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Multidisciplinary Approach and Role of PSA and Testosterone Monitoring in Prostate Cancer

Panelists: Raoul S. Concepcion, MD, FACS, The Comprehensive Prostate Center; Jorge A. Garcia, MD, FACP, Taussig Cancer Institute; Alicia K. Morgans, MD, MPH, Vanderbilt University Medical Center; Ashley E. Ross, MD, PhD, Johns Hopkins Medical Institution; Daniel R. Saltzstein, MD, Urology San Antonio
Published Online: Wednesday, Dec 21, 2016



Transcript:

Raoul S. Concepcion, MD:
Aren’t there some institutions that are actually establishing that cardio-oncology, specifically, deal with that?

Alicia K. Morgans, MD, MPH: We have that, cardio-oncology, yes.

Jorge A. Garcia, MD: That’s a great point. I think that one of the challenges, that a lot of physicians in the community practices face, is who owns the patient? Often times, it’s urology driven, often times, it’s oncology driven. And, I think, most of us, who work at a multidisciplinary approach–style practice, believe that it doesn’t really matter who owns the patient. What is important is what do we do as a group for the patient. The patient is in the middle. We try to all maximize that outcome. I think to your point, Alicia, for instance, in our place, we have a cardio-oncology clinic, and we have many other resources that we utilize when we start ADT in patients, whether we do it for the intermittent style or we do it for continuous ADT. If you were to go to Boston, you may do a little more endocrine approach because they are big into bone health, and so forth. But, often times what we do, we do nutrition, we put them in contact with exercise with the health clinic, with the cardiology, to actually work on reduction of metabolic syndrome. We also do endocrine therapy for bone-specific things. If we are treating them, we actually need to do those things for the patient.

But, I think, when you think about rising PSA syndrome, one of the biggest challenges we face, as practitioners, is all the data that we have for ADT, in the biochemical recurrence N0 space, is all over the map—because some people have used absolute PSAs to make decisions on when you trigger that re-initiation of ADT. Some people have used testosterone recurrence, some people have used 6 months of ADT, which is, probably, in my opinion, the best data that we have. The data that I follow the most are Juanita Crook’s data from Vancouver, looking at if you start someone on a rising PSA, you could do 6 months of ADT, and then you stop. Now, I don’t tend to do 6 months. I actually tend to push to 9 to 12 months, but the reality of that is between 6 to 12 months. Based on the side-effect profile, that’s what I do.

What, I think, is very important, is for people, at least, to pay attention to testosterone recovery because there are two true rationales to do intermittent therapy, in my opinion. One is the side-effect profile, maximizing the quality of life, but you need to ensure that you’ve recovered testosterone in order for you to have quality of life. If we start someone age 70 on ADT for 6 months, that patient may, very well, not recover his testosterone for 1 year, 2 years, or 3 years. They may not be getting their shots, but they are castrated by definition. The quality of life continues to be down. So, I follow testosterone. Basically, during testosterone deprivation, only do PSA side-effect management. As soon as they go off, every 3 months I check testosterone, and PSA along the way. Once I know testosterone has recovered, then I know how long it’s going to take for the patient to actually recover their quality of life, and that is the period that I think patients value the most. Because once you have full testosterone, if I have to shut down your testosterone again within 3 months, then that patient really is not benefitting from intermittent therapy. On the contrary, if you go long and your PSA takes me 1 year to 2 years to restart ADT, that patient is benefitting from that approach.

And, the second, which is a biologic rationale from the breast models from the prostate cancer models, is can we delay the onset of castration-resistant disease by doing on and off cycles? And, I don’t think we have really validated that in a scientific manner, but we still believe that if you keep patients suppressed, there may be a national pressure, selected pressure, to actually isolate those clones of CRPC or an AR-null (androgen receptor–null) disease that may eventually end up becoming CRPC.

Transcript Edited for Clarity

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Transcript:

Raoul S. Concepcion, MD:
Aren’t there some institutions that are actually establishing that cardio-oncology, specifically, deal with that?

Alicia K. Morgans, MD, MPH: We have that, cardio-oncology, yes.

Jorge A. Garcia, MD: That’s a great point. I think that one of the challenges, that a lot of physicians in the community practices face, is who owns the patient? Often times, it’s urology driven, often times, it’s oncology driven. And, I think, most of us, who work at a multidisciplinary approach–style practice, believe that it doesn’t really matter who owns the patient. What is important is what do we do as a group for the patient. The patient is in the middle. We try to all maximize that outcome. I think to your point, Alicia, for instance, in our place, we have a cardio-oncology clinic, and we have many other resources that we utilize when we start ADT in patients, whether we do it for the intermittent style or we do it for continuous ADT. If you were to go to Boston, you may do a little more endocrine approach because they are big into bone health, and so forth. But, often times what we do, we do nutrition, we put them in contact with exercise with the health clinic, with the cardiology, to actually work on reduction of metabolic syndrome. We also do endocrine therapy for bone-specific things. If we are treating them, we actually need to do those things for the patient.

But, I think, when you think about rising PSA syndrome, one of the biggest challenges we face, as practitioners, is all the data that we have for ADT, in the biochemical recurrence N0 space, is all over the map—because some people have used absolute PSAs to make decisions on when you trigger that re-initiation of ADT. Some people have used testosterone recurrence, some people have used 6 months of ADT, which is, probably, in my opinion, the best data that we have. The data that I follow the most are Juanita Crook’s data from Vancouver, looking at if you start someone on a rising PSA, you could do 6 months of ADT, and then you stop. Now, I don’t tend to do 6 months. I actually tend to push to 9 to 12 months, but the reality of that is between 6 to 12 months. Based on the side-effect profile, that’s what I do.

What, I think, is very important, is for people, at least, to pay attention to testosterone recovery because there are two true rationales to do intermittent therapy, in my opinion. One is the side-effect profile, maximizing the quality of life, but you need to ensure that you’ve recovered testosterone in order for you to have quality of life. If we start someone age 70 on ADT for 6 months, that patient may, very well, not recover his testosterone for 1 year, 2 years, or 3 years. They may not be getting their shots, but they are castrated by definition. The quality of life continues to be down. So, I follow testosterone. Basically, during testosterone deprivation, only do PSA side-effect management. As soon as they go off, every 3 months I check testosterone, and PSA along the way. Once I know testosterone has recovered, then I know how long it’s going to take for the patient to actually recover their quality of life, and that is the period that I think patients value the most. Because once you have full testosterone, if I have to shut down your testosterone again within 3 months, then that patient really is not benefitting from intermittent therapy. On the contrary, if you go long and your PSA takes me 1 year to 2 years to restart ADT, that patient is benefitting from that approach.

And, the second, which is a biologic rationale from the breast models from the prostate cancer models, is can we delay the onset of castration-resistant disease by doing on and off cycles? And, I don’t think we have really validated that in a scientific manner, but we still believe that if you keep patients suppressed, there may be a national pressure, selected pressure, to actually isolate those clones of CRPC or an AR-null (androgen receptor–null) disease that may eventually end up becoming CRPC.

Transcript Edited for Clarity
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