You are here: Home: PCU 1 | 2006: Gregory S Merrick, MD

Tracks 1-16
Track 1 Introduction
Track 2 Influence of PSA velocity on survival after local therapy
Track 3 Therapeutic approach to patients with low-risk disease
Track 4 Brachytherapy techniques
Track 5 Medical management of patients treated with brachytherapy
Track 6 Erectile dysfunction in patients treated with brachytherapy
Track 7 PSA levels after brachytherapy
Track 8 Clinical algorithm for the treatment of patients with high-risk disease
Track 9 Clinical and research strategies for patients with intermediate-risk disease
Track 10 Postprostatectomy radiation therapy
Track 11 Management of PSA recurrence
Track 12 Future role of chemotherapy for patients with prostate cancer
Track 13 Key current clinical research questions in prostate cancer
Track 14 Brachytherapy with or without external beam radiation therapy in patients with intermediate-risk disease
Track 15 Case discussion: A 58-year-old man with Gleason 8 prostate cancer and seminal vesicle invasion
Track 16 Rehabilitation after brachytherapy

Select Excerpts from the Interview

Track 2

DR LOVE: Would you discuss your treatment approach for a patient with low-risk prostate cancer who has a rapid PSA velocity?

DR MERRICK: It’s been interesting to evaluate the influence of PSA velocity on the survival parameters — biochemical, cause specific and overall. Multiple studies have confirmed that a PSA velocity of greater than 2 ng/mL in the year prior to diagnosis significantly affects those survival outcomes (D’Amico 2005; [2.1]).

DR LOVE: How have you incorporated those data into your practice?

DR MERRICK: Until these data became available, rapid PSA velocity hasn’t been something that we have considered. For patients with low-risk disease, the cause-specific survival in our brachytherapy series is 99.5 percent at 10 years.

It’s going to be difficult to alter that outcome by looking at any other parameters. What remains to be determined is how many patients fell into the cohort of this rapid PSA velocity. We have not yet examined that information.

Patients with low-risk disease are treated with monotherapy. Patients with high-risk disease receive combined-modality therapy. For patients with intermediate-risk disease, our prospective randomized trials are trying to prove that we can eliminate the supplemental external beam radiation.

Track 8

DR LOVE: Would you describe your general algorithm for a patient with high-risk prostate cancer?

DR MERRICK: In our program, high-risk disease is defined as two or three adverse prognostic factors: a clinical stage greater than or equal to T2c, a PSA greater than 10 ng/mL and a Gleason score greater than or equal to seven. In our series, all of those patients receive pelvic radiation therapy along with a palladium boost. A high percentage of those men have also received androgen deprivation therapy.

Retrospectively, we have been able to show that the men who received androgen deprivation therapy have a statistically significant improvement in eight-year biochemical progression-free survival of approximately eight percent (Merrick 2005).

We will begin a prospective randomized trial in our Wheeling and Seattle group later this year, which will randomly assign patients with a Gleason score of seven to nine and a PSA of 10 to 20 ng/mL to 45 Gray of pelvic radiation therapy and a palladium boost with or without nine months of androgen deprivation therapy. My expectation is that androgen deprivation therapy will improve biochemical outcome.

DR LOVE: Which specific androgen deprivation regimen do you use?

DR MERRICK: We’re strong proponents of total androgen suppression. These patients will receive nine months of an LHRH agonist, either goserelin or leuprolide, along with four months of bicalutamide at 50 mg daily. For all of my patients, I use total androgen suppression for four months. If the PSA is undetectable at that time, we continue the LHRH alone for the remainder of the treatment.

In the community, what we often see is an LHRH agonist with a short course of an antiandrogen to block the flare. I have not been a proponent of that approach. If you look at the RTOG studies, especially the studies that Mack Roach has conducted, they’ve all used total androgen suppression (Roach 2003; Hanks 2003).

DR LOVE: It seems that total androgen blockade is not used in the community as much as it’s used in academia. Is that your impression?

DR MERRICK: It is. I believe the real key with prostate cancer treatment is to cure the patient up front. We can talk about treatment costs, but we know that if we treat a patient and cure him with a radical prostatectomy or brachytherapy or a similar combination, we’re probably talking about a cost of $15,000 to $40,000.

Data have been published indicating that once a man experiences biochemical failure, from failure to death it costs the healthcare industry around $150,000 to $160,000. The curative treatment is always cheap in comparison to treating patients for the remainder of their lives in a palliative setting.

DR LOVE: Do you think financial issues are the main reason total androgen suppression is not used much?

DR MERRICK: This regimen does add cost for the patient. Therefore, often the choice to use it depends on whether the patient can financially afford it.

Track 11

DR LOVE: How do you approach the management of PSA relapse?

DR MERRICK: I’m relatively conservative in managing PSA recurrences. If we’re going to treat those patients with hormonal therapy, I do not recommend androgen deprivation therapy until the PSA doubling time becomes less than 12 months.

Once the PSA doubling time is less than 12 months, we have to seriously consider androgen deprivation.

The big question then is continuous versus intermittent treatment. I have always been a proponent of intermittent androgen deprivation therapy because of the better quality of life associated with it.

DR LOVE: Would you describe exactly how you use intermittent therapy?

DR MERRICK: We leave a patient on androgen deprivation therapy for nine to 12 months. If the PSA becomes undetectable, then we stop the androgen deprivation therapy until we see the PSA exceed some arbitrary PSA cut point, such as 10 or 15 ng/mL.

Track 12

DR LOVE: What are your thoughts about the potential future role of chemotherapy earlier in the natural history of the disease?

DR MERRICK: This is a reasonable question to evaluate, but it has to be done in a prospective randomized trial. The studies that Dr Petrylak and Dr Tannock performed among patients with hormone-refractory disease were important for a large number of patients. However, it’s also important to remember that the differences in overall survival were two months (Petrylak 2004; Tannock 2004). These weren’t home runs we were hitting, but they were small steps, which doesn’t minimize the importance of their work. However, I do think chemotherapy should, in select cases, be considered earlier, but it must be done in the setting of prospective randomized trials, not outside of a protocol.

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Editor
Neil Love, MD

Mark S Soloway, MD
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Gregory S Merrick, MD
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Richard G Stock, MD
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Anna C Ferrari, MD
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Faculty Disclosures

CME Information

Editor's Office