DR DEREK WILKE (Orcid ID : 0000-0003-1803-5765)

Article type : Original Research Article

Accepted Article
Testosterone Suppression With Luteinizing Hormone-Releasing Hormone (LHRH) Agonists

in Patients Receiving Radiotherapy for Prostate Cancer

Wilke Derek1, Patil Nikhilesh1, Hollenhorst Helmut1, Bowes David1, Rutledge Robert1, Ago

Casely1
1
Department of Radiation Oncology, Dalhousie University, QE II Health Sciences Centre,

Halifax, Nova Scotia, Canada

Key words: prostate cancer, radiation therapy, testosterone suppression, LHRH agonists

Conflict of Interest: Dr. Wilke reports grants and personal fees from Allergan, grants and

personal fees from AstraZeneca, grants and personal fees from AbbVie, personal fees from

Amgen, personal fees from Astellas, personal fees from Jansen, grants and personal fees

from Paladin Labs, grants and personal fees from Sanofi, outside the submitted work.

Dr.Patil reports personal fees from Ferring Pharmaceuticals outside of the submitted work.

Drs. Hollenhorst, Bowes, Rutledge, and Ago have no conflicts of interest.

This article has been accepted for publication and undergone full peer review but has not
been through the copyediting, typesetting, pagination and proofreading process, which may
lead to differences between this version and the Version of Record. Please cite this article as
doi: 10.1002/phar.2084
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 Corresponding author:

Derek Wilke
Accepted Article
Radiation Oncologist, Assistant Professor

Dalhousie University, Department of Radiation Oncology

2027, Dickson Building

5820 University Ave

Halifax, Nova Scotia, Canada B3H 1V7

Email: [email protected]

This work was presented as a poster presentation at the American Society of Clinical

Oncology, Genitourinary symposium, San Francisco, January 6-9, 2016

Abstract

Objectives

To characterize the probability of testosterone escape during a course of radiotherapy and

androgen deprivation (ADT) in patients with prostate cancer, and examine predictors of

testosterone escape, the prostate specific antigen (PSA) levels during testosterone escape,

and the impact of testosterone escape on outcome.

Patients and methods

To participate in the database review, necessary data included: (i) type of luteinizing

hormone-releasing hormone agonist (LHRHa) administered, date of initiation, and date of

cessation or duration of therapy, (ii) radiotherapy information (start date and dose) with at

least 6 months of follow-up after radiotherapy, (iii) had to have radiotherapy to the prostate

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 or prostate bed, and (iv) had to have a least one serum testosterone and PSA

measurement.
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Results

Five hundred sixty patients in the database were identified as being treated with

radiotherapy and ADT. Three hundred seventy-five patients had at least one measurement

of testosterone and PSA, and the type of LHRHa used could be determined in 361 patients.

Median follow-up of patients still living was 4.7 years. The median number of testosterone

measurements per patient was six. The incidence of testosterone escape per patient course

of treatment was: buserelin 9.3%; goserelin 10.5%; intramuscular leuprolide 11.5%;

leuprolide subcutaneously 23.9%; triptorelin 6.7% (p=0.02). There was no difference in

either biochemical failure-free survival or overall survival in patients stratified by

testosterone escape. The modal PSA level during a testosterone escape was an

undetectable PSA.

Conclusions

An undetectable PSA does not rule out the presence of higher than desired levels of

testosterone during ADT. In this cohort of patients, there appears to be no impact of

testosterone escape on either biochemical relapse-free survival or overall survival.

Testosterone suppression has been the mainstay of treatment of locally advanced and

recurrent prostate cancer. Luteinizing hormone-releasing hormone agonists (LHRHa) and

antagonists, with or without oral anti-androgens have been successfully accomplishing this

for decades. LHRHa have reasonably been assumed to produce testosterone suppression,

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 most of the time. However, 6–13% of the time, patient’s serum testosterone levels can go

above 1.74 nmol/L, or 50 ng/dL, resulting in, what is commonly defined as, a testosterone
Accepted Article
escape.1-3 A recent analysis of a large randomized study of patients with recurrent,

nonmetastatic, prostate cancer demonstrated that patients who achieve a low nadir serum

testosterone (<0.7 nmol/L or <20 ng/dL) in the first year of androgen suppression have a

superior cause-specific survival and a longer time to castration resistance, compared with

patients who have not.4 There is also evidence that ideally, testosterone levels should be

suppressed to levels below 1.1 nmol/L or 32 ng/dL ,3,5 in order to maximize survival.

This study was performed on patients with locally advanced or recurrent prostate

cancer who had a prospective measurement of testosterone as part of their treatment with

testosterone suppression and radiotherapy. We hypothesized that patient factors could

predict for testosterone escape and that testosterone escape might predict for adverse

outcomes. We were also interested in investigating what the serum level of prostate-

specific antigen (PSA) was at the time of testosterone escape, and if an undetectable PSA

would rule out testosterone escape negating the need for testosterone monitoring

especially during the time period of the adjuvant, long-term testosterone suppression.

Methods

Subjects

A retrospective chart review was conducted on patients diagnosed with nonmetastatic

prostate cancer who were treated with ADT and RT. Patients were identified from the

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 clinical database of those seen by radiation oncologists at the QE2 Health Sciences Centre in

Halifax, Nova Scotia. Data missing from the database was supplemented by hospital chart
Accepted Article
review. Serum testosterone measurements within one month of the initial injection of the

LHRHa were excluded to rule out testosterone elevation due to the initial flare. All

testosterone values above 1.74 nmol/L (which was defined as a testosterone escape) were

reviewed against the clinical record and excluded from analysis if there was a documented

administration error or delay in administration of the scheduled dose of LHRHa.

Treatment

To participate in the study, necessary data included: (i) type of LHRHa, date of initiation, and

date of cessation or duration of therapy, (ii) radiotherapy information (start date and dose)

with at least 6 months of follow-up after radiotherapy, (iii) had to have radiotherapy to the

prostate or prostate bed, and (iv) had to have a least one testosterone and PSA

measurement. Testosterone and PSA measurements were intended to be done every three

months while the patient underwent ADT. After May 2007, there was a policy that if a

testosterone escape occurred, oral bicalutamide 50 mg daily would be re-introduced until

repeat testosterone measurements revealed that the testosterone levels were less than

1.74 nmol/L.

Statistics

The primary end point of this exploratory analysis was to investigate if testosterone escape

had an impact on biochemical-free relapse rates. Biochemical failure was defined as the

‘nadir +2’, or Phoenix definition. This definition defines biochemical failure as when the

serum PSA level reaches a value of 2 or greater, above the lowest serum PSA level that the

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 patient has achieved after treatment was completed.11 The date of biochemical failure is the

date that the serum PSA was measured when it reached a value of 2 or greater, above the
Accepted Article
lowest serum PSA level achieved after treatment was completed. Time-to-event survival

analyses were conducted using the Kaplan-Meier method. Comparison of groups in the

survival analyses were conducted using the Log-Rank test. Analysis of categorical variables

was accomplished using Fisher’s Exact test (where the expected value in any one cell was

less than 5), or the Chi-Square test, where appropriate. Pairwise comparisons were

conducted using logistic regression, and where there were more than two levels in the

response variable, multinomial logistic regression was used. Analysis of continuous variables

was conducted using analysis of variance with a corrected p value and using Bonferroni’s

method for multiple pairwise comparisons.

Results

Five hundred sixty patients in the database were identified as being treated with

radiotherapy and ADT. Three hundred seventy-five patients had at least one measurement

of testosterone and PSA, and the type of LHRHa used could be determined in 361 patients.

Median follow-up of patients still living was 4.7 years. The median duration of LHRHa

treatment was 2.02 years. The median number of testosterone measurements per patient

was six. The patients who received leuprolide subcutaneously (SC) or triptorelin received a

slightly higher dose of radiotherapy than patients receiving the other LHRHa treatments

(median dose of 73 Gray versus 70 Gray, p=0.0003), and most patients treated with

leuprolide SC received intensity modulated radiotherapy, whereas, most other patients

received 3-dimensional conformal radiotherapy.

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 Table 1 illustrates that there were no differences in age, stage, Gleason score,

baseline PSA, or number of patients who received postoperative treatment across LHRHa
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treatment groups. Younger age was a predictor for patients having higher maximum

testosterone values during their course of ADT (p value on analysis of variance = 0.01,

analysis not shown). Of the 13.8% of patients in the cohort that experienced a testosterone

escape, those patients less than 67.5 years of age accounted for 9.1% of escape events

whereas older patients accounted for only 4.7% of events, nearly half the rate of

testosterone escape in the patients whose age was less than 67.5.

Table 2 illustrates that there was a higher number of patients with testosterone

values above 1.75 nmol/L in the patients receiving leuprolide subcutaneously on univariate

analysis compared with the other agents (24% for leuprolide SC compared with 6.6-11.5%

for the other LHRHa treatments).

Univariate logistic regression revealed that increasing age and fewer number of

testosterone measurements were associated with statistically significant lower testosterone

categories. Duration of ADT was not different between the different LHRHa treatments

(analysis not shown). Depot duration and the likelihood of a testosterone escape cannot be

analyzed as 96% of the patients on leuprolide SC were on a 6-month depot and 65 to 100%

of patients on the other LHRHa treatments were on 3-month depot injections; the

differential effect of LHRH agonist type versus depot duration cannot be separated in this

study.

In patients with six or fewer testosterone measurements, the probability of

testosterone escape was 0 to 9% across LHRHa treatments, whereas in patients with more

than 6 measurements the probability of testosterone escape was in the range of 10 to 26%.

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 The comparisons within and across tables where not statistically significant, but when

number of testosterone measures were analyzed as a continuous variable in logistic

Accepted Article
regression (a more robust analysis) it was a significant predictor.

Table 3 illustrates when a multinomial logistic regression model was analyzed

incorporating age, number of testosterone measurements, and type of LHRHa. Age and

number of testosterone measurements remained statistically significant to predict

testosterone suppression, whereas overall type of LHRHa utilized did not. In a subgroup

analysis, there was a suggestion that there is better testosterone suppression with

triptorelin compared with leuprolide SC, however this was not statistically significant when

corrected for multiple pairwise comparisons, and was therefore only for hypothesis

generation.

Biochemical-free relapse rates of patients with maximum testosterone values less

than 0.70 nmol/L, 0.70 nmol/L to 1.74 nmol/L or greater than 1.74 nmol/L, were not

statistically different (Log-Rank p value = 0.26) using the ‘nadir +2’ or Phoenix definition. In

addition, the overall survival rates of patients with maximum testosterone values less than

0.70 nmol/L, 0.70 nmol/L to 1.74 nmol/L or greater than 1.74 nmol/L were not statistically

different (Log-Rank p value = 0.38).

PSA values at the time of testosterone escape are summarized in Figure 1 which

illustrates that the PSA at the time of testosterone escape (> 1.75 nmol/L; 69 testosterone

escapes in 50 patients) was relatively low. The modal PSA level was in the undetectable

range (representing 25% of the PSA values), with a median PSA of 0.1 and a mean PSA of

0.94. The median testosterone level at the time of testosterone escape was 2.1 nmol/L, with

the modal value being 1.8 nmol/L.

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 Discussion

Whereas it is more comforting to clinicians to assume that all testosterone lowering agents
Accepted Article
work perfectly, to suppress testosterone to castrate levels, this may not be the most robust

assumption for our patients. Some clinicians pragmatically believe that if the PSA is

undetectable, then there should be no concern of testosterone escape and therefore no

need to measure testosterone. This study would cast doubt on that belief, especially in

younger patients at higher risk of testosterone escape whom clinicians should be more

concerned about. Therefore, if clinicians want to try to provide the optimal treatment for

patients and ensure that they achieve adequate, reliable testosterone suppression, at the

very least, testosterone should be measured on a regular basis despite the finding in this

cohort of patients that testosterone levels did not impact short-term outcomes.

Follow-up in this study was relatively short, and even if a difference in survival

stratified by degree of testosterone suppression did exist, one would not expect to see a

difference until the median follow-up was in the range of 7 to 10 years. Despite the lack of

impact of testosterone escape on outcome in this study, several interesting findings are

worth discussing. First, one of the strengths of this study was a relatively high number of

testosterone measurements per patient. Second, there was an appreciable rate of

testosterone escape with LHRHa treatment, and the modal PSA value at the time of

testosterone escape was an undetectable PSA. This illustrates the importance of

testosterone monitoring during therapy, as one cannot rely on an undetectable serum PSA

to rule out testosterone escape. Third, the incidence of testosterone escape was higher in

younger patients and in patients with closer monitoring of serum levels of testosterone on

multivariable analysis. This suggests that the more often testosterone levels are measured,

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 the more cases of testosterone escape will be identified. When accounting for patient age

and number of measurements of testosterone, there is likely a minimal impact of which

Accepted Article
LHRHa is used. This study cannot assess the performance of LHRH antagonists, like

degarelix. This study also cannot evaluate the performance of different testosterone assays,

some of which may lead to unreliable testosterone measurements at very low levels.5

Despite the fact that testosterone suppression has been used to treat prostate

cancer for over half a century, several questions remain. Which is more important: to induce

as low a level of testosterone as possible, or to avoid testosterone escapes? Is there a

period when having a low testosterone matters most? Is it mostly, or entirely, in the first 6

to 12 months of treatment, or it is important throughout the entire duration of testosterone

suppression? In addition, is the degree of testosterone suppression more important in

patients who are being treated with curative intent, for example in patients receiving ADT as

part of a course of curative radiotherapy? Or is it more important to have as low a

testosterone as possible in patients being treated with palliative intent, as in those with

newly diagnosed symptomatic metastatic prostate cancer?

Several studies suggest that it is the ‘induction phase’ of treatment for prostate

cancer that is the most important,4, 6 ,7 almost drawing an analogy to how acute leukemia is

treated. Furthermore, it is clear that the ‘induction’ treatment that produces benefit can be

multi-modal. For example, the early introduction of radiotherapy in patients with locally

advanced prostate cancer,8, 9

upfront chemotherapy in patients with extensive stage,

metastatic prostate cancer6 and also select patients with locally advanced nonmetastatic

prostate cancer, as those treated in the STAMPEDE study.7 The lack of harm of intermittent

androgen deprivation compared with continuous androgen deprivation as illustrated by the

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 National Cancer Institute of Canada ‘PR7’ study10 suggests that a low testosterone is not key

throughout the entire duration of a proposed course of ADT, and perhaps, may be mostly
Accepted Article
important only in the initial phase of treatment.

Conclusion

In this cohort of patients, an undetectable PSA does not rule out the presence of higher than

desired levels of testosterone, reinforcing the need to monitor testosterone levels,

especially in younger patients. There appears to be no impact of testosterone escape on

either biochemical relapse-free survival or overall survival in the short term. The incidence

of testosterone escape is higher in younger patients and in patients with more frequent

monitoring of serum levels of testosterone.

Acknowledgements

The authors would like to thank Chris Parker for review of the manuscript.

References

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advanced prostate cancer: can we improve on androgen deprivation therapy? BJU Int

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2. Zinner NR, Bidair M, Centeno A, Tomera K. Similar frequency of testosterone surge

after repeat injections of goserelin (Zoladex) 3.6 mg and 10.8 mg: results of a randomized

open-label trial. Urology 2004;64(6):1177–81.

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 3. Morote J, Esquena S, Abascal JM, et al. Failure to maintain a suppressed level of

serum testosterone during long-acting depot luteinizing hormone-releasing hormone

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agonist therapy in patients with advanced prostate cancer. Urol Int 2006;77(2):135–38.

4. Klotz L, O’Callaghan C, Ding K, et al. Nadir testosterone within first year of androgen-

deprivation therapy (ADT) predicts for time to castration-resistant progression: a secondary

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Clin Oncol 2015;33(10):1151–6.

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suppression with luteinizing hormone-releasing hormone agonists: does it happen and does

it matter? BJU Int 2012;110(11 Pt B):E500-7.

6. Sweeney CJ, Chen Y-H, Carducci M, et al. Chemohormonal therapy in metastatic

hormone-sensitive prostate cancer. N Engl J Med 2015;373(8):737–46.

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both to first-line long-term hormone therapy in prostate cancer (STAMPEDE): survival

results from an adaptive, multiarm, multistage, platform randomised controlled trial. Lancet

2016;387(10024):1163–77.

8. Mason MD, Parulekar WR, Sydes MR, et al. Final report of the intergroup

randomized study of combined androgen-deprivation therapy plus radiotherapy versus

androgen-deprivation therapy alone in locally advanced prostate cancer. J Clin Oncol

2015;33(19):2143–50.

9. Fosså SD, Wiklund F, Klepp O, et al. Ten- and 15-yr prostate cancer-specific mortality

in patients with nonmetastatic locally advanced or aggressive intermediate prostate cancer,

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 randomized to lifelong endocrine treatment alone or combined with radiotherapy: final

results of the Scandinavian prostate cancer group-7. Eur Urol 2016;70(4):684-691.

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10. Crook JM, O’Callaghan CJ, Duncan G, et al. Intermittent androgen suppression for

rising PSA level after radiotherapy. N Engl J Med 2012;367(10):895–903.

11. Roach M, Hanks G, Thames H, Schellhammer P, Shipley WU, Sokol GH, et al. Defining

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J Radiat Oncol Biol Phys. 2006 ;65(4):965–74.

Figure

Figure 1. Distribution of PSA values at time of testosterone escape. PSA = prostate specific

antigen.

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 Table 1. Baseline Characteristics
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Leuprolide Leuprolide P
Characteristic Buserelin Goserelin Triptorelin
IM SC value

No. Analyzable 43 114 78 96 30

Age

Median (yr) 65.2 68.5 67.0 66.4 70.1 0.31a

Range (yr) 54-82 45-82 44-80 47-79 58-82

T Category, Clinical [N
(%)]

T1c-T2a 11 (25.6) 38 (33.3) 36 (40.7) 19 (19.9) 13 (43.3)

NSb
T2b-T2c 7 (16.3) 26 (22.8) 16 (18.6) 18 (18.8) 5 (16.7)

T3a-T3b 23 (53.4) 47 (41.2) 24 (35.6) 60 (62.5) 12 (40)

Unknown 2 (4.7) 2 (1.7) 2 (5.1) 0 0

Gleason Score, on
biopsy

[N (%)]

6 10 (23.3) 21 (18.4) 13 (16.7) 16 (16.7) 5 (16.7) NSb

7 18 (41.9) 44 (38.6) 32 (41.0) 34 (35.4) 11 (36.7)

8-10 13 (30.2) 48 (42.1) 30 (38.5) 46 (47.9) 14 (46.6)

Unknown 2 (4.65) 1 (0.9) 3 (3.8) 0 0

Post-RP [N (%)] 9 (20.9) 13 (11.4) 17 (21.8) 24 (25.0) 8 (26.7) NSb

Baseline PSA (µg/L)

Median 14.8 12.9 14.2 11.6 12.5

0.75 a
0.03-
Range 0.04-95.5 2.05-66.2 0.22-103 2.2-163
82.90

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 IM = intramuscular; T = tumor stage; NS = not statistically significant; PSA = prostate
specific antigen; RP = radical prostatectomy; SC = subcutaneous.
a
For analysis of variance using multiple pairwise comparisons, using the Bonnferroni
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correction method.
b
For Fisher’s Exact test, not statistically significant (NS).

Table 2. Distribution of Minimum, Median, and Maximum Testosterone Levels at Each

Level

Testosterone (nmol/L)

0.7 0.7-1.7 ≥1.7 Total

Variable Level % Level % Level % Level %

Testosterone

Level during

ADT

Minimum 280 77.6 80 22.1 1 0.3 361 100

Median 172 47.6 187 51.8 2 0.6 361 100

Maximum 75 21 236 65 50 14 361 100

Mean age, years 67.8 66.8 63.4 66.6

P value 0.01a

ADT = androgen-deprivation therapy.

a
Analysis of variance test, on maximum testosterone comparison.

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 Table 3. Number of Maximum Testosterone Levels Within Each Category by Course of
LHRH Agonist
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Testosterone
Buserelin Goserelin Leuprolide IM Leuprolide SC Triptorelin P valuea
(nmol/L)

≤ 0.7 [N (%)] 6 (14) 21 (21.1) 25 (32.1) 11 (11.5) 9 (30)

0.7 - 1.74 [N (%)] 33 (76.7) 78 (68.4) 44 (56.4) 62 (64.5) 19 (63.3) 0.003

 1.75 [N (%)] 4 (9.3) 12 (10.5) 9 (11.5) 23 (24) 2 (6.67)

IM = intramuscular; LHRH = luteinizing hormone-releasing hormone; SC = subcutaneous.

a
For Fisher’s Exact test.

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 Table 4. Number of Maximum Testosterone Levels Within Each Category by Course of
LHRH Agonist in Patients With Six or Less Testosterone Measurements Per Patient
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Maximum Total Number
Testosterone of Patients
Leuprolide
Buserelin Goserelin Leuprolide SC Triptorelin With ≤ 6
Category IM
Testosterone
(nmol/L) Measurements

≤ 0.7 [N (%)] 5 (20) 21 (26.9) 19 (37.2) 5 (45.5) 4 (44.4)

0.7 - 1.74 [N (%)] 19 (76) 52 (66.7) 28 (54.9) 5 (45.5) 5 (55.6) 174

 1.75 [N (%)] 1 (4) 5 (6.4) 4 (7.9) 1 (9.0) 0 (0)

IM = intramuscular; LHRH = luteinizing hormone-releasing hormone; SC = subcutaneous.

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 Table 5. Number of Maximum Testosterone Levels Within Each Category by Course of
LHRH Agonist in Patients More Than Six Testosterone Measurements Per Patient
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Maximum Total Number
Testosterone of Patients
Buserelin Goserelin Leuprolide IM Leuprolide SC Triptorelin With > 6
Category Testosterone
(nmol/L) Measurements

≤ 0.7 [N (%)] 1 (5.6) 3 (8.3) 6 (22.2) 6 (7.1) 5 (23.8)

0.7 - 1.74 [N (%)] 14 (77.8) 26 (72.2) 16 (59.3) 57 (67.1) 14 (66.7) 187

> 1.75 [N (%)] 3 (16.6) 7 (19.5) 5 (18.5) 22 (25.8) 2 (9.5)

IM = intramuscular; LHRH = luteinizing hormone-releasing hormone; SC = subcutaneous.

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 Table 6. Odds Ratios From the Multinomial Logistic Regression of the Predictors of
Testosterone Suppression
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Odds Ratio Estimates

Point 95% Wald

Variable
Estimate Confidence Limits

Age 1.039 1.009 1.071

Number of testosterone measurements 0.830 0.772 0.891

Buserelina 0.472 0.177 1.261

Goserelina 0.471 0.201 1.100

Leuprolide IMa 0.745 0.309 1.800

Leuprolide SCa 0.390 0.162 0.941

IM = intramuscular; OR = odds ratio; SC = subcutaneous.

a
Probability of testosterone suppression compared with triptorelin (OR < 1 indicating a
lesser probability of testosterone suppression, statistically significant if upper 95%
confidence interval < 1.0 and OR > 1 indicating a greater probability of testosterone
suppression, statistically significant if lower 95% confidence interval > 1.0).

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 Number of PSA values Distribution of PSA values at time of TTE
62 0
5 4
1 8 Distribution of PSA values at time of TTE
0 12
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70
0 16 62
0 20 60

Number of PSA measurements

1 24
50

40

30

20

10 5
1 0 0 0 1
0
0 4 8 12 16 20 24
PSA value (µg/L)

Summary of PSA values at time of

Testosterone escape above 1.75 nmol/L or
50mg/dL (N values = 69)
Mode = 0.04
Median = 0.10
Mean = 0.94
Minimum = 0.00
Maximum = 23.70

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