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I have been struck by how many patients ask me to measure their lipid panels as we work our way through the management for their prostate cancer. To be sure, it is important to know about cholesterol, triglycerides, and cardiac risks for both men and women. If you have never had a fasting lipid panel, you should get one. If you are not on a statin, you might consider that and read about the benefits for prostate cancer patients in one of my previous posts here or here. Knowing about cardiac risks for the general population is a terrific public health idea, and you can check out your own risks here. (If you are otherwise healthy, with good blood pressure and a non-smoker, it is sobering to play with that calculator and watch what happens to your risk with increasing age…the one thing you can’t do much about!)
But why continue to worry about heart disease once you have prostate cancer, especially if you have metastases and become resistant to hormonal manipulation? Do you need to continue to take your statin? There is a reasonable literature looking at the downside of polypharmacy in patients as they age, and the potential cost savings, and even improvement in quality of life by stopping some medications. Read this brief article for a good discussion on the topic.
Expanding this thinking to what blood tests we should worry about and how often to do them is an important exercise. In particular, I think we are all addicted (often too addicted) to the PSA test as I discussed in the PSA clock blog. There were many comments pointing out the necessity of following PSA to know the efficacy of changing treatments, and I agree with that. On the other hand, obsessing about PSA can definitely be a negative for your mental health and enjoyment of life. Don’t fall for the idea of daily measurements if someone comes out with a finger stick blood test for PSA!
Testosterone measurements, on the other hand, may be too infrequently measured in caring for prostate cancer patients, and compared to the costs of the newer ADT agents, or even the GnRH injections, they can be highly cost effective. A quick search suggests that measuring your T could be as little as $50 or probably 2-3x that in a hospital. If you have metastatic prostate cancer it is key to have the T level as low as possible. Some cancer cells become hypersensitive to even low levels of circulating T by over expressing the androgen receptor, and of course this led to the research on further blocking testosterone synthesis by drugs like abiraterone or the receptor by the “lutamides” (bicalutamide, enzalutamide, apalutamide, duralutamide). These drugs can cost in the range of $10K/month, so measuring T levels has minimal impact on the overall cost of care. However, in two abstracts presented at the recent ASCO meeting, the possibility of stopping GnRH injections in patients on abiraterone was studied. It makes sense that if abi completely blocks T synthesis in the testis, adrenal gland, and cancer cells, you might not need the injections. There is a good review of one of the abstracts here. I had always wondered about this, and it was nice to see it studied. The cost savings if this became a standard could be in the millions. (caution however – would need to be studied more carefully, and if someone missed abi doses, very rapid T increases would be seen due to high LH levels no longer suppressed by GnRH analog injections).
I realize this is far into the weeds for most patients, but maybe a take home message could be to discuss measuring your T levels once in a while with your physician, rather than just the PSA. And maybe you could go over what meds you might consider stopping at this point in your care. We doctors are too often pill pushers and as I try to say to every patient at every visit, [Please CLICK ON THIS ONE:] there is nothing more effective in general than increasing your exercise – often as effective as ANY additional pill or blood test!
10 responses to “Blood tests and stopping medications”
Great article. While you are cautious not to recommend eliminating the agonists , there is the hope that men can keep their testosterone and prevent its “ fueling effect “ on PCA. A reduction in side effects would be fantastic.
Separately, could you opine on the issue of whether the advanced use of these secondary hormone treatments will accelerate time to castration resistance . It seems that the net result of early use could accelerate time chemo and nuclides.
I think there is a lot of room to study the potential reduction in side effects of various forms of ADT. The use of the better lutamides as single agents is a possible example. There is also the question of time to resistance. The Hopkins group had an interesting abstract at ASCO regarding waiting until mets show up in slow doubling time patients before starting ADT that deserves attention. The financial costs and toxicities of the “new ADT” are considerable, and their use later in the disease and/or intermittently instead of continuously should definitely be studied. Tailoring timing, sequencing, and which agents to use in individual patients is somewhat of an “art of medicine” issue for now. And the side effects of treatment vary considerably among patients.
Dr. Glode, I have heard that monotherapy with the “lutamides” greatly increases the incidence of gynecomastia due to the action of “unopposed estrogen” at the receptors. Would you expect to see this same phenomenon using abiraterone (+ prednisone) as monotherapy?
Abiraterone blocks the synthesis of T (and also some other steroids, hence the need for prednisone). Patients on abi mono therapy would likely have little in the way of gynecomastia. On the other hand, blocking the androgen receptor with any of the “lutamides” results in the body/brain thinking it is deprived of T. The LH levels (from the pituitary) go up, driving more T synthesis by the testis, some of which is converted (aromatized) to estrogen unopposed (as you point out) by the androgen/androgen receptor axis. Hence gynecomastia. (LH release is blocked by the GnRH analogs in the combined ADT mode we have been using for years.) Aromatase inhibitors would block this, but now we are talking about many pills and polypharmacy…
The advantage of the lutamides is the non necessity of taking prednisone required with abi. If one has a sensitivity to prednisone….which is exacerbated by longer term use….then the lutamides make sense .
As one person said “ big man boobs or a fat face …take your choice”.
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Is it the case that after a course of Abireterone for 12 or 18 months the patient’s T level will be near zero and remain there for many months or years? Or is it expected the T level will creep up—and that is ok as long as it stays below a certain level? Is that level 4.0–or do I have that confused?
T levels on GnRH should be less than 50 (ideally less than 20). They are usually undetectable when also on abiraterone/prednisone. When both drugs (GnRH and abi/pred) are stopped, it is anticipated T will slowly rise to normal (typically in the 300ng/ml range). The longer someone is on ADT and the older they are, the slower the recovery.
Maybe a bit fundamental, but is there some way to stop taking metformin but get the glucose down? Trying to give the kidneys a break. Promise to get up to 3×50 exercise, too.
Glad to hear about exercise. Metformin should be discussed in person with your physicians.