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Saturday, December 26, 2009

Blog Updates for December 2009

Dec 25/09. In Testosterone Metabolism and Prostate Cancer we added (referring to the simple model in which testosterone "fuels" prostate cancer: An example of using this simple model is Gat's hypothesis [prostatecancerinfolink article] [PMID: 19737278] that an age-related malfunction can allow a very much higher than normal amount of testosterone to reach the prostate from the testes. By performing microsurgery to block this transmission he was apparently was able to reverse prostate cancer in 5 out of 6 patients. (Note that the models discussed below could lead to other explanations.)

Dec 22/09. In Biochemical PSA Recurrence we added: Trock et al (2008) [PMID: 18560003] [Full Text] present a retrospective study of 635 men with a median follow up of 6 years after recurrence and 9 years after surgery. They found that:
  • 22% of men with recurrence and no salvage therapy died in the follow up period vs.
  • 11% of those who had salvage radiation and
  • 12% of those who received salvage radiation + hormones
After case mix adjustment the group with radiation salvage had 3x the survival rate of the no salvage group. Salvage therapy had to be administered within 2 years of recurrence and PSA doubling time had to be less than 6 months for salvage radiation to be effective. The authors recommended that the results be validated in a randomized trial.

Stephenson published a nomogram for Recurrence after Salvage Radiotherapy that can be found in the section of that name on our Calculators page.

Dec 19/09. In Advice to the Newly Diagnosed we added: In a December 2009 NY Times article Natasha Singer writes:
A print advertisement for prostate cancer surgery at Mount Sinai Medical Center in Manhattan is typical of the way many elite research and teaching hospitals sell hope to the public.

"Our newest prostate specialist, ..., has pioneered a minimally invasive approach that allows him to retain the highest cancer cure rates with the lowest risk of side effects," says the ad.

Highest cure rates. Lowest risk. What evidence does the medical center have to back up such superlatives?
This doctor may be an excellent doctor, e.g. see [testimonial], but as the New York Times article goes on to say the claims in the ad are based on antecdotal remarks by patients. This represents a level of evidence that the FTC would never allow drug companies to use. On the other hand, non-profit medical centers can get away with claiming "highest cure rates" with virtually no evidence comparing the cure rate there and elsewhere.

Dec 15/09. In Radiation risks associated with Prostate Cancer we added: Estimating Mortality from CT Scans Using data from a large insurance database, in [Table 1] of [Full Text] published in Dec 2009 Archives of Internal Medicine, Berrington de Gonzalez et al estimated the risk of dying from CT scans to the abdomen at 5, 3 and 2 deaths for men age 30, 50 and 70 respectively per 10,000 CT scans. They further estimated that 29,000 excess cancers and 15,000 deaths in the US would occur due to the radiation exposure from CT scans performed in 2007 alone. The cancer and mortality numbers were based on CT scans to any part of the body, not just pelvic CT scans that might be done for urology, and excluded CT scans conducted after a diagnosis of cancer or scans performed in the last 5 years of life.

Actual Measured Dosages. A second study [Full Text] in the same Dec 2009 Archives of Internal Medicine issue examined the 11 most common types of CT studies in 1119 adult patients at 4 San Francisco Bay hospitals and concluded that actual dosages being given are substantially higher and more variable than previously thought:
We documented higher and more variable doses than what is typically quoted from the most common types of diagnostic CT studies performed in clinical practice. For example, the median effective dose of an abdomen and pelvis CT scan (the most common type of CT examination performed in the United States12) is often quoted as 8 to 10 mSv. Yet we found that the median dose of a routine abdomen and pelvis CT scan was 66% higher, and the median dose of a multiphase abdomen and pelvis CT scan was nearly 4-fold higher. Furthermore, we found substantial variation in doses within and across institutions, with a mean 13-fold variation between the highest and lowest dose for each CT study type included. Thus, depending on where an individual patient received imaging and the specific technical parameters used, the effective dose received could substantially exceed the median. While some of this variation may be clinically indicated to accommodate patients of different size or the specifics of the clinical question that was being addressed, the variation in effective dose was dramatic and of greater magnitude than widely considered acceptable, particularly considering that the patients were already stratified within relatively well-defined clinical groups. The variation in dose across the 4 clinical sites reflects site-specific methods of choosing different technical parameters to answer the same clinical question.
The data is shown in [Table 2] of that paper which shows that median dosages of actual measurements for routine abdomen-pelvis CT scans with contrast were 16mSv per scan ranging from 10mSv - 20mSv equating to about 220 chest radiographs. In [Table 4] they estimate one death per 660 pelvic CT scans given to men age 60.

Dec 9/09. In Advice to the Newly Diagnosed we added the following disadvantage of conservative treatment: Repeated biopsies can induce fibrosis making eventual nerve sparing treatment impossible. See Slide 11 of [Catalona 2009 NY AUA presentation].

Dec 8/09. In Prostate Cancer Calculators we added: In [Full text] [PMID: 19918337] Lowrance (papers) and Scardino (papers) discuss predictive models for prostate cancer covering methods that use risk classifications(e.g. d'Amico risk groups), tables (e.g. Partin tables), risk scores (e.g. CAPRA score), nomograms (e.g. Kattan nomograms) and systems pathology which refers to using a wider range of variables than the traditional clinical variables (e.g. Aureon Labs' Px method). See [Table 1]. Future methods will likely incorporate genetic inputs to improve prediction accuracy. The authors point out that the need to discretize variables into a number of groups potentially reduces the accuracy of risk classifications, tables and risk scores whereas nomograms do not suffer from this problem (however, whether this potential loss of prediction accuracy is material is not discussed).

Dec 8/09. Added to the Links box in the right margin on the "Guidelines - Eur" line this German guideline (in German): [de]

Dec 7/09. In PSA Screening and Early Detection Part 2 we add regarding the USPTF recommendation against screening: A rebuttal by Dr. William Catalona to the task force recommendations appeared in the Washington Post [full text] on August 26, 2008 page A13 and discussed in greater detail in his [2009 Northwestern University Presentation] where he disputes the over diagnosis figures commonly cited and points out that the ESPRC trial provided level 1 evidence in favor of screening and should not be confused with the PLCO trial which was uninformative due to contamination (i.e. many men in the control group has been screened or pre-screened). Also see these articles by Catalona in the Winter2009 issue of Quest. [article3] and [article4].

Dec 6/09. In PSA Screening and Early Detection Part 2 we add: Effect of DRE has been disputed; however, Dr. William J. Catalona" says patients should wait 48 hours after a DRE before getting a PSA test. [Quest Fall 2009]. The time needed to wait for PSA testing after biopsy is said to be one month by each of these two papers (on PSA and fPSA) [PMID: 12479122], [PMID: 10197848] while this article says 8-12 weeks. Dr. William J. Catalona" says patients should wait 6-7 weeks after a biopsy before getting a PSA test.

Dec 5/09. In Biochemical PSA Recurrence we added: One phenomenon to note is that frequently there is a temporary rise in PSA after radiation thought to be due to inflammation induced by the procedure itself. This rise is known as PSA Bounce and is further discussed [here].

Dec 5/09. In Advice to the Newly Diagnosed we added: North Carolina Prostate Cancer CoalitionThe NCPCC in conjunction with Dr. J. Moul has put together a set of materials for the newly diagnosed available [here]. These include [Newly Diagnosed Patient Workbook] and a set of [guidelines and other documents]

Dec 5/09. Added [PCNCC Screening] to the "Guidelines - US" line in the Links box in the right margin.

Dec 3/09. In How Long Can Prostate Cancer Treatment be Delayed After Treatment we added a number of comments from a recent NY AUA presentation by Catalona:

In a 2009 NY AUA presentation William J. Catalona (papers) pointed out that the Warwick study's definition of curable vs. non-curable was based on statistical criteria rather than on specific pathology features and so the results may be less meaningful. See slide 29 of [Catalona presentation].

A 2006 study by Freedman et al at John Hopkins University specifically studied the effect of wait time from biopsy to surgery and found that "time from biopsy to surgery was not significantly related to high grade disease in the RP specimen, positive surgical margins or extraprostatic extension (all p-trend >0.05)"; however, if the patients waited for more than 6 months then "after adjustment for multiple clinical covariates a longer time from biopsy to surgery was significantly associated with an increased risk of biochemical progression (p-trend = 0.002)". In the same [Catalona presentation] cited earlier Catalona pointed out that after the 180 day period the risk of cancer progression after treatment increased to be 2.73x those who had immediate treatment.

The [Catalona presentation] cited earlier points out that criteria for detecting significant prostate cancer are much more accurate than criteria for detecting low risk prostate cancer. He points out that there are no validated criteria for low risk disease and as far as the existing non-validated criteria are concerned when they conclude low risk disease they are wrong about 30% of the time. The danger is that if one delays too long then the window of opportunity when the cancer is most treatable will be lost or else more aggressive treatment will be necessary with consequent worse side effects.

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