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Medical Forum / Diseases and Disorders / Prostate Cancer / December 2004Obtaining ultrasensitive PSA testing
Hello to the group. I have a question for anyone who has found a strategy for dealing with this problem. I am located in CT and have been getting ultrasensitive PSA tests (MRL of .01 ng/dl) through Dianon/Labcorp (I had an RP). Nobody else in CT offers the ultrasensitive PSA test that I know of. More than half the time, they do the wrong test, and even if they do the correct test they don't cc the results to me (even though it says so on the lab slip). There are valid reasons for me to get the ultrasensitive test (my MD agrees); has anyone found a solution in the Northeast? Thanks! Feel free to e-mail responses.  SignatureFrom rraport3 at infionline.net (delete the three) > Hello to the group. I have a question for anyone who has found a strategy > for dealing with this problem. [quoted text clipped - 11 lines] > > Feel free to e-mail responses. Richard, My first response didn't make it. I don't have an answer to your question, but I'm curious about the ultra sensitive test. What is the added value? Would you be willing to have radiation or hormones prior to reaching PSA of 0.1? Steve Hi Steve...There are several potential advantages to ultrasensitive PSA testing. First, it gives you more time and data to use in the decision making process. I think we'd all agree that earlier treatment of recurrence is generally more effective than later treatment, so with ultrasensitive testing you can usually be positioned to make a call on recurrence (after RP) somewhat before or when the PSA hits 0.2. Second, for RP, RT and HT (Dr. Strum uses the ultrasensitive test for his HT patients) treatment, the lower the PSA the better. Again, the ultrasensitive test will give you data to make a judgement on treatmeant efficacy. Along these same lines, "how low you go" has also been used to assess the risk of long-term biochemical freedom from disease...Best wishes and good health, Ron > Hi Steve...There are several potential advantages to ultrasensitive PSA > testing. First, it gives you more time and data to use in the decision > making process. I think we'd all agree that earlier treatment of > recurrence is generally more effective than later treatment, so with > ultrasensitive testing you can usually be positioned to make a call on > recurrence (after RP) somewhat before or when the PSA hits 0.2. Ron, I think that there is still considerable controversy about that. As you may know, Walsh presents data in his book which suggests that nothing is lost if one waits a bit to begin followup radiation therapy. He presents other data suggesting that waiting to begin hormone therapy makes sense. I'm aware that there are some more recent results which suggest that in certain situations beginning hormone therapy early makes a difference. But the trouble is that it is very easy to compare apples and oranges in this sort of thing. I think it is fair to say that we don't really know at present if early hormone therapy makes a difference in situations detectable by ultrasensitive testing. > Second, for RP, RT and HT (Dr. Strum uses the ultrasensitive test for > his HT patients) treatment, the lower the PSA the better. Again, the > ultrasensitive test will give you data to make a judgement on > treatmeant efficacy. Along these same lines, "how low you go" has also > been used to assess the risk of long-term biochemical freedom from > disease...Best wishes and good health, Ron The argument my erudite doc makes for early post-RP adjuvant HT is that it has a better chance of permanently eradicating an undetectable micromet now than it does an established small tumor pumping out detectable PSA later. He feels it has a better shot at a few thousand cells than at a few million (billion?). (In my case his advice is based on my one seminal vesicle involvement, bilateral lobe involvement, and Grade 8, but it wouldn't surprise me if he advised early HT any time the statistics implied any chance of recurrence.) I like Walsh's approach better . . . unless it kills us, and he doesn't think it will. It makes sense to me to watch the ultrasensitive PSA tests (quarterly?) and look for a discernable pattern that may indicate real data rather than random physiological fluctuations or test vagaries. If we can see a genuine PSA ramp, even if it's in the second decimal point, maybe it's time to act; my PSA over the past few years formed a beautiful (technically), consistent curve, leaving no doubt that it was real data. If I saw a curve like that in my ultrasensitive PSA data, I would be much more inclined to try at least try HT based more on my doc's philosophy than on Walsh's experience . . . with more research, of course. Maybe Walsh himself may think differently in locally advanced cases (such as T3c) with some measurable threat of recurrence. I.P. > > Hi Steve...There are several potential advantages to ultrasensitive PSA > > testing. First, it gives you more time and data to use in the decision [quoted text clipped - 15 lines] > that we don't really know at present if early hormone therapy makes a > difference in situations detectable by ultrasensitive testing. The question of early HT treatment seems to me to have superficially reasonable answers on each side. On the side of early treatment: Perhaps micrometastases can be not just controlled, but killed, if the number of metastatic cells is still extremely small. On the side of late treatment: Conditioning PCa cells to hormone deprivation early on may accelerate the development of androgen indpendent cancer cells. So we can make up theories on each side. What we really need now is facts. Unfortunately, we don't have them. Alan Which readily takes us back to an earlier post somewhere, which quoted one of the > The question of early HT treatment seems to me to have > superficially reasonable answers on each side. [quoted text clipped - 15 lines] > > Alan Belay my truncated post; when my computer decides to SEND, it SENDs, no matter what I tell it. As I was starting to say, that's a vote for choosing treatment based on known SEs rather than hypothetical or statistical benefits. At least one author supports it, and it has merit in many cases. And although doctors who define their success rates by heartbeat may not like it, it may become increasingly common as more people beome aware of PSA and PC and SEs. I.P. > The question of early HT treatment seems to me to have > superficially reasonable answers on each side. [quoted text clipped - 13 lines] > So we can make up theories on each side. What we really > need now is facts. Unfortunately, we don't have them. Here is the example I used to argue w/ my uro re getting the ultrasensitive test: You have 3 quarterly tests done w/ the standard assay and get 3 straight at .2. Great - nothing happening - right? Well, let's say that portions of the samples of each of those tests were also subjected to the ultrasensitive test and came back .15, .19, and .24. Note that all of these round off to the same .2 using the standard assay. Now what do you see? A PSA rise of 60% over a 6-month period, a PSADT of less than a year. Totally different story. Bill Denton RP 2/12/02 Memphis > Here is the example I used to argue w/ my uro re getting the > ultrasensitive test: [quoted text clipped - 5 lines] > you see? A PSA rise of 60% over a 6-month period, a PSADT of less than > a year. Totally different story. Bingo! Uncomfortable with some things happening -- and not happening -- with my rad onc, I consulted a med onc (contrary to the former's advice) last Friday. What an eye-opener! Among other things, she did not much like the 0.1 PSA result of the 11/22 test, saying that the ADT I'm on should have forced it much lower. The ADT may be failing (testosterone too high, too). Yesterday, I had blood drawn for another T assay, plus "ultrasensitive" PSA and PAP. The latter test should have been done a year ago, BTW. I am to have ultrasensitive PSA's done monthly for the next six months. We shall see. As for the T assay, the 11/22 reading was 36 ng/dL. This is almost twice as high as the standard (per Strum and the med onc) of <20. The rad onc says that "many of the studies have also used <50 as a cut-off." Having never heard of such a thing, I intend to do some research on this. Anyone have any input? Regards, Steve J __ "Never give in--never, never, never, never, in nothing great or small, large or petty, never give in except to convictions of honour and good sense. Never yield to force; never yield to the apparently overwhelming might of the enemy.'' --Sir Winston L. S. Churchill Yup: I'd be leary of too much bias in any physician who advised me not to consult another type of physician for a reality check. And one author I ran across (I'm guessing Strum or Scholz) said that although T must be below 20 for ADT to be really effective, it may be even more effective if we can lower T even further. I.P. "Stephen Jordan" <mycroftscj@earthlink.net> wrote > > Uncomfortable with some things happening -- and not happening -- with my > rad onc, I consulted a med onc (contrary to the former's advice) last > Friday. > Anyone have any input? On December 21, I.P. Freely replied to me: > Yup: I'd be leary of too much bias in any physician who advised me not to > consult another type of physician for a reality check. And one author I ran > across (I'm guessing Strum or Scholz) said that although T must be below 20 > for ADT to be really effective, it may be even more effective if we can > lower T even further. Dunno about Scholz. Do know that Strum states in several places in his book that T must be lowered to *less than* 20 ng/dL. Guess that at least indirectly reinforces what IP sez. One way to do that would be to supress the T that is manufactured by the adrenal cortexes. This is ~10% of total T. It is not affected by LHRH agonists such as Lupron. It is affected by Casodex and Proscar. CHB (aka "ADT3," using Casodex, Proscar and an LHRH agonist) means that both the testicular and the adrenal sources of T are reduced to an effective zero. That's *lower* than castrate level. BTW, IP has elsewhere mentioned mebbe going to Casodex monotherapy. That would have a list of SE's all its own. I suggest that IP might want to make up his mind that there is nothing he can do that does not have SE's. And that includes doing nothing :-( Regards, Steve J But the expected Casodex SEs (and thus QOL impact) are far less than those of "normal" ADT, and WW often has no "SEs" for years, whereas ADT SEs are NOW and sometimes IN YER FACE. I.P. "Stephen Jordan" <mycroftscj@earthlink.net> wrote > > BTW, IP has elsewhere mentioned mebbe going to Casodex monotherapy. That > would have a list of SE's all its own. I suggest that IP might want to > make up his mind that there is nothing he can do that does not have > SE's. And that includes doing nothing :-( On December 21, the top-posting I.P. Freely replied to me: > But the expected Casodex SEs (and thus QOL impact) are far less than those > of "normal" ADT, and WW often has no "SEs" for years, whereas ADT SEs are > NOW and sometimes IN YER FACE. To my brother IP: I am on ADT, and can live with the SE's in lieu of dying a horrible death. Today, I met with my cardiologist for a six-month followup. I broke down. It was the ADT. She was understanding. And my heart is in great condition. It's your body, your prostate, and your life. And you have sole responsibility for your treatment. The choice to which you have pretty much committed would not be mine. But that's what makes horse races. Regards, Steve J If I could find any indication that early post-RP adjuvant HT in the absence of symptoms or PSA would add to my quality time on the planet, I'd change my tune. I.P. "Stephen Jordan" <mycroftscj@earthlink.net> wrote > > It's your body, your prostate, and your life. > > And you have sole responsibility for your treatment. > > The choice to which you have pretty much committed would not be mine. Excellent argument. Same for me. My .07, .05 (-28%), .06 (+20%) looks a whole lot better at .1, .1, .1 SignatureProstate Cancer Survivor (so far), not a doctor PSA 16 10/17/2000 @ 46 Biopsy 11/01/2000 G7 (3+4), T2c RRP 12/15/2000 G7 (3+4), T3bN0M0 PSA .1 .1 .1 .27 .37 .75 EBRT 05-07/2002 @ 47 PSA .34 .22 .15 .21 .32 Lupron (1 mo) 07/21/2003 @ 48 PSA .07 .05 .06 Lupron (3 mo) 8/03 (48), 12/03, 4/04 (49), 09/04 (50) non Illegitimi carborundum > Here is the example I used to argue w/ my uro re getting the > ultrasensitive test: [quoted text clipped - 9 lines] > RP 2/12/02 > Memphis I just realized, by arbitrarily moving the decimal another notch, I would be 16, 0, 0, 0, 0, 0, 1, 0, 0, 0, 0, 0, 0, 0. > Excellent argument. Same for me. My .07, .05 (-28%), .06 (+20%) looks a > whole lot better at .1, .1, .1 [quoted text clipped - 12 lines] > > RP 2/12/02 > > Memphis We spend 6 months in MA and 6 months in FL and had a problem with getting consistent ultrasensitive PSA results. . Finally settled on Quest that has labs in both states. Had a conference call with both Andover MA main lab and Tampa FL main lab and they advised me to always request the "ultra sensitive enhanced Nichols" from the Quest Nichols lab in California. The code number for the test is 6791N. This test is sensitive to 0.01 . The phone for the Nichols lab is 1-800-553-5445 . Hope this helps...Bowich > We spend 6 months in MA and 6 months in FL and had a problem with > getting consistent ultrasensitive PSA results. [quoted text clipped - 8 lines] > . > Hope this helps...Bowich Hi Bowich, What do you mean by "consistent"? Were the result varying? If so, in what range? My Uro claims they're accurate down to 0.00 but I'm skeptical. Thanks Don |
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