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Select Excerpts from the Interview
Track 2
For example, Dr Tom Stamey, who’s contributed a tremendous amount to our field and to the use of PSA, came out two years ago and basically said that PSA was no good (Stamey 2004). That incident set the field on edge. The reality is that PSA is still the best marker we’ve ever had, but it certainly isn’t perfect, and we have to use it in a smarter way as we move further and further into the PSA era. With that background, we tried to see if the rate of change of PSA was more predictive of prostate cancer than PSA itself. Most men that we see now already know their PSA level. They’ve seen their primary care doctor or their internist or even their urologist, and they have had a series of PSA tests. So can we look at that change to predict prostate cancer? The bottom line — with a large data set including men of various ages — is that the rate of PSA change with or without cancer is different for younger men than for older men. Younger men have a lower slope for their PSA — slower-rising PSA levels. Those subtle rises in young men are more predictive of prostate cancer because BPH isn’t as common and there isn’t as much prostatitis in this group. Fewer confounding conditions are present. We’re finding that if you measure PSA at 40 to 59 years of age — in that 20-year time span for a man — a change in PSA of more than about a half a point per year is predictive of prostate cancer. The reason that’s important is that 14 years ago, Bal Carter from Johns Hopkins was the first person to propose PSA velocity as a screening tool for prostate cancer (Carter 1992). Bal said that if a patient’s PSA level increased more than about three quarters of a point per year, that was a red flag for prostate cancer. We’re finding that Bal’s data do hold for older men, but for younger men in their forties and fifties, it’s probably more appropriate to use a slightly lower cut point for PSA velocity, to the tune of about 0.4 to 0.6 ng/mL. We’re fine-tuning this right now in an effort to produce something that’s easy to remember so doctors in the trenches can use it.
Track 4
The answer remains controversial. Our data from 2004 indicated that you certainly couldn’t be criticized for starting hormonal therapy early for men at high risk, such as those with a rapid PSA doubling time or those with higher Gleason scores, because they’re not going to do well with watchful waiting (D’Amico 2004). More recently, Steve Freedland, who recently joined us at Duke, published a nice paper in JAMA (Freedland 2005), in which he examined the Johns Hopkins data set (2.2). It was actually a follow-up to the Pound paper (Pound 1999). The bottom line was that Steve created a nomogram, which showed 10-year mortality after PSA recurrence. In other words, he evaluated patients who had a biochemical recurrence after surgery and then asked what the chances were of dying from prostate cancer 10 years later. He found that PSA doubling time, Gleason score and time of PSA recurrence (ie, earlier versus later than three years after the surgery) were good predictors of death from prostate cancer. The good news is that we can predict who will die of prostate cancer. The bad news is that we’re still not sure if we can alter the natural history if we put those patients on hormonal therapy. Combining the data from Steve Freedland’s paper with those of our paper from the military would suggest that using hormonal therapy for those high-risk PSA recurrences is reasonable, but we need a randomized trial to address the question.
Track 5
Nevertheless, the outcome comparisons between robotic prostatectomy and what I still consider the gold standard — open radical prostatectomy through a small, low, midline incision — have not demonstrated better outcomes with the robotics (Tewari 2006). In fact, no good outcome studies have evaluated this. We’re desperately trying to do that at Duke. It’s not a randomized study; however, we’re trying to get all the patients who undergo either type of surgery to fill out thorough quality-of-life instruments before the surgery and then periodically over the first two years. So far, we’re not demonstrating any statistically significant benefits in using the robot, except for lower blood loss with no difference in transfusion rates. For those men who have strenuous, physical-labor type jobs, the robotic surgery might confer about a five- to seven-day benefit in the ability to return to full activity. Other than that, we haven’t proved the difference in potency rates, and we haven’t proved a difference in continence rates. We haven’t shown a difference in hospital stay, but we’ve definitely shown a difference in cost. The robotic surgery is a tremendously more expensive procedure for our country and our healthcare system. The disposables associated with its use add to the cost, and the operating room time alone — even in the best of hands — adds an hour to an hour and a half to an open prostatectomy. Track 8
It is interesting that you bring that up because I’m trying to reevaluate that issue using our database. When I was at Walter Reed, we made a first-pass effort observing the natural history of that issue (Chen 2004). The bottom line was that survival was much longer among those men than among the traditional patients with hormone-refractory prostate cancer — to the tune of about a five-year survival versus two to three years for the men with more traditional hormone-refractory metastatic disease. |
Editor Meet The Professors Case 1: from the practice of Case 2: from the practice of Case 3: from the practice of Richard Davi, MD Case 4: from the practice of Dr Nieder Case 5: from the practice of Benjamin M Tripp, MD INTERVIEWS Judd W Moul, MD Daniel P Petrylak, MD
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