Saturday, June 30, 2007

Stick a fork in me

Fifteen years ago I wrote a science fiction novel that was never published. The idea was good -- what life would be like after global warming had begun to cause the collapse of society -- but the execution was poor. It was one of those projects that I figured I’d take another look at one day, when my dialog and plotting skills had improved. Alas, CLL came to pass and Phaeton’s Run shall forever remain on the back burner.

Speaking of burners, which exude heat, it will be 108 degrees here in Sedona on July 4. This is pretty near a record for us, being 4500 feet above sea level in the high desert of northern Arizona. Those
are Phoenix temperatures, and I cannot bring myself to imagine how hot America’s fifth largest city will be on that day. The National Weather Service predicts it will be 116, but it will probably feel hotter. There is a lot of concrete and asphalt there, which traps the heat, so what doesn’t kill you from above can kill you from below, or at least melt cheap pairs of sandals into the pavement.

In my novel, the hero and his girlfriend h
ead south from Lake Tahoe into Arizona to rescue her family, which had stayed behind in the remnants of Phoenix. In my not-too-distant future, summer temperatures are regularly in the 130s, electricity is spotty, municipal services like water have begun to fail, and most sane people have headed well to the north.

Not ever
yone can hack it even today, of course. Last year, as were driving on I-40 toward New Mexico, we were passed by an SUV with Arizona plates and the windows painted with festive messages: “Going home to Minnesota!” “Go Vikings!” “Goodbye sun! Hello snow!”

In fact, out of every ten people that move here, four eventually leave. It's the summer that gets to them, and
how close my novel is to being science fact, and not fiction, is rather scary.

In 1940, before air conditioning became widely available, the entire popul
ation of the state was half a million. Most of these hardy folks survived thanks to evaporative cooling, which ceases to work effectively well before the 100-degree mark. The arrival of air conditioning contributed to Arizona’s population boom, and today there are 6 million souls here, most of whom live in places where it gets too hot to go outside for more than 15 minutes between 10 a.m. and 6 p.m. from June through September. (And more and more homes are being built in places where there is no guaranteed water supply, but that’s another story.)

“It’s a dry heat,” we tell ourselves, even as the temperatures give one a b
urning-at-the-stake feel. Local TV news shows do the obligatory story about someone frying an egg on the sidewalk. Then there is the occasional report of tourists from places like Norway succumbing to conditions such as “muscle melt,” or of foolish people who go hiking without water and are found three weeks later, having provided a tasty repast for coyotes.

When I was growing up here, in the 1960s, many Arizonans kept a gallon container or two of water in the trunk of their cars. This was before cell phones and emergency road service, when either you or your radiator might need a little shot of water to survive. Today, people wander around the cities with plastic bottles of spring water, and those who venture onto the sidewalks are sometimes protected by misting devices that line the storefronts. These spray teensy droplets of water on passersby, as if basting them for some purpose. Those are modern conveniences we didn’t have when I was six years old, sitting in our evaporatively-cooled apartment near the Colorado River, riding out 122-degree temperatures by keeping still, turning the lights off, drinking Coca-Cola, sticking ice on our heads, and fanning ourselves. How the cat managed without keeling over under all that fur, I don’t know. (For the record, cats can hold up to six ice cubes when laying on their sides.)

Today, we have central air conditioning courtesy of a monstrous Lennox unit that sits outside the house, but it is merely an improvement, not a panacea. We live in
a condo that was foolishly built out of wood, and which sits on a hill with a lovely view and a bullseye on the roof that says “bake me.” We can run the AC 24/7 on hot days and we’re lucky if it gets below 90 degrees upstairs during the middle of the day. Downstairs, protected by that vast insulation known as the upper story, and with walls made of concrete block -- basically a raised 8-foot foundation that we renovated into living space -- the temperature is 10 to 15 degrees cooler. This is where we moved our bedroom to.

My daily attire is shorts, and nothing else. I keep a fan on myself when working upstairs on the laptop, and I also keep the fan on the laptop, which is already elevated on a metal grid (aka cooling sheet for cookies) to keep it from overheating. Sometimes I enjoy chocolates from the pantry, stuck together in a big glob.

Ah, but the view is worth it, especially during wildfire season when you can see the orange glow that threatens to march into town and dispossess us. Open the wind
ow at night for a cool breeze -- when we’re not threatening to break temperature records it gets down to 70 degrees in the middle of the night -- and you can smell the smoke from huge fires a hundred miles away.

“Another day in paradise” is a common local expression. We’ll just keep telling ourselves that.

Monday, June 18, 2007

Low- dose Rituxan – first round results

I have now completed my 12-week protocol of low-dose Rituxan, accompanied by methylprednisolone -- 72 mg a day over nine days. The purpose was to treat both my chronic lymphocytic leukemia and a nasty bout of autoimmune hemolytic anemia (AIHA) that reached its nadir on March 14.

The early returns are in, and the protocol did a pretty good job: It reduced my bulky lymph nodes by about 50% and lowered my absolute lymphocyte count (ALC) to within a few
thousand points of normal. It did this while putting the kabosh (my medical term) on the anemia and restoring my red counts to at or near normal.

The jury is still out on how long these effects will last -- and that is a crucial question -- but so far, so goo
d. Tomorrow I will finally be getting an infusion of IVIg, which should further help with the AIHA and which should also give me some much-needed immunity against infection, which was driving my white count up when treatment started March 12, and which also may have triggered the AIHA.

It is at this poi
nt that I should remind everyone that my results are what the researchers call anecdotal; that this was not a randomized, controlled study; and that your mileage may vary and probably will.


The idea behind this protocol was inspired by the R + HDMP (Rituxan + high dose methylprednisolone) trials at UC San Diego. As readers know, I have used single-agent Rituxan several times over three years with diminishing results. So I looked into what could be done to boost my respo
nse without dipping my toes into traditional chemotherapy; as tempting as some of those chemo protocols are, the problem is that one can and will develop disease resistance to them. They cannot be reused indefinitely and they come with their own set of potentially dangerous toxicities. Ergo, it is best not to use them until you really, truly have to.

R + HDMP was one of the few ideas out there that did not involve either
alkalyting agents (chlorambucil, cyclophosphamide) or purine anologues (fludarabine, pentostatin). UCSD has conducted two trials of R + HDMP in chemo-naive patients, one in 2004 and one just completed. I have corresponded with patients who have been in the trials and last year I made a trip to San Diego to see Dr. Januario Castro, one of the principal investigators in the trials.

Overall -- and this is my impression based on everything I have been able to learn -- it appears that participants are getting decent results, including normalized white counts, elimination of most or all lymph nodes, and dramatic reduction of CLL in the bone marrow. It also appears, from the perspective of time and distance, that these remissions are perhaps not as deep as those that can be obtained by such protocols as FR and FCR; rarely do they seem to be minimum residual disease negative, and patients are almost always offered Campath as a follow-up. Campath, a highly immunosuppressive monoclonal antibody, deepens and extends the remission.

When I saw Dr. Castro last May, he predicted I would get about 18 months o
ut of R+HDMP. But there were certain factors that mitigated against my doing it. First, because I had had Rituxan in the past, I did not qualify for the trial at UCSD, nor would my insurance have covered regular treatment there; I believe the protocol is sufficiently tricky (read: potentially dangerous) that it should be done in a controlled setting where the doctors are experienced with it. Dr. Castro essentially agreed with me on that point and is not a fan of doing it off-study, aka “off-label.”

My then-new doctor, Dr. Belle, was also not interested in doing it off-label. She
thought the amount of steroid used (1 gram/m2 of methylprednisolone x 3 cycles) was way over the top.

Indeed, I had to ask myself: Even if I could do R+HDMP in San Diego, would it be worth it for a relatively short 18-month remission? Would I want to follow up with Campath
, which is an important drug – the only thing besides steroids that works on 17p-deleted CLL – that cannot be reused indefinitely?

In the end, all these factors conspired to cause me to abandon the thought of doing R+HDMP. So I began to think in the opposite way: could less be more, or could it at least be adequate? If I am probably not going to get a sterling, extremely durable CR regardless, what can I do to just control the
CLL a little better?

Last year, around the time that I saw Dr. Castro, Dr. Ron Taylor of the University
of Virginia was speaking at conferences about his studies of low-dose Rituxan in CLL. I went into this subject in some detail here.

If Rituxan has synergy with methylprednisolone, which it apparently does, based on both the San Diego studies and studies in the UK, then what can they do together at lower doses?

Dr. Belle w
as sympathetic to my quest to control CLL by low-toxicity means, and thus a little, informal protocol was born: LDR + LDMP (Low-dose Rituxan + low dose -- at least comparatively -- methylprednisolone).

I would be getting 20 mg/m2 of LDR three days a week for 12 weeks, and we would add the steroid in midway, after the blood counts had been reduced. This plan w
as turned on its head by the arrival of the AIHA, which coincided almost perfectly with the start of the LDR. As Dr. Belle said on March 14, while I sat in the infusion chair for my second dose of LDR, looking rather peaked with a hemoglobin of 8.9, “It looks like you have AIHA. How would you like to start the steroid early?”

And so we di
d. Starting March 14, and for nine days following, I took 72 mg of methylprednisolone each day (this being based on the standard amount of prednisone used to treat AIHA, recalculated to reflect my body mass and the differences in the pharmacokinetics of the steroids). After the ninth day, we stepped the steroid down over the following month.

My LDR + LDMP experience

The LDR, all 42 mg of it, was infused each time without premeds. Only once, when the bag was run through a bit too quickly, did I get an infusion reaction. Keep in mind that I am an experienced Rituxan user and that I know my limits, as it were. My advice t
o anyone using Rituxan for the first time, in whatever dose, is to make sure you are adequately premedicated with IV Benadryl, Tagamet, and a steroid such as Solu-Cortef -- all these things are designed to tamp down any infusion reaction before it begins. I did take allopurinol to guard against tumor lysis.

Some pati
ents have had LDR at home via a self-administered subcutaneous shot. My insurance plan and the doctor’s office both had policies precluding this, which would have been convenient as we live two hours from the infusion center. This three-day-a-week schlep became so burdensome that we experimented, halfway through, with cutting back the infusions to two days a week (Monday and Friday). As it turned out, this made no difference in the rate at which the counts reduced, so we stuck with two days a week. Each infusion took about 20 minutes, and then we were off searching out yet another Vietnamese restaurant or buying unnecessarily large packages of things at Costco.

I took the methyl
prednisolone in 4mg tablets, meaning I was popping 18 of them a day at the height of it all. Overall, the steroid experience was a long, strange trip.

On the plus side, the steroid initially reduced my disease bulk by about 90%. I lost six pounds in the first two days,
a lot of it probably lymph node and spleen weight. My neck was at its pre-CLL appearance within 72 hours.

But I continued losing weight; at first I thought it was muscle loss but the steroid appeared to be burning up fat cells instead. I lost 20 pounds over nine days and wrote here about my desperate efforts t
o eat enough to avoid losing too much weight (talk about living in a bizarro world . . .). As much as I hoped that I would be able to keep most of the weight off when I was done with the steroid, I hadn’t counted on the AIHA making aerobic exercise impossible. Not only did I not feel up to it much of the time, my heart was working overtime (I had less oxygen in my blood and it was under enough strain already. AIHA is not for the faint of heart, so to speak.) Gradually, then, I have regained just about all of the weight.

Steroids are also
known for some other physical and psychological effects. My sleep was disturbed to some extent, and I found myself getting up earlier than usual and then having to take naps. Sometimes I had a little more energy than I should have had, but the AIHA tended to counter that. At certain times I had a sense of well-being that I am not generally used to; indeed, I found myself being a little more extroverted than normal. Sometimes, however, I would get worried, and I would obsess over a perceived problem or symptom. I wouldn’t call it paranoia, just a greater state of concern than usual.

One legitimate concern for me when it came to steroids was my history of squamous cell skin cancers. The immunosuppressive nature of steroids can lead to such cancers, as well as to infections running amok. Midway through the steroids I had my dermatologist gave me a complete exam, which I passed. As to infections, I was on several prophylactic meds to guard against them: Bactrim, acyclovir, diflucan, and later augmentin. Dr. Belle also ordered herpes, CMV and EBV titers to see if any of these posed a hidden danger. The last two were negative but the former was “high,” which led to the acyclovir: the last thing I needed in the midst of all this was to come down with shingles.

Steroids can cause a
dramatic reduction of nodes in CLL, but the effects are rather transitory. I have been fortunate in that my nodes did not return completely within a month or two. Overall, I am guessing that they are at about 50% of what they were when I started. The painful pelvic nodes have quieted down considerably. My neck is still reasonably svelte. My disease bulk has probably been set back by about a year.

None of my previous Rituxan treatments were very effective on nodes 2.5 - 3 cm or larger. I tried adding Neupogen
, EGCG, and Beta Glucan as boosters at various times but the steroid was the first thing that made a difference. I always intuitively felt that it would.

I do not know the extent to which the LDR may have prevented a complete return of the nodes once the steroid was tapered down. I did notice that, after an infusion, the nodes in my neck would recede a bit,
feel a bit smaller. But this effect was transient and after a couple of days they would return to their baseline. Now that I am done with the LDR, it will be interesting (in a watching-a-traffic-accident kind of way) to see how fast they grow.

One of the mysteries in my results has to do with the reduction of the ALC. When I started on March 12, it was 162k and rapidly rising, probably due to an infection that may also have triggered the AIHA. After the steroids pushed things out of the nodes and marrow, the count went to a high of 361k on March 20. Then it dropped to 263k on March 26 and 92k on April 2.

Why such a dramatic drop? The LDR could not have been responsible for the entire reduction, especially as I wasn’
t even using it one of those weeks (long story, another post). The steroid would not have been responsible for that much of the cell kill. My theory is that the antibiotics and antiviral drugs I was on finally put an end to that infection I mentioned, and that the CLL therefore naturally ramped down. It is also entirely possible that some of the CLL could have sneaked back into the spleen, liver and less noticeable nodes as the steroid was stepped down during that time.

I do know that once my counts were below 100k, the LDR reduced them, consistently, by 10-15k per week until a plateau was reached. The only bump upward came when, after I was off the prophylactic Ba
ctrim, it appeared I had caught a new bug, or the old one had returned (monocytes and granulocytes also increased). I began the augmentin then and the counts resumed their downward course. They hit 8.6 on May 21 and then began to dither around, rising a bit, then falling again to a low of 7.3 on June 5. On June 11 they were at 8.4 and they were at 12.1 by June 15. Essentially, then, I hit my plateau about eight or nine weeks in. A whole 12 weeks of LDR is probably not necessary in my case.

That bottom number, 7.3, was lower than the low reached during my previous Rituxan therapy, last October, when the ALC dropped to 22.6. I was then using Dr. John Byrd’s thrice-a-week protocol of standard-dose Rituxan.

By comparison, here are my other lowest ALCs following Rituxan therapy, dating back to January 2004: First tre
atment 2.3, second 4.9, third 5.1. Considering how much Rituxan I’ve had since I started – almost 20,000 mg total – I think the 7.3 is a pretty good result. Keep in mind that it was reached by using the amount of Rituxan that would normally be given in less than two standard doses.

Worth a mention here is the effect that all this had on my platelets. They were at 197 when treatment began on Marc
h 12. They reached a high of 325 on March 19, likely because the steroids had emptied out the spleen. There was a slow decline to 151 on May 11. Then they dropped like a rock to below normal (baseline of 130) for the first time ever -- to 99 on May 18 and then to 85 on May 21. Dr. Lord made the assumption that I had developed ITP and now had Evans Syndrome, which is the double booby prize of having both AIHA and ITP. But it turns out he was wrong. The platelets began to climb back into the normal range, and were 135 by June 15. An anti-platelet antibody test turned out negative.

So, what knocked the platelets down? Going on nothing other than a hunch, I suspect the Rituxan. Last October, w
hen I did standard-dose Rituxan three days a week, my platelets took a big hit during the first 48 hours, then they slowly recovered. I am guessing that some tipping point in their relation to Rituxan was reached this time.

It should also be noted that my immunoglobulins declined during the treatment, my IGG dropping from 746 on March 20 to 382 on June 15. It is suspected that Rituxan can erode IGG, but none of my previous Rituxans appeared to cause a decline, even though a lo
t more of the antibody was in my system then. Was it the Rituxan? Was it fate? What I do know is that at the higher number my IGG was pretty much ineffective at keeping away infections, so IVIg was in the cards for me regardless.

Last but by no means least, there’s the AIHA. (I say “by no means least” because once you’ve had it, you never want to have it again.) The rather dramatic hemolysis stopped immediately after I started taking the steroid. But I have been surprised at how long it has taken for my red counts to return to a semblance of normalcy. Apparently this is not uncommon and I am rather lucky: there are people who are on steroids for months and months to get a handle on AIHA. (Given my weight loss problem, I am not sure how I could have managed that.) Here are my red counts at their worst,
on March 14: RBC 2.65, HGB 8.9, HCT 26.9.
On June 11, RBC was 4.07, HGB 12.8, HCT 38.5
(Normal: RBC 4.7 - 6.10; HGB 13.0 - 17.0; HCT 36.0 - 52.0)

The bigger picture

In a discussion of AIHA on the ACOR list, Dr. Terry Hamblin once wrote, “Some cases of CLL present with AIHA, and indeed once the AIHA has been treated with steroids,
the CLL is barely detectable.”

Given my bulky disease, it would have been too much for me to hope that the CLL would resolve along with the AIHA. But in some patients, those with fewer nodes and more indolent CLL, LDR+LDMP may enhance the chance of just such a remission.

Chlorambucil (CB) plus prednisone was once a fairly standard treatment for CLL. CB killed the CLL while the steroid reduced the nodes. Studies showed no improved survival by adding the prednisone, but it did help relieve discomfort.

Nowadays, with Rituxan available, some of that same cell kill can be accomplished without adding an alkylating agent. The methylprednisolone, which has established cell kill properties at higher doses, may retain some of them at lower ones, though this is not definitely established by any means, and it may also still exhibit some synergy with Rituxan.

In some patients, this combination may provide CLL control at minimal cost in terms of toxicity (while having the added bonus of combatting AIHA, which is a prope
rty of Rituxan as well as the steroid). Besides reducing nodes, it also clears out the marrow better than Rituxan alone.

Ideally, such a soft-glove approach should have been administered to me a year or two ago when my lymphadenopathy was less extensive. I did in fact suggest to my second hem/onc, Dr. Chopin, that prednisone be added to my standard-dose Rituxan in October 2005. She refused to do it, saying simply, “It’s not done.”

Well, folks, there’s a first time for everything. As far as I’m concerned, low-dose Rituxan is a no-brainer for most patients using the drug as a single agent. (I say this not only based upon my personal experience, but also upon Ron Taylor’s pilot studies and anecdotal reports from other patients.) Adding pulsed doses of methylprednisone that are consonant with the steroid dosages normally used in CLL is also logical.

Now, in my case, it remains to be seen how well this will ultimately work. Dr. Belle and I realized that the first 12 weeks would be just the beginning. On the very day she was dismissed from practice, we talked about doing another cycle or two --
pulsed steroid and four weeks of LDR starting one month after completion of the first cycle, and so on. The idea is to reduce the overall bulk with each cycle until it is down to a more acceptable and manageable level.

Would it have worked? Will I ever know? Since Dr. Belle is gone, I am now seeing Dr. O’Leary, who is open to the approach, but who is thinking of using it as maintenance at three month intervals. I’ll be seeing him in one month to see where my counts and nodes are and to discuss whether it can wait that long.

Dr. O’Leary, by the way, told me that he has had good luck with Rituxan and cyclophosphamide, which is the kissing cousin of good old chlorambucil. Most of us know by now that Dr. Hamblin has advocated R + CB as a useful treatment. It is interesting to note that I have stumbled across another doctor who is impressed by the results he gets with something very similar.

Certainly the question of “What next?” has been on my mind if and when LDR + LDMP ceases to hold the fort. Should I dip my toes in the chemo waters and add something that starts with a “C,” perhaps? In a future post I’ll discuss my thinking on where to go from here.

A LDR clinical trial note

There is a study of LDR underway at the NIH in Bethesda, MD. I understand they still have openings. If you’re interested in LDR, consider giving them a call. This link explains the trial and has contact information.

Sunday, June 10, 2007

Thus saith the Lord

Those who follow this blog know that I am an agnostic, but I have now found God: He is about 6' 2" tall and practices his craft in Phoenix, Arizona. There may be another God in Heaven, but the one I encountered definitely thinks he rules on Earth.

I am talking, of course, about a doctor, with whom I consulted recently, and who had been voted one of the "top doctors" in an annual poll of doctors in Phoenix. Having doctors name each other "top doctor" is probably a bad thing, as it might, like too many people in a crowd chanting "Long live our great leader Kim Jong Il!," go to the head.

I should pause here and say that, despite my blogging about the fallibility of doctors, I have found most of them to be not unpleasant and not unreasonable. Indeed, when I was a waiter in the Catskills as a teenager, doctors were known to be only the third craziest class of customers, after lawyers and, the very worst, magicians.

This doctor, who I’ll call Dr. Lord, is the seventh I have seen about my CLL. I went to him on the recommendation of my former physician, Dr. Belle, the one who was dismissed from practice at the place I’ve been going for more than three years. She referred all her patients to Dr. Lord for some reason, and I entered the office with the expectation of switching to his care. Later, after our experience, Marilyn theorized that perhaps Dr. Belle’s recommendation was part of a Machiavellian plot: Her patients, having experienced the overbearing Lord, will come running back to her in droves when she opens her own practice.

Now I can hear a few of you, probably the doctors who read this blog, thinking that I must be exaggerating, that I must be suffering from hemolysis of the brain or something. Maybe I have unreasonable expectations, or I was having a bad day.

Well, maybe he was having a bad day, because I have never had such a lousy experience in a doctor’s office, and that includes my visit with a 50-something GP who wore matching yellow hip-hop clothes and used a matching yellow pen. LL Cool Doc sprinkled his analysis of everything with jokes so bad that you couldn't tell if he was being serious or not, and he was obsessed with those obnoxious plug-in air fresheners, which left me wheezing and gasping in every room of his office.

Dr. Lord, on the other hand, looked the part. Yet he managed to sum up for me in one towering package almost everything that is wrong in doctoring.

* * *

The visit began with a conversation in his office, in which Marilyn and I waited for about 20 minutes before the door opened and a bald vision in a white monogrammed coat stepped forward. Unsmiling, all business, he shook our hands, picked my file up off his chair, where it had been arranged just-so by the nurse, and sat down. Now I don’t really mind the unsmiling part, and businesslike people can be very helpful, so at this point I was still optimistic that I might learn something of value and have some of my pressing concerns answered.

One such concern was my fear, borne out by recent CBCs, that my AIHA could be backsliding. Another was a very recent rock-like drop in my platelets, which had always been in the normal range until tested a few days before my visit. It might have been nice to discuss these issues, as well as my low immunoglobulins and my still unrequited quest for IVIg, but Dr. Lord would have none of that.

Now, to be fair, he needed to start where he needed to start, He was pretty ignorant of my case, and it was apparent that the copies of the medical records sent by the office where I had been going were random and inadequate, as if chosen from my phone-book sized file by a chimpanzee given 60 seconds to complete the task. (I believe in privacy rights and I don’t necessarily trust computer databases to keep things secure, but the idea of having medical records available online is not such a bad one.)

Dr. Lord began by asking about my date of diagnosis and treatment history. It became clear almost immediately that, in his view, I should have had chemotherapy back in 2003, at the very beginning. This is because my WBC was 144,000 upon diagnosis and my first hem/onc, Dr. Lippencot, wanted me to have chemo. He even made a point of saying that he knew Dr. Lippencot personally.

Lippencot had insisted that I use single-agent fludarabine and appeared to be a rituximabophobe, but I sensed that it would not have gone down very well to have discussed why I was hesitant to pursue that course. So I talked about how I changed doctors and opted for Rituxan monotherapy because I was otherwise in good health and thought, based upon the one prognostic test available to me at the time (CD 38), that I had a reasonably indolent case. It was obvious that he didn’t approve; hindsight is always 20/20, though it can be argued, even in hindsight, that I was not wrong in my thinking.

I should say here that I am aware that a somewhat informed patient can come across as a little threatening, perhaps, when visiting a doctor, especially for the first time. But I was not there to impress him or to convert him to a certain philosophy; I was there to (try to) have a conversation between adults. I was not shopping for a doctor who would always agree with me; I was shopping for a doctor who I felt I could trust. There was nothing about me that should have put him off; I am fundamentally a polite individual, not given to being overbearing (except, occasionally, in print). My goal was to learn; as informed as we patients may be, our doctors have a breadth of experience that we do not, and it behooves us to give them a fair hearing. As part of that process, it also behooves them to listen to our questions and concerns.

It soon became apparent that Dr. Lord was not interested in anything I had to say, or in anything I wanted to discuss. When I tried to explain the idea that CLL is incurable and that treatments need to be intelligently staggered and that there was actually some debate among experts about when watch and wait should end and what treatment is most beneficial when it does, I might as well have been talking to an immovable statue, as the Greeks did at the temple of Zeus. (I got the sense that if he could have thrown a thunderbolt or two at me, he would have; indeed, as time went on, he would lob a couple of metaphorical ones my way.)

In a vain effort to explain my current treatment, I handed him some abstracts on low-dose Rituxan, which he was not familiar with. He scanned the abstracts brusquely, annoyed.

I was obviously interfering with his Mind, which was already Made Up, and which had been so within the first few minutes since we entered his Presence, and after viewing medical records prepared by monkeys. He did not even bother asking about any of my treatment history past April 2005, nor did he ask about symptoms, and at one point he just assumed I was having night sweats although the opposite is true.

When, in an exasperated effort to build even the tiniest bit of credibility with him, I mentioned that I had seen a couple of CLL experts, and named their names, including Dr. John Byrd, it backfired. This was because, I realized, Thou shalt have no other gods before me.

Even then, I was willing to give him a chance. He might be a little touchy, but still I might learn something.

"At my age, given my disease," I told him, "I expect one day that I’ll need a stem cell transplant. Dr. Byrd, who told me last year to watch and wait and then use Rituxan again, said I should save FCR for transplant preparation."

I may as well have gone into a mosque in Teheran wearing a tallit, bearing the Torah, and throwing kreplach at portraits of the Ayatollah.

"I don’t believe in transplants," he declared.

There was a heavy silence in the room, and then I asked why.

"I did a couple of those and the blood cleared for a year or a year and a half and then the disease came back," he said. "I had one person who had a transplant and had a lot of problems for the next 18 years."

I wanted to say, "You mean you did a transplant on a CLL patient who got 18 years out of it? Maybe you are a god!" But somehow I got the impression that this was not the form of worship he wanted to experience.

I tried telling Lord that a transplant might be my only hope for long-term survival, but he essentially said to stop worrying about it and just do chemotherapy.

"Treating CLL is not rocket science," he said, annoyed. "We’ve been doing it since the 1950s. You’ve got to kill the clone."

Yes, but what do you do when the clone comes back?

At this point I realized things had no chance of going well, since "no transplant" was a tenet of his faith, as was "don’t worry about it" when you relapse from chemo.

Just believe.

Alas, this did not inspire a great deal of faith on my part in Dr. Lord.

* * *

The transplant issue is interesting as it relates to communication, as well as the establishment of trust and confidence. Later, another patient I know saw Dr. Lord and was given the same line about transplants. This patient had the presence of mind to ask, "Do you mean autologous or allogenic?" and Lord replied that he did approve of the mini-allo, not the traditional autologous with its attendant heavy-duty radiation.

Now, was it my role as the patient to suss out what the doctor meant when he said, with great solemnity, ‘I don’t believe in transplants.’? Am I a patient, or am I a psychic? Lord's unwillingness to expand on the transplants he believes in and the transplants he doesn't created a crucial problem between us -- it was at this point that I decided that he must be pigheaded and set in his ways, as well as a little out of touch with current practice. A willingness to discuss the transplant question with me in a little more detail might have avoided this misunderstanding, but he was dismissive of my concerns throughout the interview, even big ones like "eventually I think I'll need a transplant or I'll die."

* * *

The second part of our rather rapid audience, er appointment, involved retiring to the examination room and some poking, prodding, and out-and-out pontificating.

It was interesting, because Dr. Byrd gave me the impression last June that it was doubtful that I had ever needed treatment up to that point, even while I was doing all that Rituxan. Dr. Lord insisted that my care had been "completely mismanaged" from the beginning by not being treated at the outset with something heavy-duty. I had "futzed around" with Rituxan and might very well pay with my life. I could be "using it up" right now, in fact. (That low-dose Rituxan has lowered my ALC to within a few thousand points of normal, which is far lower than standard-dose did last time, would have been fodder for further derision, had I been given a moment to talk about it.)

When, speaking of monoclonals, Marilyn innocently mentioned that HuMax CD-20 would be on the market in a year or so, he looked straight at me and said "If you live that long."

The giver of life was, at this point, passing a death sentence.

Fans of the TV show Stargate SG-1 will appreciate the fact that, at about this point, I was expecting his eyes to light up and his voice to deepen, and to hear the words, "Bow before your God!"

Now, I am not arguing that the time for big-gun treatment may be getting closer, especially as I seem to have some autoimmune issues. And certainly there are those who make cogent arguments that a deep remission might ultimately be beneficial for some CLL patients. Whether they are right about this is a matter of debate, of course, at least outside Lord's office.

Dr. Lord laid his hands upon my abdomen and neck and determined that I had a few 4 cm lymph nodes, a spleen 5 cm below the costal margin and a liver about 2 cm below the costal margin. This served as confirmation to him that I am indeed an idiot, even though those numbers are somewhat shy of meeting the NCI Guidelines for Treatment.

Big-gun therapy would not be easy, Dr. Lord warned, piling it on with a certain relish. "There is a 70% chance you will end up in the hospital with sepsis," he prophesied. "You will have to be on all sorts of medications: Bactrim, diflucan, acyclovir . . ." as if this was something I had brought upon myself by not undergoing the One, True Treatment sooner. The fact that I had just been on all those drugs while doing steroids for AIHA, and that some of them are standard prophylactics for CLL patients who undergo immunosuppressive therapy, did not enter the picture.

The moment of highest drama -– next to the pronouncement of my death sentence of course -– came when Marilyn reached into the briefcase we had brought (Oh you leather repository of insolence!) and took out a study by Dr. Byrd that shows results of FR therapy by FISH and mutational status.

Dr. Lord scowled, looked across the room at the paper in her hand and said he "would not be intimidated" by "patients who try to intimidate the doctor."

You’d think we were there in metal-studded black leather jackets, flashing switchblades, and that Marilyn was curling her lip and popping gum as she spat out the words, "Yo, Dr. John Boid says here in this study that my man here is only gettin’ two years outa that there freakin’ therapy."

What she did manage to get out edgewise was the word "prognostics," which led to this commandment from Dr. Lord: "Ignore the prognostics. Just do the treatment and go on with your life."

"But what do we do when he relapses?" Marilyn asked. "I don’t want to be a widow!"

"We have R-CHOP and some other things we can do," he said. R-CHOP, ay? Dr. Lord’s religion is based on some rather ancient texts, I guess.

"So," I finally asked, asking the only question I could ask, the only one that would elicit any kind of response that did not involve being insolent in the eyes of the Lord. "What do you think I should do?"

"FCR," he replied, and then, as he scribbled some notes, he added that he usually recommends PCR (pentostatin instead of fludarabine).

"So why are you suggesting FCR?" I asked.

"Because you mentioned it before."

I was floored, and not in a brought-to-my-knees-in-prostration kind of way. He was treating me on the basis of my having mentioned a treatment? Not a lot of thought was going into this, I surmised.

Dr. Lord finished his scribbling, which involved orders for a number of tests that he didn’t bother to explain to me, and stood up, signaling that it was time to go.

"I’ll be gone for several weeks during the summer," he said. "My nurse practitioner will handle the details."

Me, 70% sepsis boy, doing whatever-it-is plus CR under the aegis of a nurse practitioner? Talk about tests of faith . . .

* * *

As we left, we found that Lord’s office is run like a cattle yard, with patients herded through this and that process by people who are either clueless or apathetic. The order is handed down by Lord, and then the patient retires to the waiting room until someone shows up and calls their name for whatever it is that needs to be done -- blood test, scheduling, getting a question answered.

Indeed, in the spirit of its leader, the office is not geared toward answering questions. When I was in the blood lab and asked what tests Dr. Lord was running, the chirpy tech in the white coat said "Lots!"

Marilyn was beginning to grit her teeth and turn red and I sensed that if the tech did not respond with a better answer soon, her entrails would be wrapped around her neck.
So I asked to actually see the order, and I was looked at like I was an alien from outer space, and then finally handed the document. There was the usual stuff, and there was also a FISH test, and I figured it would not hurt to check the FISH after my recent low-dose Rituxan and steroid therapy, so I went ahead with the tests.

Later, at checkout, we discovered that Dr. Lord had ordered a CT scan of my chest and abdomen and also a chest X-ray. The obvious question, which had to be asked, was "Why a chest X-ray when I'll be getting a CT of the chest?" The scheduler was clueless but said the doctor was now "too busy" to answer the question and that she would find someone to help us if we would just retire to the waiting room and wait until my name was called.

A nurse of some kind showed up.

"Isn’t the chest X-ray a redundant test and extra radiation that I don’t need?" I asked. She fumbled for words and seemed unable to answer and Marilyn tried repeating the question several different ways, each time with a slightly louder and more impatient tone, and finally the nurse gave the only answer that really made any sense given our experience that day:
"Because he wants it done!"

Thy will be done, on Earth as it is in Heaven.

* * *


We left, shell-shocked, and over a bowl of pho at a Vietnamese restaurant realized that Dr. Lord wasn’t right for us. The experience left me dazed and confused emotionally, and it took me a few more days to get past it, frankly. When a doctor tells you your death is reasonably nigh, there’s a small part of you -– the part that has been conditioned to believe what doctors say -– that thinks, at least for awhile, "Maybe he’s right."

Later that week, back at the old practice, I saw one of the doctor partners who had fired Dr. Belle, which, of course, had upset me greatly. He turned out to be a reasonable human being, with a decent knowledge of current thinking about CLL. He examined me also, and noted the size of the spleen and liver without curling his lips in disgust. "I’d be surprised if they weren’t swollen," he said. He gladly took the abstracts about low-dose Rituxan and was quite impressed at how well it had brought down my counts, insisting that I continue with it for three more weeks, completing the 12-week protocol. We also touched on various other treatment options, and I expect we will discuss them in detail soon.

And more good news: As if by magic, both my red counts and platelets turned around dramatically for the better when tested just before my meeting with the second doctor. Maybe Dr. Lord had put the fear of God into them.

I left with the feeling that I could probably trust this new doctor and that I could work with him. A good doctor-patient relationship is a partnership, which involves some give and take and a willingness to question assumptions in both sides. This process is what builds trust and respect.

I could not, and would not, leave my care up to someone with a God complex, no matter how many diplomas on the wall, or how many votes received in a poll. Dr. Lord might even be a good doctor in some respects -- who knows, I might even follow his advice about treatment -- but trust, like faith, must be earned, not assumed. And personally, I have always responded better to the concept of a compassionate God than to a vengeful one.


Some time later I found out that Dr. Belle was not recommending that her patients see Dr. Lord but rather another doctor in Lord's practice. This message got muddied, however, as word circulated from patient to patient. Eventually Dr. Belle formed her new practice in partnership with this other doctor, who had been working at Lord's and who was glad to get out of there. I had a chance to speak to him and he described Lord as being akin to "the great and powerful Oz." I had to laugh, and it was reassuring to know that someone who worked intimately with the Great One had reached the same conclusions as I. -- November 19, 2007