This is a monoallele deletion, which means the relevant bit is broken off of the long arm of one of the set of two chromosomes #11. A biallele deletion would mean that both of the chromosomes 11 have lost the ATM gene. So hey, I’ve still got one arm to hang paper with, it seems. (A cautionary note is worth inserting here: As we all should know by now, the FISH test doesn’t probe for all possible chromosomal abnormalities that may eventually prove important in CLL. No news is good news in my case, but it may not be all the news, if you know what I mean.)

So by some measures -– including how I feel on any given day -– I am just sort of trucking along with this thing in neutral. But it ain’t quite so. There are those abdominal nodes remember, none over 5 cm, but a whole, whole lot of them. My B2M is 4.8, a little over the line MD Anderson sets (4.0) to divide between those with better disease and those with worse. For me, the action is taking place in the abdomen.

Plus I’ve got the AIHA, with its hemolysis shoe always waiting to drop, a sign that CLL has gummed up immune function and still continues to do so. I also have squamous cell skin cancer issues. I've had two SCCs removed surgically since 2005, several actinic keratoses frozen off, and I am on far-too-intimate terms with a tube of Efudex. SCCs can be deadly serious in CLLers, whose T cell surveillance function is weakened, because it is T cell surveillance that helps keep those squamous cells in check. CLLer T cells take a hit because of the lowered immunity that accompanies disease progression, and they can further tank due to immunosuppressive therapy, notably fludarabine and Campath.

I haven’t had fludarabine or Campath, which brings us to the menu of choices I now face:

Looking at all the data tells me that my disease is stable-ish but also growing, more or less behaving but capable of getting that much worse if I don’t attend to it. For years I attended to it with single-agent Rituxan, but AIHA changed that game and while Rituxan was clearing the blood the disease found other avenues for growth.

So attending to it for about the past two years has consisted of costlier therapy, RCD, or rituximab, cyclophosphamide and dexamethasone. A recent DEXA scan shows my bones are no worse than they were two years ago, marginally osteopenic here and there. But steroids are not a long-term solution. Cyclophosphamide has done me good so far, nailing hemolysis when it occurs, but it is a potentially mutagenic agent and one to which, if I’m like most other people, I will only develop disease resistance to over time.

So RCD as “maintenance” is not realistic, and “maintenance” to me now means something a lot tougher and potentially more problematic than single-agent Ritxan. I have come to the end of Easy Street and there’s a big sign there that says “Road Closed.”

* * *

So, what to do? Besides lenalidomide, or Revlimid, the FDA has approved ofatumumab, aka Arzerra, aka HuMax-CD20, aka the Monoclonal Antibody Formerly Known as Prince, for use in CLL. This is the bigger, badder, fully humanized anti-CD20 antibody, none of that wussy mouse shit. For someone who has used Rituxan to the max, its presence represents a potential new lease on life, or at least on effectiveness.

And because of that, it is an important drug in my arsenal. I am not treating it the same way I treated Rituxan. Sure, I might get a year or two of stability out of it by using it as a single agent, but then what? I think it is wiser to save Arzerra for combination therapy, the good old FCA, when that becomes front-and-center my only choice.

Which it almost is at this point: FCA, followed by a transplant at relapse, the CLL end game. But enter lenalidomide, an immunomodulator drug that intrigues and mystifies the experts. Some interesting data came out of December’s ASH conference, including a report from MD Anderson, which ran a trial of Revlimid and Rituxan in relapsed patients.

How len seems to help some CLLers is explained succinctly in this online interview with Dr. Asher Chanan-Khan, “Mr. Revlimid” himself, who goes over all the highlights from ASH, including a discussion of len at the end.

When it works -– and it doesn’t work on everyone -– lenalidomide seems to have a way of rebalancing the immune system, weakening the CLL cells themselves and compromising the nurse-like cells that protect them. Len can improve T cell and NK cell function, actually get the immune system to go toe to toe with the CLL. It works on high-risk cytogenetics such as my 11q. And while you have to watch for low neutrophils and low platelets while on the drug -– not to mention tumor flare, rashes, fatigue, nausea, and so on –- it does not appear to have the potentially mutagenic, viral-reactivating, Richtersy transformative potential of immunosuppressive chemo.

And keep in mind, for someone with AIHA, the idea of restoring an equilibrium in the immune system is powerful catnip. I have it on the best authority that two transfusion-dependent, hemolysing AIHA patients were treated with Revlimid; in both cases the hemolysis resolved and one patient is still with us three years later, free of the AIHA curse.

That, plus some added squamous control, plus the prospect of making a dent against that abdominal bulk, makes Dave a potentially very happy man. Which, defined in CLL terms, means someone who is able to control his disease, possibly even weaken it, for a long period of time without really compromising future therapy choices.

So, it’s worth a try. My insurance has rejected it, of course. It costs $60 a day per pill times 365 days and the insurance won’t even give it to patents with multiple myeloma, for which it has FDA approval. But my hem/onc, who now runs her own kick-ass office with a bent on getting patients the care they need come hell or high water, is optimistic that I can qualify for assistance from the maker, Celgene. We’re waiting on that, and on a few other details –- is it better to do with or without Rituxan, for example? –- but I hope to start soon.

* * *

Here's hoping all of you are doing well in your struggles with CLL. Even more, here's hoping you're out there living your lives to the fullest. Nobody gets off this planet alive, whether it is CLL that takes you or something else. Don't die with your regrets intact. Get real and deal and rock and roll. You only go around once, and this is it. Punch cancer in the nose and kiss life on the face.

My six years of CLL, and six things I’ve learned

September 3 is here, the sixth anniversary of my big doo-doo surprise. It was on this date in 2003 that I awoke from a dream in which the room was spinning. It turns out that the room really was spinning, which meant a visit to the ER, which was followed after a couple of hours by my diagnosis of chronic lymphocytic leukemia. I was told it was a “good cancer” and sent home.

The room, as it were, has not stopped spinning since.

I was going to title this post “Six years of this crap,” but I think it’s best to look back with a more even temperament at some of the big screaming bullet points that I have run across. These are things that may be the most help to those of you who are waking up into your own CLL bad dreams.

Since 2003 I have come some distance in my understanding of the disease and what it means to cope with it. Time is a teacher, and I’m sure it has a lot more to throw my way — at least I hope it does, if you catch my drift. At six years in, I’m in my CLL middle age, both in terms of disease progression and knowledge. When it comes to the latter, I'm no longer wet behind the ears, yet wise enough to know that the learning curve goes on forever.

Here are some things I’ve learned, sometimes the hard way. They may represent a change or an evolution in thinking over some older posts in the blog. They are the truth as I see it today:

1. CLL is not the same disease for everyone. The “CLL is an indolent disease/good cancer” monster has to be staked through the heart every time it gets out of its coffin to suck your blood. It is the old, cobwebby way of thinking about CLL. Wipe those cobwebs from your eyes, unless you enjoy being mesmerized while your life drains away.

Some of us have relatively mild CLL, some of us don’t. Some of us respond really, really well to easy, breezy treatments, and others of us barely respond to nuclear chemo. This is because, for all practical purposes, we don’t have the same disease. A dog is a dog is a dog, but not all dogs are alike: Paris Hilton would look a lot more chewed up if she were carrying around a pit bull instead of a chihuahua.

Figuring out what kind of CLL you have does not involve reading tea leaves, poring over entrails, or consulting the shell of the prescient tortoise. It’s a matter of looking at the results of the tests available — IgVH mutational status, ZAP-70, FISH, CD38 — and at your clinical history (how fast your nodes are growing, how quickly your lymphocyte count is doubling, how far your hemoglobin and platelets are dropping). When I was diagnosed, the only readily-available test was CD38, so a lot has happened in six years. If you want to know what you’re dealing with, get your tests done.

2. See a a CLL expert (or two) at the very outset. Ol’ Doc Lippencot, highly regarded as she is around these parts for curin’ breast cancer and lice and possum infestations and such, didn’t know much about CLL. This is often the case with the local doctor, whose stock in trade is usually not going to be a disease that affects almost nobody.

And while patient networks and educational websites are excellent for moral support, learning about case histories, and keeping up with the latest research news, they are of limited medical expertise. This is because they are filled with seekers and guessers such as yourself, not to mention the occasional insufferable blowhard. Some of these people are downright brilliant, some of them are extraordinarily helpful. But in the final analysis they are, like yours truly, amateurs — what the dictionary defines as “lacking the skill of a professional.”

Which brings us to the professionals. Experts live and breathe CLL and have seen hundreds of people just like you, with all the variants of your disease. They have a clue. This does not make them infallible. Having consulted a few, I can say that they don’t always agree. Just as painters see the world differently, so do those who practice the art of medicine. So see a couple of the big names — or even a few, the worse your case is — just to get a consensus, or maybe that much more confused.

Our CLL experts are a great bunch — many of them are approachable by e-mail — but they’re not miracle workers and they’re not gods. Sometimes they run out of things they can do to save your life. Dr. Terry Hamblin told me in an e-mail once that, the way things stand today, doctors can only keep me alive for so long. I forgot how long “so” was — it appears to be at least six years — but the point was well taken, which leads me to:

3. The battle has a beginning and an end, and you need to be ready to fight. For those of us who don’t have indolent “goody-two-shoes” cancer, the day will come when we beat it or are beaten by it. The opening round came when that first mutant CLL clone got out of your own personal Pandora’s Box. The final round will come when it comes, and for many of us younger patients it will probably end with a transplant, win or lose (or there can even be a draw, of sorts).

Obviously, you need to be as prepared as possible. That is why patient education is important, getting the lay of the land is important, staying up with truly useful news is important, staggering your treatments intelligently is important, doing all the strategy and tactics stuff is important.

And that is also why learning to cope emotionally is important, and why this battle hinges at its heart on more than science and medicine. Healing is a big, mysterious thing. Books have been written. Bullshit has been blathered. But there is a lot about the mind-body connection that we don’t understand. Well-respected, level-headed doctors see “medical miracles” during their years of practice. I believe your chances of healing are better if you put your heart and soul into it, and the evidence seems to back me up.

Emotional preparedness can also help you cope with the inevitable surprises and slip-ups, the disruptions and disappointments (and occasional triumphs) that come with fighting cancer. It is a rough journey, a test of your faith and your stamina, something that demands that you get your inward act together.

You can walk out into the ring with all the technical skills, having read hundreds of papers and abstracts, having consulted every expert doctor within a ten thousand mile radius — but if you don’t learn to float like a butterfly and sting like a bee, if you can’t get in your groove, make knowledge and soul work together, you are fighting with one hand tied behind your back.

4. Be a pain in the ass. No, I don’t mean be a cry-baby or a whiner or a ninny (take that blood draw like an adult!). I mean learn to stand up for yourself in medical settings, learn to question things if you are uncomfortable, learn to say “No” and “Are you sure?” Do not be railroaded by doctors, office staff, or well-meaning family or friends. Be as diplomatic as the situation allows, but keep in mind the words of Teddy Roosevelt: “Speak softly and carry a big stick.”

This is where those emotional/intuitive clues come in handy. If someone says, “This is right,” but it doesn’t feel right, honor that thought. Float like a butterfly, and whack! with that stick. And the bigger the thing, the bigger the pain you must be. Do not stand on ceremony or save face; it will be at your own peril. The face you save could be you own.

5. You cannot predict the future with certainty. So far, CLL has humbled the great minds of medicine, so get your humble on. Nobody can predict the future. Nobody can know an outcome for certain. Sure, a lot of cases follow the conventional wisdom; things often, unfortunately, go by the book.

But there are exceptions. Let me tell you a story:

A patient has a sudden relapse, finds herself refractory to every therapy, has to live on transfusions. Like a Greek chorus, there is whispering offstage: “She should go into hospice.”

And now, two years later, like some mighty Greek goddess who has triumphed in an epic battle, she has survived a sudden transplant and is doing pretty well, thank you.

Bad things often happen in CLL, but good things can, too. This is not an article of faith, it is a matter of medical fact. There really IS hope, tempered as it is by this thought:

6. In the end, it often comes down to luck. Dr. Allan Hamilton is a respected neurosurgeon, and the author of a book called The Scalpel and The Soul, and his number one piece of advice after decades of practice is this: “Never underestimate luck — good or bad.”

The more I see of CLL, the more I believe this to be true.

Why do some people live and some die? My ever-practical younger brother puts it this way: “When your number’s up, your number’s up.”

It’s called Fate. This is why the best-prepared sometimes fail, why the least-prepared sometimes live. That’s no reason not to care, no reason not to make the odds as much in your favor as you think you can make them.

But nobody gets off this planet alive. Dr. Hamilton has a blog, and he talks rather poignantly (tearjerker alert) about a couple who drive up a mountain to share a glass of wine in the twilight of life.

So enjoy wine and a sunset, whatever day it is for you. Life is not all about the battles we wage to stay here. It is about how we live it while we are blessed to be here.

That can be easy to forget when you’re in the trenches battling cancer. But with time and wisdom, we can learn to savor what life is about despite the challenge it has thrown at us. And life can become all the more sweet in the face of the dangers ahead.

Nobody said beating CLL was going to be easy, but nobody who knows what they’re talking about says it can’t be done.

So here’s to six more years (come to think of it, I think the number “12" was in Dr. H’s e-mail somewhere).


With this post, I am stepping back from the blog for awhile. I have some fighting trim to get into. There are other things in life I must attend to. Over the years I have said a lot, but sometimes there is wisdom in being quiet and listening. I promise to post every few months, and I will let you know if I encounter any big health emergencies or breakthroughs. In the meantime, no news is good news. Take care, and stay as healthy as you can.

The chemo monster mash: FCR vs. FCA

An interesting therapy comparison has come out in recent days, worth a mention to those who want to update their scorecards.

In this corner, weighing in at a zillion tons, breathing enough fire to melt Mt. Fuji, is our current champion, the Godzilla of CLL clemotherapy -- FCR (Fludarabine, Cyclophosphomide, and Rituximab, Genentech's long-standing anti-CD20 monoclonal antibody).

And in this corner, causing the earth to shake with the whip of its newly-minted tail, is the Mechagodzilla of CLL chemotherapy -- FCA (Fludarabine, Cyclophosphamide, and Arzerra — aka ofatumumbab, Genmab’s competing anti-CD20 monoclonal that is now very close to approval by the FDA).

We all know that the loser is going to be Tokyo. And the winner is . . .

Both, or neither, depending on how you look at it!

Genmab just announced the Phase II results of a trial of 61 chemo-naive patients who were treated with FCA. Those who received the largest dose of ofatumumab (which also used to be known as HuMax-CD20) got a 50% complete response rate as measured by the 1996 National Cancer Institute CLL guidelines. (According to Genmab, the CR rate was 32% in patients who received 500 mg of ofatumumab and 50% in those who received 1000 mg. The overall response rate was 77% in the 500 mg group and a slightly lower -- go figure! -- 73% in the 1000 mg treatment group.) Obviously, the study is ongoing, so we don’t have any idea how long those “complete responses” will last.

Compare Genmab's results to those reported by the respected German CLL8 study group in 2008 in a trial of 817 patients randomized to receive either FCR or FC. The FCR group received a 52% CR rate using the 1996 NCI criteria. Assuming some basic equivalency between the studies, that’s a two percent difference, statistically insignificant.

Progression-free survival in the German study was 76.6% at 2 years in the FCR arm and 62.3% in the FC arm. But the difference for overall survival was not significant (91% v 88% at 2 years).

(MD Anderson has been providing its own ongoing retrospective, non-randomized information that paints a rosier picture of FCR; it is worth noting Dr. Terry Hamblin's comments here.)

Which brings us again to the perennial question: What's the "best" choice for your first therapy, and how does that impact what you do after relapse, when it's time for that second act that we often tend not to think about?

In my case, having pretty much used up Rituxan, it’s going to involve some Arzerra in the hope that it works better as a second-act agent, which it does appear to do. It is now being considered for FDA approval for those who are considered double-refractory to fludarabine and alemtuzumab (Campath), neither of which I have had yet -- but neither of which, the more I use chemotherapy of any kind, is going to work as well as it would have had it been my first choice out of the box.

So welcome to the boxed-in world we CLL patients live in. What do you chose for your first act? How does that impact what you choose for your second? (And, transplant planners, how do those choices impact that third and probably final -- and I mean "final" in the hopeful "cure" sense -- act?)

Which brings us to another bit of recently-reported information, floating around the air like Mothra:

“First-line fludarabine not superior to chlorambucil in older CLL patients”

In a study of patients over age 65, the German CLL Study Group randomized 95 patients between fludarabine and chlorambucil.

Progression-free survival was similar in the fludarabine group (19 months) and the chlorambucil group (18 months); however, clinical significance was not reached. Overall survival was also similar between the two groups (46 months vs. 64 months), but again, clinical significance was not reached.

The bottom line is that fludarabine provided a more robust response (as well as more bone marrow toxicity) but in the end that deeper remission didn’t mean the patients were living any longer, at least as of this writing. Keep in mind the OS non-difference between FCR and FC as reported by the German CLL8 group.

Of course, the trick is to track these things over a much longer time period, to see how overall survival of Regimen A vs. Regimen B goes on year after year after year.

Unless, of course, your CLL isn't giving you a decade or two to watch all the data dribble in.

Then you have to pick your monster and place your bet.

Hello Kitty, anyone?

The Hello Kitty Darth Vader, a sure sign that the end of civilization is near.

The dog days of August

Anyone who has Googled "chronic lymphocytic leukemia" has run across references to the disease in dogs and, more rarely, cats. If you give Fido some chlorambucil, he goes on merrily chasing his tail, usually for a normal life span.

Recently I received a phone call from someone who read my letter to the local paper in which I explained that I have CLL and that I support health care reform. The caller left a message on my answering machine. She said she supports reform also, and then began to talk about her dog, which was recently diagnosed with CLL. If it would not be a bother, she asked, would I mind calling her back and telling her a little bit about the disease and what might be done to treat her dog?

When Marilyn and I heard the message, our reaction was the same: laughter, of the disbelieving kind. I don't mind talking about CLL to fellow patients, or to my neighbors, or to a complete stranger who has some interest in the disease. But I'm not a veterinarian.

My gut level response, to my surprise, was anger. I love animals, and I like dogs, but I have seen too many friends and acquaintances die of this disease. I have seen too many struggle with impossibly difficult choices. For every great remission I have seen great disappointment. I have spent almost six years struggling with CLL, not always successfully. If I thought the last six years were bad, the next six promise to be worse. So pardon me if I don't have a lot of energy left over to counsel people whose dogs have leukemia.

Sometimes I think I'm being a little hard-hearted about this, but I cannot bring myself to call her back. I know she means nothing by it, that she's probably not aware that a CLL patient might develop some emotional baggage after awhile. Is she being a little insensitive? Or am I being oversensitive?

I empathize with her and her dog, but all I want to say to her is "Use your freakin' Google."

Am I right or am I wrong?

The runaway shopping cart CLL fitness test

On Tuesday night we were at Bashas', our favorite local supermarket, which is built on a sloped lot. After we loaded the car with groceries, our shopping cart, to make a long story short, escaped. It was heading downhill, and at first looked like it would come to rest against a metal railing. But the gimpy wheel that had annoyed us during our trek through the store came into play, setting the cart on a subtle curve right toward someone's car, and it was picking up speed as it went.

It would not be right, I thought, to allow it to bang up someone's vehicle, so I took off after it, running as fast as I could. I caught up with it about three feet from the car it was heading for, which I saved from a scratch or a dent. I was not so lucky. As I grabbed hold of it, both it and I fell, me on my left side.

I bruised my shoulder, got some long scratches on my leg, and the bumpy asphalt was particularly unkind to the area just below and to the left of my knee. This was not helped by the fact that I was wearing shorts, leaving bare skin to come in contact with the ground. I came away with a bloody sore about 2" by 2", part of it black.

Nurse Marilyn drove us home, I took a shower, and she administered Neosporin and a bandage to the wound. The next day we saw our primary care doctor, just to make sure everything was OK. This is where the CLL comes in, because if I did not have lowered immunity -- made worse by my neutrophils being at their nadir due to recent chemotherapy -- it's unlikely that we would have felt the need to be so cautious.

The doctor complimented Marilyn on her bandaging ability, and the black spot was determined to be asphalt, which had embedded itself in the skin, and which we were told would gradually work its way out as the wound healed. He was pleased to hear that I was on prophylactic Bactrim, which is one of the precautions I am taking while doing RCD (Rituxan, Cyclophosphamide, and Dexamethasone) therapy for CLL and AIHA (autoimmune hemolytic anemia). Apparently, Bactrim is used to fight staph infections, among other things. I was sent away with a clean bill of health, or as clean as a CLL patient with a bloody sore can get.

One of my first reactions to the incident, besides "ouch," was to put it in the context of CLL. It was as if I had been subjected to an impromptu physical fitness test: Did I have enough hemoglobin to run at full speed and tackle a shopping cart? Were my platelets numerous enough to insure proper clotting of the wound? Was my immunity good enough to avoid infection? Have my bones survived steroid therapy well enough to avoid breaking or fracturing when my 200-pound body hits the ground?

I was pleased to have passed on all counts, and to know that I can still endanger myself by stopping speeding metal objects. After awhile, one learns to take nothing for granted about life with CLL, especially after having lived with periods when the disease, in the form of its AIHA complication, has impacted my ability to do things like I used to.

There is a fitness scale for cancer patients, called the ECOG performance status, named after the Eastern Cooperative Oncology Group. The scale runs from 0 to 5, with 0 being the best, "Fully active, able to carry on all pre-disease performance without restriction." For most of my CLL life, I have been at that level. But the AIHA, with its red-blood-cell-destroying hemolysis, has put me at ECOG 1 or 2 at times. Two, for example, is ""Ambulatory and capable of all selfcare but unable to carry out any work activities. Up and about more than 50% of waking hours."

I suppose I am lucky that I am generally a 0, as the shopping cart chase demonstrated. I hope to avoid ECOG performance status level 5, which is described succinctly in the chart as "Dead." Those at level 5 don't put in much of a performance, evidently.

There's no toxin like Cytoxan

Well, there probably is, but new lyrics are running through old songs in my post-chemo haze. “There’s no business like show business” is the tune, and I suppose that having had a round of RCD last week was getting down to business, so that’s why it turned into a rather annoying song looping through my head.

RCD is Rituxan + Cyclophosphamide (aka Cytoxan) + Dexamethasone, which is a protocol used by Dr. Kanti Rai and his group to combat autoimmune disorders, such as AIHA and ITP, in CLL patients. I, of course, am graced with the AIHA (autoimmune hemolytic anemia), a side effect of CLL gumming up the immune system, which periodically leads to bouts of hemolysis, in which macrophages destroy my red blood cells.

I had a variant of RCD for three rounds at the end of 2007 -- click on "AIHA" under "Posts by Topic" on the right for the whole saga -- which held me pretty well. But it did not involve the same steroid program as used in the protocol, which is 12 mg of dex given over seven days. I entered treatment then in a severe hemolytic crisis, made worse by the failure of my hapless Dr. O’Leary to see the depth of the problem, which necessitated a change of doctors in the middle of the red blood stream. Fortunately for me, my beloved Dr. Belle had just resumed her practice. For a couple of weeks there, I was on my own, doctorless, taking 72 mg of methylpredisolone daily in a desperate attempt to slow the loss of hemoglobin, which fell to 6.6 at its worst.

As we began the treatments — first with a little vincristine, which we quickly dropped due to side effects — we stepped down the methylprednisolone. The Cytoxan was doing the work.

Well, chronic disease is chronic disease. And like an annoying, insistent, door-to-door missionary, CLL is always capable of ringing the bell. It did that again shortly before Christmas 2008, which I wrote about here. I was put on 4 mg of dex, upped to 8 mg when that stopped working so well, to control the AIHA over the holidays, then given Rituxan and Cytoxan in January to nail it.

Readers know that Dr. Belle and I have been experimenting with treatments since then, starting with the rather useless R-FFP. I noticed that my red counts were beginning to head south again at some point not too long after R-FFP concluded, so seeking to nip hemolysis in the bud, we did a week of pulsed dexamethasone (four days of 40 mg/day — quite a dose, but similar to what is given to ITP patients) and one round of standard-dose 375mg/m2 Rituxan. It did wonders, for a month, but while the numbers held, the nodes began to creep back. Then we decided to try more pulsed steroids -- this time, a gram of methylprednisolone by IV on one day, plus that standard-dose Rituxan.

The theory, which has been demonstrated in studies, is that there is a synergy between the methylprednisolone and Rituxan that seems to be more powerful than that between Rituxan and dex. But, then again, there's the real world of the particular patient. I have had a lot of methylprednisolone since my AIHA diagnosis in March 2007, with the resulting time to grow refractory to it. We tried the pulsed dose recently to see how I would respond, this being a sort of trial run at the idea of maybe doing R-HDMP.

Well — surprise, surprise — just a couple of weeks afterward the red counts began to show a subtle drop again, I was alerted to this by more-orange-than-average urine (hemolysis warning sign No. 1) that I have described in the past. The conclusion: methylprednisolone is not going to do much for me, and neither is Rituxan along with it.

The RCD protocol no doubt involves the “D” for a reason, and this time we followed it close to religiously, other than my starting the seven days of dex a little ahead of schedule to keep the hemolysis in check over the weekend. I am pleased to report that Friday’s CBC shows a remarkable recovery of the red counts — heck, my hemoglobin went from 12 to 14 in a week, and the overall RBC jumped from 3.91 to 4.43.

Some conclusions

Part of the purpose of this post, which I am dashing off during what is laughingly referred to as a “day off” around here, is to put forward some insights on steroids, AIHA, and treatment based on my experiences. They come with that anecdotal warning, as well as that internet adage, YMMV:

AIHA patients often face a progressive order of attempting to control the condition. First steroids are usually given, but those can cease to work. Rituxan may be next (or may be given with the steroids), and that can cease to work. At that point, you’re looking at heavier-duty chemo. R-CVP is similar to RCD but involves vincristine, which can lead to neurological problems and which by my experience should be avoided unless truly necessary. RCD is gentler and (for me, so far) quite adequate to the task.

It does involve Cytoxan, which is a venerable old toxic drug used in many cancers, and which may be somewhat better than average at getting at 11q-deleted CLL, which I have. Cytoxan (good PDF here, and yes, the more powerful the drug the more fire you play with; this beggar can't be as choosy as he used to be) gives me few side effects, at least that I can see or feel anyway. Lord knows if it's setting up some mutagenic condition that could lead to another cancer, or to further disease resistance on the part of my CLL clones, but remember that line about beggars.

I don't lose my hair, but I don’t have much left to lose anyway. The drug tends to destroy rapidly-reproducing cells, taxing the stomach lining, but it has not given me nausea, only the desire to eat bland food for a few days. I do get GERD, which I find to be easily controlled with Prilosec OTC.

Speaking of food, with all those steroids as well as the Cytoxan, be aware of your glucose. I avoid sugary, carby things as much as possible during the treatment window and I have no hint of diabetes. Still, my glucose, when tested, goes higher than the norm.

I also get more easily fatigued by the changes the drugs wreak in my body, especially when Cytoxan is part of the equation. I have lost at least 15 pounds in a week, much of which appears to be lymph node weight. (People say I look wonderful after chemo.) The neck nodes, which were brought down nicely by the pulsed steroids without the Cytoxan, were brought down much more dramatically with the Cytoxan. I have a lot of abdominal nodes, and for the last couple of nights have been able to sleep comfortably on my stomach — a sign that progress has been made in these unseen areas, too.

Because of tumor lysis — CLL cell kill, with all the dead cells making their way through your kidneys — it is important to stay well hydrated. I drink at least a gallon of water the day before, of, and after my treatment. (And I use allopurinol -– a commonly-given drug that helps control uric acid -– a few days before, and continue it as long as the cell kill remains.) Then I keep on drinking as much water as I can stand. Even with all that, Friday’s blood test showed my BUN was high, not untypical considering all the cell-kill my body had been through.

The water also helps protect your bladder from the Cytoxan, and you should go with the flow, pee whenever you need to just to keep the stuff moving through. Watch the serum sodium results on your metabolic panel, as well — this can dip, so you may want to consider drinking salty water or eating salty foods for a week or so after treatment.

Keep in mind also that steroids are immunosuppressive and that Cytoxan is immunosuppressive, so staying on prophylactic meds -- acyclovir, diflucan, Bactrim -- during this period are part of the tools of the trade of the appropriately cautious doctor and patient.

RCD (dex pills in photo below) works for me where Rituxan alone, and Rituxan with pulsed methylprednisolone (HDMP), do not.

I have been around the steroid block enough now to have some feel for how I react to them. Steroids are excellent though transient reducers of lymph nodes. But they come with enough bad side effects — osteoporsis for one — especially when given in smaller, long-term doses, that they should be used sparingly. (Big, pulsed doses appear to be safer, based on information from UC San Diego and elsewhere, but that's still powerful stuff going into your veins.)

I find that node reduction in steroid-Rituxan combinations still rests largely with the ability of the steroids. (The Rituxan helps more with the cell kill, providing a somewhat deeper, though still shallow, remission.) Once you add Cytoxan, the game changes, at least in me. The nodes reduce as much again as before, and the remission lasts far longer.

Another thing I have noticed along the way is that the mental effects of the 'roids (such as sleeplessness) seem more pronounced when I am on smaller doses than when I have undergone the big pulses. Methylprednisolone at 72 mg and less tended to make me worry things a little, but not at 1 gram. Forty milligrams of dex over four days had the mental effect of drinking water, but give me 12 mg and my brain shoots into overdrive, getting very detailed about things, and I have trouble sleeping. (It should go without saying that dose equivalencies among steroids vary greatly -- this converter can come in handy.)

I expect to be undergoing more rounds of RCD, then perhaps to have a CT scan to see where the nodes stand abdominally, where they are worse than neckly and underarmly, to coin some medical phrases.

Right now I look like a slimmed down picture-of-health, ready to absorb all those laudatory comments from friends and acquaintances who wonder what kind of a marvelous crash diet I've been on.

Living the not-so-good life in Sedona

Our little city of Sedona, nestled amid the red rocks of Northern Arizona, is a resort community and tourist destination. A lot of people retire here to live the good life, or choose to live and work here for the same reason.

It's reasonably affordable, as such places go -- unless you come down with a catastrophic illness and are subject to the whims and foibles of our health care system. I am not talking about myself here. I am talking about a couple in town who lost pretty much everything in a futile attempt to battle the wife's colon cancer. This was reported recently in our local newspaper, the Sedona Red Rock News. Here's a link to the story, entitled "Health system fails Sedona couple." Here are some excerpts:

It wasn’t long before all of the DiMarcos’ days were consumed with medical appointments, arguing with insurance companies and pleading for help from state agencies.

By 2007, their lifelong savings had dwindled to nothing, exhausted by treatments and drugs deemed ineligible for coverage by their insurance company. With no money left, Joseph turned to credit cards to pay for hotel rooms near hospitals, for co-pays and for pain medication.

. . . In spite of hundreds of thousands of dollars of tests and treatment, painful procedures and mind-numbing drugs, by 2008 Andrea’s doctors held little hope for her recovery and she was referred to RTA Hospice and Palliative Care in Sedona. She passed away two months later.

Joseph is left with the memories of a woman he describes as his soulmate, a twin flame with whom he wanted to grow old. He is also left with a mountain of bills, having to choose which one to pay each month.

In the latest print edition is another story (not online), this time about a patient with heart problems who faced the unfairness of the system first-hand. This involves the "churning" of insurance applications, in which private insurers look for an old condition or treatment you may have forgotten to mention and use it as an excuse to cancel your plan rather than pay for the care you desperately need.

My point here is that in any community -- even one of 15,000 people -- there is story after story like this. Health care reform is needed not only for the 50 million uninsured, but also for the many millions more who are insured, only to find that the system fails them when they need it most.

Here's a letter I just wrote to the editor of the News:

I’d like to commend the Red Rock News for its recent series of articles on how failures in our health care system have caused heartache and pain for local residents who are the victims of cancer and other serious diseases.

I am one of those stories. In 2003, I was diagnosed with chronic lymphocytic leukemia. Mine is a fairly aggressive form of the disease and I have required several rounds of chemotherapy. Fortunately, this has been covered by my health insurance, a state-sponsored program for small businesses. But the plan has its limits. It specifically excludes adult stem cell (bone marrow) transplants. I am 52 years old and the expert doctors I have traveled to see out of state (at my own expense, since my plan only covers a limited in-state network), have told me that I am unlikely to see 60 unless I get a transplant. These can run upwards of a million dollars out of pocket, well beyond my capacity to pay.

As you might imagine, private plans that cover transplants want nothing to do with me. Unless there is health care reform in Washington that requires all insurers to take patients with preexisting conditions, I face a bleak future.

I am all for keeping private insurers, but I also strongly favor a public option. Some mechanism has to be put in place to keep private providers honest, as your most recent article about the “churning” of health care applications demonstrates. If people cannot rely on their private insurance in a pinch, then they deserve an option where care is truly guaranteed.

To those who were recently seen protesting here against “Obamacare” and who argue that they don’t want the government managing their health care, I have this to say: What is so offensive about creating a system that preserves your sacred private insurance but also gives people like me a chance to receive life-saving care? Is it really preferable to have penny-pinching private insurance bureaucrats finding excuses not to give you the procedures and drugs you need? I’d take a government bureaucrat any day -- I’ve been dealing with them at the state level for years -- since they don’t have that vested interest in finding ways to deny me, or my doctor. Finally, if you really hate “socialized medicine,” then give up your Medicare coverage on principle. I’d gladly take it.

Sincerely,
David Arenson

THE COMPANY WE KEEP

Counties in blue have some sort of universal health care system. Countries in green are trying to institute one. Countries in orange -- Iraq and Afghanistan -- have universal systems instituted by the United States after they were invaded. Perhaps we have to declare war on ourselves to get universal care?