Time to death among men with nmCRPC by NCCN risk group


One of the abstracts to be presented at ASCO this year gives us some insight into risk for and time to death among men with non-metastatic but castration-resistant prostate cancer (nmCRPC). This is a group of men for whom therapeutic options are currently poorly defined and of limited effectiveness.

Macomson et al. used data from the Optum electronic health database to identify a total of 1,008 men who met all relevant criteria for a diagnosis of nmCRPC between 2007 and 2016.

They categorized these men into one of four different risk groups:

  • Group A: Men initially diagnosed with NCCN low-risk prostate cancer (Gleason ≤ 6 and PSA < 10 ng/ml)
  • Group B: Men initially diagnosed with a PSA level of < 10 ng/ml and who had no assigned Gleason score
  • Group C: Men initially diagnosed with NCCN intermediate-risk prostate cancer (Gleason = 7 or PSA ≥ 10 and ≤ 20 ng/ml)
  • Group D: Men initially diagnosed with NCCN high-risk prostate cancer (Gleason ≥ 8 or PSA > 20 ng/ml).

Here is a summary of the study findings:

  • The average (mean) age of the patients was 76 years.
  • 121/1,008 patients (12 percent) were African Americans.
  • 553/1,008 patients (percent) developed metastases.
  • 430/1,008 (percent) patients died during follow-up.
  • Average (mean) time to metastasis was
    • 28 months for men in Group A (among 9/29 patients or 31 percent)
    • 22 months for men in Group B (among 131/285 patients or 46 percent)
    • 15 months for men in Group C (among 175/320 patients or 55 percent)
    • 13 months for men in Group D (among 238/374 patients or 64 percent)
  • Average (mean) time to death was
    • 32 months for men in Group A (among 8/29 patients or 28 percent)
    • 30 months for men in Group B (among 101/285 patients or 35 percent)
    • 24 months for men in Group C (among 124/320 patients or 39 percent),
    • 21 months for men in Group D (among 197/374 patients or 53 percent)
  • Men in Group D (the high-risk group) were more likely to develop metastasis during the first year and die within the first 2 years than those in any other risk group.

What is probably still surprising about these “real world” data is that

  • More than half of nmCRPC patients with high-risk disease still die within 21 months of onset of nmCRPC.
  • Nearly 40 percent of nmCRPC patients with intermediate-risk disease still die within 2 years of onset of nmCRPC.

We are very clearly still dealing with a subset of men with an aggressive form (or forms) of prostate cancer who are at very high risk for early metastasis and death once they stop responding to standard forms of androgen deprivation therapy (ADT).

20 Responses

  1. Either I don’t understand this summary or there are problems in phraseology.

    First: The eight sub-bullets purport to report the “average (mean) time to” an event. I think this is wrong, and I suspect that what is reported is average (median) instead. Why?

    — The mean cannot be calculated until the entire population has encountered metastasis and/or death.

    — The two final bullets conclude something about “half the men”, surely indicating median rather than mean.

    This is not as nitpick-y as some of my past statistical comments have been. In a population of this sort, the two “averages” can be quite different, and their interpretation is quite different.

    Secondly: I don’t understand what was meant by this phraseology: “months for men in Group (among M1/M2 patients …)”

    Whether median or mean, how was itcalculated?

    — If median, it must have been a projection, not a calculation, for those groups where fewer than 50% had encountered the event.

    — If mean, how was the tail of the curve projected?

    Thirdly: It seems odd to stratify men according to their initial diagnostic findings, when (IIRC) 20% of men who undergo second — or subsequent — biopsies and 30% of men who undergo surgery have upgraded Gleason scores. (Mine is such a case.)

    Fourthly: It is worthwhile noting that the time to metastasis and time to death are measured from the diagnosis specifically with castration-resistant prostate cancer (CRPC) — a diagnosis that might occur decades after the initial diagnosis.

    Finally: It would have been helpful to compare this cohort of men with two cohorts of similar demographics (age, race, co-morbidities) each with one key difference: (a) men without prostate cancer, and (b) men with hormone-responsive nonmetastatic prostate cancer.

    Off the top of my head, I couldn’t tell you whether a man in Group A could expect to live another 100 months or 400 as a median or mean, or whether a man in Group B could expect to live another 50 months or 500 as a median or mean.

  2. So, this begs the question, “Why are there almost no clinical trials open to nmCRPC patients?” Why do these men have to wait until they are metastatic before they become eligible for clinical trials?

  3. Dear Paul:

    I agree with you that this abstract was very poorly written. I haven’t seen the text of the full paper. I did the best I could, but some of your comments and criticisms may be entirely accurate, and frankly I couldn’t tell when the authors were applying the NCCN criteria to these patients, but the “customary” time to do this is at initial diagnosis, not later on.

  4. Dear Len:

    Actually if you really looked through ClinicalTrials.gov (which is hard work) you might find many more trials of men with nmCRPC than you expected. However, …

    (1) One of the biggest problems is that until only a few years ago we had no good drugs that might have been expected to be effective and safe in the treatment of nmCRPC.

    (2) A second problem is that abiraterone acetate (Zytiga) will lose patent protection before any trial of this drug in treatment of nmCRPC could report results, so the manufacturer would have had to make a huge investment in such a trial with no likelihhod of a significant financial return on that investment.

    (3) The manufacturer of enzalutamide (Xtandi) chose to “skip” the nmCRPC patient group and go directly to whether adding enzalutamide to radiation therapy and surgery in high-risk patients could show a clinical benefit. I assume this was a straightforward business decision.

    (4) As a consequence, most trials of drugs in nmCRPC are small Phase II trials at one or two institutions that have not led to any major findings of clinical benefit that would encourage the necessary major investment in Phase III trials that are needed to lead to the approval of drugs for that indication by the FDA.

  5. I think it’s worth mentioning a few points:

    • As always, when they say “metastatic” or “non-metastatic,” they really mean “not detectably metastatic or non-metastatic based on whatever diagnostic methods were used (typically bone scan/CT).

    • Non-metastatic and castration-resistant is a relatively rare situation. Usually castration resistance sets in well after metastases have been discovered. Sometimes these rare types are quite virulent, but not always.

    • To PaulC’s point about means and medians — this was a retrospective data analysis and not a prospective trial. That means they did know what the mean was because they have hindsight. I think (but don’t hold me to it) what they did is remove the zeros — so more accurately, they should have stated: “among those who died/developed metastases, the mean time to death/developing metastases was X.” But I agree that looking at the survival/metastasis curves would be more enlightening.

    • To Len’s point — Because of the rarity of this presentation, such clinical trials are very hard to recruit for. We have discussed on this site one such trial I am extremely hopeful about, and which I understand is going through a very slow recruitment process. That would be the be the trial of Lu-177-J591 + ketoconazole (see this link).

  6. Allen, I agree that there is a false distinction between nmCRPC and mCRPC and I’m sure most medical oncologists would agree, so why can’t practitioners and insurers agree to open up all therapies, whether approved or in clinical trials, for patients as soon as they become CRPC? This would allow such patients to have an earlier start with therapies like enzalutamide, abiraterone, Provenge, etc., instead of standing around while the cancer advances to the point of radiographic progression. Do we really need to prove (through clinical trials?) that nmCRPC will eventually progress to mCRPC?

    Regarding the lutetium-177 trial, I suspect that recruitment is very slow because this trial was first designed (I think) before abiraterone was approved, so they used ketoconazole which has since been completely displaced by abiraterone. If they modified the protocol to substitute abiraterone for ketoconazole, I’ll bet recruitment could be accelerated. I think that Mike’s comment earlier about Zytiga losing patent protection before any current trials could yield results may not apply here because the manufacturer could apply for a “use patent” (to extend the life of the original patent) for the combination of Zytiga with Lu-177.

  7. Dear Len:

    No insurance company (or Medicare) is going to “open up” use of approved therapies for patients as soon as they become nmCRPC for the very simple reason that they aren’t approved for such treatment by regulatory authorities because we don’t yet know whether patients who are non-metastatic will benefit from any such available therapy. The cost risk for the insurance companies is too high. Also, any patient who is nmCRPC can already enroll in any clinical trial they are eligible for (usually at no cost).

    And respectfully, I am pretty sure the costs involved in conducting a trial of abiraterone + Lu-177 in men with nmCRPC would be far higher than any amount of money the company could hope to recover within the possible 3-year patent extension that was exclusive to the use of Lu-177 + abiraterone in men with nmCRPC, which is a small subset of patients.

    With regard to the issue of slow enrollment in the Lu-177 + ketoconazole trial, I think it is much more likely that at the time this trial was being designed the manufacturer of abiraterone acetate was unwilling to have this (at the time) pretty much untested drug (Lu-177) be given in combination with abiraterone because of the risk for unknown side effects. Therefore they wouldn’t have been willing to contribute free drug for conduct of the trial. The consequence of that was that — since abiraterone is not approved for the treatment of nmCRPC — patients would have had to pay for the abiraterone themselves (or the developers of Lu-177 would have). That would have been a pretty hefty bill for anyone to be paying.

  8. The reason that clinical trials are such powerful evidence is because the protocols are uniform. If, for example, a man with nmCRPC has a very different reaction to some treatment compared to a man with mCRPC, then the overall results are “polluted” by the inclusion of two very disparate groups. Imagine a clinical trial for a new hormonal agent, for example, that allowed in a man with small cell prostate cancer that wasn’t detectably metastatic and was CRPC. He will not respond to any hormonal agent, and his inclusion in the total will make the results seem worse than they really are.

    The lead investigator told me that recruiting is slow because it is a rare group — not because it doesn’t include Zytiga. Zytiga is only approved for mCRPC, so including it in a clinical trial for Lu-177-PSMA would doubly confuse the results — what caused the benefit, if there was one? Since such patients could not get Zytiga, they would probably be thrilled to have the option of the nuclear medicine with ketoconazole. They could always get Zytiga later, after they developed detactable metastases (if they ever did).

  9. Still Puzzled After All These Years: Discrepant Survival Medians For CRPC Survival: Oefelein 60 Months (Median) Vs. Halabi 2014 Updated Nomogram For Metastatic Patients (17 – 30 Months, Median), And This Abstract For CRPC Patients (21-32 Months, Reportedly The Mean)

    The survival durations reported above strike me as within striking distance of the typical ranges for prognosis of overall survival for men with metastatic CRPC to be treated with first line chemotherapy, per the well-known and now updated (2014) Halabi nomogram, which is fairly close in survival duration to the prior 2003 version. Granted, it generally takes a little time for men to move from CRPC, as in the above abstract, to metastatic disease, as in the Halabi nomogram, but the above abstract suggests that the time is fairly short in the above study for the minority of men dying early, about 4 to 8 months for groups A to D.

    However, in a 2004 paper in the Journal of Urology, three authors from Case Western Reserve University (Cleveland), Oefelein MG1, Agarwal PK, and Resnick MI, presented quite different prognoses for patients with what was then called “hormone refractory” prostate cancer (now known as CRPC). Case Western Reserve is noted as a prostate cancer research institution, and the late Dr. Resnick was a distinguished leader in the field, once head of the American Urological Association. Here is a link to their paper. In essence, they were struck by their impression, which they were able to prove, of substantially longer survival durations of hormone refractory (CRPC) patients at their institution than the norms commonly reported. Here is the key line from their results: “Median survival after hormone refractory prostate cancer developed in patients initially staged with and without skeletal metastasis was 40 and 68 months, respectively.”

    By the way, as one of about 100 survivor representatives present, I was able to highlight the encouraging Oefelein survival figures with an audience question to the panel on which Dr. Susan Halabi, Dr. Nick Vogelzang, Dr. Eric Small, Dr. Howard Scher, and Dr. Ou were participating at the 2007 IMPaCT Conference (Innovative Minds in Prostate Cancer Today), which was a review of results of sponsored research and an exchange of expert views under the auspices of the US Department of Defense managed Prostate Cancer Research Program of the Congressionally Directed Medical Research Program (CDMRP). The panel was Symposium Sub-Session 18-5 entitled “A Novel Intermediate Endpoint for Predicting Overall Survival in Men with Metastatic Castration-recurrent Prostate Cancer (CRPC): An Analysis of Nine CALGB Studies.” At that time the 2003 Halabi Nomogram was current. My question created quite a stir, with Dr. Vogelzang asserting with some spirit that the figures I had mentioned must be flawed. I was really impressed that Dr. Halabi approached me afterward to get the exact citation of the Oefelein study. This memory is why I put “after all these years” in the title. (And it’s an example of some of the cool and meaningful contributions we survivors can make as activists, challenging the conventional wisdom!)

    But back to the main point: what accounts for the marked difference in survival figures? Perhaps a key factor for the above study is that most men were still alive as of the study’s cut off (72%, 65%, 61% and 47% for groups A, B, C, and D respectively), whereas the Oefelein study was mature as all patients were no longer alive. These facts suggest that final survival time figures will be considerably larger than in this interim analysis of the above study when all patients in groups A through D have passed on. Indeed, nearly half the men in the study had not yet even developed metastatic disease, with figures for those who had metastatic disease ranging from about a third, about half, about half, to about two thirds for groups A through D respectively.

    One minor difference, perhaps adding one to a few months added survival for those dying early, which may not represent the situation for the total group, is the difference in starting the survival clock; the Oefelein study counted time from the first PSA increase (in a series of increases) for men being treated with ADT who had a “castrate level of testosterone,” very likely < 50 ng/dl which was in contrast to starting the clock at the second increased PSA result in the above abstract. That said, men in the above abstracted study were likely monitored with frequent PSA tests, perhaps as frequently as each month, so the average gap between the first and second PSA increase may have been short.

    The Halabi nomogram is based on research where the clock was started at the time of trial enrollment, which might lag considerably behind the first detection of metastatic disease, which in turn usually lags development of metastatic disease. This would seem to explain some of the difference between median survival of 48 months for men with metastatic disease in the Oefelein study and the considerably shorter survival ranges indicated by even the updated 2014 Halabi nomogram. Also, as noted above, the Halabi nomogram does not include time from the first indication of CRPC to the first indication of metastatic disease. (Additionally, it specifically is geared for use of docetaxel and does not cover use of the exciting drugs approved in recent years.)

    What does all this mean for us? I am convinced it means that survival is almost surely substantially longer for us after diagnosis of CRPC than is evident from the above study. The study, at its current state of maturity (with a majority still alive at the research cut-off date), is arguably somewhat helpful in suggesting a rough lower boundary for the length of survival for men with CRPC who may be expected to have shorter than average survival after developing CRPC. For me personally, when I became aware of the Oefelein study — probably around the fifth year into a still life-threatening case under treatment with intermittent triple ADT at that time — I was overjoyed! I knew I was not yet in the CRPC state, and that meant I would likely enjoy at least a number of years before becoming resistant to ADT (never happened by the 14th year, when I ceased ADT, except dutasteride as part of my safety net) and then would likely enjoy around 5 more years of survival, with advances in technology each year that might help me beat this thing. (My PSA of May 10 — 4 years and a month after a curative attempt with radiation, and 3 years and a month after my supportive triple ADT expired — was again < 0.05.)

  10. A correction to my previous post:

    The above text reads: “The Halabi nomogram is based on research where the clock was started at the time of trial enrollment, which might lag considerably behind the first detection of metastatic disease, which in turn usually lags development of metastatic disease.”

    It should read: “The Halabi nomogram is based on research where the clock was started at the time of trial enrollment, which might lag considerably behind the first detection of metastatic disease, which in turn usually lags development of castrate-resistant disease.”

  11. I hope I’m not beating two dead horses here, but I’m not sure they’ve been properly understood or addressed.

    Here’s a very simple illustration of the median-vs-mean problem:

    • Suppose that, in 2019, 10 men are diagnosed.
    • One man dies in 2019, another in 2020, …; the fifth dies in 2024.
    • The median time to death is established the moment the fifth man dies. We now know it precisely for that 10-man cohort, and no future event can change it.
    • But as for the mean time to death for the cohort, we can only guess. We cannot calculate it until the last man dies.

    Why?

    — If the remaining five all die in 2025, the mean time to death is ~ 3.5 years.
    — If the remaining five all die in 2040, the mean time to death is > 11 years.
    — If the last man proves to be immortal, the mean time to death is infinite.

    I am aware of statistical tools to extrapolate from a less-than-complete sample. All of them are based on models (e.g., Poisson distribution) that produce estimates with margins of error. Actuaries use such tools all the time, and life-insurance companies depend on them. They are very accurate for large populations and large samples.

    But I’m not aware of any tools that could produce a meaningful extrapolation from eight or nine time-based events occurring out a population of 29. When I look at a simple Poisson distribution, I emerge with figures like “28 ± 12” months or “32 ± 11” months.

    To a physician those error bars are important; to a patient, they are enormously important.

    And here’s a restatement of my issue with the “metastatic” label:

    The “m” in “nmCRPC” is not just poorly defined, it’s a moving target. Using the accepted terminology, a metastasis just barely detectable today was a nonmetastasis 10 years ago, when the technology was worse. And a suspicious nonmetastasis today might well be a metastasis by imaging technology 10 years hence, when the technology is better.

    Thus the same pathology — the exact same physical condition — can be “nm” in one year and “m” in another, simply because the snapshots are sharper. Metrology should not change according to fashion. People don’t become more diseased because of advances in imaging technology.

    If comparisons are to be made between groups from 10 or 20 years ago and groups of today or 10 years hence (and they should), then calibrating corrections must be made and disclosed.

  12. PaulC,

    In a normal distribution, the mean, median, and mode are all the same. I don’t think you understand how a retrospective study, like this one, differs from a prospective study, like a clinical trial.

    With a retrospective study, all deaths have occurred, and they can calculate the mean, median, and mode among all non-metastatic men from the time they reached castration-resistance to the time they died. Unless, there were significant subgroups that might create a bimodal (or trimodal, etc) distribution, the means, medians, and modes will most likely be normally distributed and would coincide. (Numerous, small subgroups are OK.) No extrapolation is necessary, and, except for the “low risk” group, the sample size here was large enough so that the differences are statistically significant. In a prospective study, on the other hand, they can calculate the median as soon as half have died, but they can’t calculate a mean until all have died.

    Metastases are, for the most part, detected pretty much the same way now that they have been for at least the last 30 years — bone scan and CT. PET detection is relatively new and is not very widespread.

  13. Thanks for the clarification, Allen.

    I had no idea that all men in this study had already died. If so, that makes all the difference in the world.

    But I don’t see anything in the summary that indicates this, and it seems implausible to me that all men diagnosed with nmCRPC between 2007 and 2016 would have died.

    How do you interpret the parenthetical comment mean in this bullet?

    • “32 months for men in Group A (among 8/29 patients or 28 percent)”

    My interpretation — apparently a misinterpretation — was that it meant “(of 29 patients, 8 died)”

    But if all have died, I don’t know what different interpretation to place on it.

    About the issue of what does and doesn’t qualify as metastasis in various decades: When I wrote “technology”, I was referring mostly to imaging technology. Perhaps I should have been clearer.

    I agree that bone scans and CT scans are decades old, but the important difference is the ability to image — just as in cellphones, cameras have much better imaging today than 10 years ago, let alone 20.

    Even in my own experience and with my own inexpert eyes, I can see the difference in image quality between a CT scan in 2007 and one in 2013.

  14. No — All men in the study didn’t die, but they computed the mean time till death among those who did, as I said in my first response.

    I’m not aware of any major changes in bone scan or CT technology, especially during the years of this study 2007-2016. Bone scans are limited by the rather unspecific technetium indicator and the poor gamma camera/SPECT resolution. CTs still deem a lesion positive if > 1.2 cm, as always. I have seen no indication from any study I’ve seen that detection rates have increased due to enhancements in bone scan or CT technology, have you?

  15. Wonderful advances in bone and soft tissue imaging over the past decade

    Re changes in bone or CT technology, as raised by Paul and reflected in Allen’s 5/25 7:22 pm response

    Indeed there have been highly significant changes during the 2007-2016 period! In fact, these changes are what persuaded me that the small metastases my doctors and I suspected could be spotted and or ruled out, and that a curative attempt might be possible with radiation, perhaps including spot radiation or spot surgery if the disease turned out to be oligometastatic.

    The major breakthrough in bone imaging was the Na18F PET/CT scan, which is far more effective, with very high sensitivity, than the technetium bone scan. Mine, done in 2011, turned out to be negative. While there has been some debate among physicians whether they can make use of that greatly enhanced accuracy, it is excellent at ruling out bone metastases. I just got 40 hits after searching PubMed for: sodium fluoride bone scan AND prostate cancer. The oldest was from 1999, the second oldest from 2009, and most were more recent.

    The development on the front for lymph node imaging, previously the domain of fairly insensitive and unspecific CT imaging, was the emergence of two excellent methods for lymph node and soft tissue imaging, also covering bone to some extent. One is the C-11 choline PET/CT, until recently only available at the Mayo Clinic, in Rochester, Minnesota, approved for Mayo by the FDA in 2012, where it is heavily used by Dr. Eugene Kwon and his colleagues, and the other is the C-11 acetate PET/CT in Phoenix, Arizona, under the direction of Dr. Fabio Almeida. Both participated in the 2016 Conference on Prostate Cancer last September in LA. Dr. Kwon stated that they do 4,500 to 5,000 C-11 choline scans a year (conference DVD set, Disc 2, 3:42).

    My own soft tissue imaging in 2012 was a feraheme USPIO MRI/CT scan done at Sand Lake, Florida, by Dr. Stephen Bravo, as part of a clinical trial. That also was fortunately and surprisingly negative. Unfortunately, while feraheme imaging is highly effective, there were safety problems related to potentially deadly anaphylactic shock, and that technology is no longer available. (I’m wondering if that could be solved by use of a pre-scan test for allergy to the scan elements.)

    Previous to that, excellent Combidex imaging, fairly similar to feraheme, was available in Holland under the management of radiologist Dr Jelle Barantsz; apparently it has recently become available again with reestablishment of the supply of imaging agent. A number of US oncologists sent a stream of patients to Holland for that imaging before C-11 imaging became available in the US.

    I got 19 hits for “C-11 PET AND prostate cancer”, and 37 for “Combidex AND prostate cancer”.

    The bottom line is that there has been wonderful progress in prostate cancer imaging that is now highly useful in the clinic!

  16. Dear Jim:

    These tests simply aren’t available to 95% to 99% of prostate cancer patients — for geographic, logistical, and financial reasons.

  17. Availability of advanced prostate cancer imaging for recurring patients in the US
    (re Sitemaster 5/26 1:25 pm)

    Dear Sitemaster,

    You are putting me to work again! That is actually something I appreciate as it helps me build knowledge and perspective beyond the leading-edge sources to which I pay most attention.

    Your statement surprised me, but I was also surprised to learn recently that “Nearly 1 in 5 Americans older than 65 do not have a single real tooth left” (Washington Post, 5/13/17), a bleak indicator of the stark financial reality facing many Americans. So I looked into the details.

    I’m finding a somewhat mixed bag in response to your statement that the availability of advanced imaging is quite limited because of several constraints. I looked at three scans (but not the new Axumin scan):

    — Na18F PET/CT for bone
    — [11C]choline PET/CT and
    — [11C]acetate PET/CT

    The latter two require cyclotrons on site. Also, these scans are almost exclusively intended for recurring patients and patients with challenging cases; they are not needed or useful for the vast majority of prostate cancer patients.

    Geographic and logistical availability differs greatly. The Na18FPET/CT scan for bone is available as of today’s listing on the Centers for Medicare Services site at exactly 2,000 listed locations in the US, with many states represented. That did not surprise me as my local site, where I had my own scan, is about 5 miles away. The carbon-11 scans will, at this time, require travel for most of us. The only two sites I could confirm were the original [11C]choline site at the Mayo Clinic in Rochester, Minnesota, and a site at Decator Memorial Hospital, Decator, Illinois, which was approved about a year ago. However, the Zevacor company, which supplies the Decator site, planned to have [11C]choline production at all its distribution sites. I was not able to find the geographic or schedule details. The C-11 acetate scans are available at Dr. Almeida’s Phoenix, Arizona site and at the University of Kansas under Dr. Dursing.

    Cost and affordability: Medicare covers the Na F18 PET/CT bone scan and the [11C]choline PET/CT scan. My own Na18F PET/CT bone scan was well covered by my retiree insurance plan. Dr. Kwon’s experience at Mayo is that costs are very well covered by Medicaid/Medicare. However, he said there is a wide range of coverage by private insurers, and that the full out-of-pocket cost ranges from $8,500 to $10,000. (PCRI, 2016 Conference on Prostate Cancer, Disc 2, 48:32)

    Current target population and use: Estimates indicate there are about 100,000 newly recurring prostate cancer patients each year. Most likely a substantial proportion have such mild recurrences, with such slow PSA doubling time that they only need ordinary monitoring without the need for sophisticated scanning. In 2016 Dr. Kwon said about 4,500 to 5,000 patients were getting the [11C]choline scan each year (with some getting more than one scan and possibly being double counted). If the Decator site could handle that many, a total of 10,000 could be getting that scan in 2017, though they may need to take some time to ramp-up. If Zevacor follows through, that number could increase substantially. The now approved Axumin scan would also cover a portion of the target patient population. Also, the [11C]acetate scan, still apparently in investigational status, covers additional patients, but I could not find evidence of how many. (The feraheme USPIO scan, had it not flunked the important safety issue, would have been very widely available. I had to travel to Florida for mine, and, with the agent not covered by insurance as it was investigational, had to pay somewhat more than $1,000 plus the cost of the trip.)

  18. Dear Jim:

    While I applaud all this research, I think you are missing one of my key points, which is that most of America doesn’t have even $500 in the bank to get their car fixed if they have a problem — let alone worry about whether Medicare is going to pay for a form of prostate cancer scan that (even with Medicare or Medicaid) comes with some form of co-pay (however small) under most circumstances. They certainly don’t have the money for a plane fare (and probably an overnight hotel room somewhere) to the Mayo or anywhere else.

    To make your research complete, I would suggest you see if you can determine the total cost of travel and all other costs associated with having such a test — when covered by Medicare — at one of those 2000 centers that offer Na18F PET/CT scans for a man who lives 50 miles from such a center (who will be a significant percentage of the target audience). You may be surprised.

  19. Jim,

    The cost/availability situation is much more complex than you’re making out. NaF PETs are only covered by Medicare if it is part of a registry or clinical trial. Even the [11C]choline PET at Mayo is only sometimes covered by Medicare — it can vary regionally and by plan. No one is going to adopt them anymore because of the better PET scans now becoming available and in clinical trials, and which do not require on-site production. 11C is already a relic, but only the largest tertiary care centers can afford to keep up. At any rate, the point PaulC was making was about improvements in technetium bone scan technology, which has nothing to do with any of your comments.

  20. The observations I was making boiled down to: a lot of us who need these scans can and are getting them, and that a lot of us are not.

    Thanks for clarifying the Medicare situation on the NaF PETs. I saw that as I was following up on Sitemaster’s suggestion but was not sure it was still current. I was not aware of the C-11 PET variation in coverage at Mayo. Dr. Kwon did not include that detail in his comment; sometimes he generalizes a bit.

    I am not aware of improvement in the technetium bone scan. What’s involved?

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