biopsies we detected high-grade prostate cancer in only one
Althoughtestosterone therapyandprostatecancerremain
a matter of debate, these studies suggest that TST might not
lead to an increased risk of prostate cancer. The prospective
nature and sample size of the study by Haider and colleagues
add credibility to this debate. It is important to note that
caution is warranted in men with specific risk factors
for prostate cancer, such as African race or family history,
until further studies can definitively elucidate the role of
testosterone in the development and progression of prostatic
cancer. The growing body of evidence should allay concerns
regarding prostate cancer that practitioners or patients
might have when considering initiation of testosterone
supplementation to relieve symptoms of hypogonadism.
Conflicts of interest:
Larry I. Lipshultz has participated in clinical trials
and received consultant and speaker fees from Auxilium and Endo. The
remaining authors have nothing to disclose.
Morgentaler A. Testosterone therapy in men with prostate cancer:
scientiFc and ethical considerations. J Urol 2014;189(Suppl 1):
Marks LS, Mazer NA, Mostaghel E, et al. Effect of testosterone re-
placement therapy on prostate tissue in men with late-onset hypo-
gonadism: a randomized controlled trial. JAMA 2006;296:2351–61.
Lacy JM, Kyprianou N. A tale of two trials: the impact of 5
reductase inhibition on prostate cancer (review). Oncol Lett 2014;
Pastuszak AW, Pearlman AM, Lai WS, et al. Testosterone replace-
ment therapy in patients with prostate cancer after radical prosta-
tectomy. J Urol 2013;190:639–44.
Pastuszak AW, Pearlman AM, Godoy G, Miles BJ, Lipshultz LI, Khera
M. Testosterone replacement therapy in the setting of prostate
cancer treated with radiation. Int J Impot Res 2013;25:24–8.
Morgentaler A, Lipshultz LI, Bennett R, Sweeney M, Avila D, Khera
M. Testosterone therapy in men with untreated prostate cancer.
J Urol 2011;185:1256–61.
Peter Butler, Jason M. Scovell, Ranjith Ramasamy,
Larry I. Lipshultz
Department of Urology, Baylor College of Medicine, Houston, TX, USA
*Corresponding author. Department of Urology, Baylor College of
Medicine, 6624 ±annin Street, #1700, Houston, TX 77030, USA.
E-mail address:
(L.I. Lipshultz).
Re: Multiparametric Magnetic Resonance Imaging (MRI)
and Subsequent MRI/Ultrasonography Fusion-guided
Biopsy Increase the Detection of Anteriorly Located
Prostate Cancers
Volkin D, Turkbey B, Hoang AN, et al.
BJU Int 2014;114:E43–9
Experts’ summary:
Anteriorly located prostate cancer (PCa) is challenging for the
urologist to diagnose by digital rectal examination (DRE) and
transrectal ultrasound (TRUS), given the distance of the tumour
farthest from the rectum. Volkin and colleagues asked whether,
after multiparametric magnetic resonance imaging (mpMRI),
an MRI/ultrasound (US) fusion-guided biopsy (±GB) is better
at detecting anterior PCa compared with TRUS biopsy. Of
499 patients who had 3-T mpMRI of the prostate, 162 were
found to have 241 anteriorly located suspicious lesions. All
162 patients went on to have 12-core extended sextant
TRUS-guided biopsy (blinded to the MRI findings) and, in the
same biopsy session, MRI/US ±GB. Of the 241 anterior lesions,
121 were positive on biopsy. Of these, 24 were positive on
TRUS-guided biopsy cores only, 59 were positive on targeted
±GB cores only, and a further 38 were positive on cores taken by
a detection rate of 25.7%; targeted ±GB had a detection rate of
40.3%. When stratified by high and moderate suspicion by MRI,
±GB increased cancer detection by 118% (
= 0.001) and 50%
= 0.017), respectively, when compared with TRUS-guided
biopsy results alone. Of all 121 patients having positive biopsies
by both ±GB-targeted and TRUS-guided techniques, 57% had at
least one previous negative standard-of-care TRUS-guided bi-
opsy. A further 10% of the study cohort had undergone four or
more negative biopsy sessions before enrolment in this study.
Experts’ comments:
This study further demonstrates the problems inherent in
relying on DRE and TRUS-guided prostate biopsies alone for
the diagnosis of PCa, particularly when PCa originates in the
anterior gland.
It is worthwhile pointing out a few issues. ±irst, it should
be noted that ±GB missed 24 anterior lesions that were found
to have PCa on TRUS-guided biopsy, thereby reminding us
that ±GB still has some errors. Second, it would have been
helpful if the authors had reported on the characteristics of
the 120 mpMRI lesions in 45 patients in whom neither ±GB
nor TRUS biopsy found cancer. Did these patients proceed to
repeat biopsy attempts, surveillance, or intervention? Such
information wouldbehelpfulinfurtherassessing the value of
current clinical application and the future role of targeted
±GB. Third, although the authors quite rightly point out that
their results are not validated against more precise reference
standards, such as transperineal mapping biopsies
whole-mount radical prostatectomy, it is reassuring that
other reporters have done so and demonstrated that MRI-
targeted biopsies miss only 4% of clinically significant lesions
when validated against whole-mount prostatectomy speci-
. Last, the application of a 3-scale scoring system
might be questioned by many who now promulgate the use
of a 5-point system or the prostate imaging-reporting and
data system (PI-RADS) scoring. However, the 3-scale system
is relatively straightforward and both clinician and patient
friendly in that the decision for biopsy or no biopsy can be
One must recognise that cancers originating from the
anterior prostate represent many cancers missed on initial
12-core transrectal biopsy
; that detection of anterior
tumours are often the reason for patients transitioning to
EUROPEAN UROLOGY 67 (2015) 1186–1192