refers to synthetic testosterone derivatives not used
for clinical management of hypogonadism.
Since the Bay Area Laboratory Co-Operative
(BALCO) scandal in 2003, which brought AAS use
by professional and Olympic athletes into the
media, the illicit use of performance enhancing
drugs has become widely recognized. Initially
popularized by bodybuilders and athletes in the
1970s, AASs are currently used most often to
increase muscular development or enhance athletic
performance.
3
Middle-aged men seeking rejuvena-
tion comprise a new demographic of AAS users that
recently appeared. It was estimated that there are
up to 3 million AAS users in the United States.
4,5
Multiple studies show that 4% to 6% of high school
males have used AASs.
6
±
8
Most large epidemiolog-
ical studies estimate that the lifetime prevalence of
AAS use in men is at least 3%.
9
AASs are known to cause hypogonadotropic
hypogonadism as a result of suppressing gonado-
tropin releasing hormone, luteinizing hormone
and follicle-stimulating hormone. The duration of
this
ASIH
is
unclear.
Some
studies
suggest
that ASIH lasts only 4 to 12 months after AAS
discontinuation
10,11
but others describe a subset of
men with long-term or permanent gonadotropin
suppression.
12
±
15
Depending on the cumulative
dose and duration of AAS exposure ASIH may last
indefinitely.
16
With increased focus in the lay press hypo-
gonadism is increasingly diagnosed and treated in
younger men. An idiopathic age related decrease in
testosterone is recognized in 38.7% of men older
than 45 years
17
but the etiology of hypogonadism in
younger men can be difficult to identify. A potential
etiology that is often overlooked is ASIH, especially
in men who may have experimented with AAS in
their youth and now seek evaluation for hypo-
gonadal symptoms.
Given the overall paucity of information on AAS
use in hypogonadal men, we examined the impact,
prevalence and prior use patterns of AAS in hypo-
gonadal men.
MATERIALS AND METHODS
After receiving institutional review board approval we
analyzed an established database of all 6,033 men evalu-
ated for hypogonadism from 2005 to 2010 at an academic
based urology practice. The charts of the 97 men who
presented with profound hypogonadism, defined as total
testosterone 50 ng/dl or less, were reviewed for clinical
data. Given the high prevalence of men with profound
hypogonadism who acknowledged prior AAS use (42 of 97
or 43%), an anonymous survey was subsequently designed
to separately assess AAS use in the patient population
currently being treated for hypogonadism.
After receiving adjunctive institutional review board
approval the survey was distributed from September to
December 2012 to all men with hypogonadism listed as a
diagnosis for the followup appointment. The survey was
self-administered in the waiting room with written in-
structions explaining the purpose of the questionnaire
and emphasizing its confidential, anonymous nature. For
inclusion in analysis patients must have been currently
receiving TRT for hypogonadism and must return for a
followup appointment and be willing to participate.
Surveys were excluded if patients were not currently on
TRT or questions pertaining to previous AAS exposure
were not completed.
The first portion of the survey assessed all patients
receiving TRT and included basic patient demographics,
such as age, sexual orientation, marital status, education
level and income. Only men who reported prior AAS
exposure were prompted to complete the second portion of
the survey, which gathered data on the nature of prior
AAS use, including age at first use, drugs used previously
and side effects while using AAS.
Data were analyzed using the Student t test for scalar
variables and the Fisher exact test for categorical vari-
ables. Correlation analysis between variables was per-
formed using the Spearman rank correlation and ORs
were calculated as appropriate. Analysis was performed
using Microsoft
Ò
Excel
Ò
and SPSS
Ò
, version 21 with
p
²
0.05 considered statistically significant.
RESULTS
Profound hypogonadism, defined as total testos-
terone 50 ng/dl or less, was identified in 97 men
(1.6%) from a database of 6,033 seen from 2005 to
2010 (table 1). Of these men 71 (73%) presented
with symptoms of hypogonadism, while 26 (27%)
Table 1.
Database analysis of etiology in 97 of 6,033 men
presenting with profound hypogonadism
No. Pts (%)
Total No. (%)
Presenting symptom:
e
97 (1.6)*
Hypogonadism
71 (73)
Infertility
26 (27)
Hypergonadotropic hypogonadism:
Idiopathic primary testicular failure
7
(35)
7
(7)
Surgical anorchia
7
(35)
7
(7)
Klinefelter
4
(20)
4
(4)
Traumatic anorchia
2
(10)
2
(2)
Totals
20 (20.6)
97 (100)
Prior AAS exposure†
42
(55)
42 (43)
Androgen deprivation therapy for prostate Ca
12
(16)
12 (12)
Idiopathic/unknown
11
(14)
11 (11)
Androgen deprivation therapy for hypersexuality
6
(8)
6
(6)
Estrogen replacement for gender dysphoria
2 (2.6)
2
(2)
Pituitary adenoma
2 (2.6)
2
(2)
Kallman syndrome
2 (2.6)
2
(2)
Totals
77 (79.4)
97 (100)
*Mean age 46 years.
†p
<
0.05.
ANABOLIC STEROID INDUCED HYPOGONADISM IN YOUNG MEN
2201