azoospermia, invasive procedures such as microdissection

testicular sperm extraction (micro-TESE) may be used for

the exceedingly rare case of unrelenting azoospermia that

does not resolve after a thorough attempt at medical

treatment has been made.

Regarding testicular atrophy, hCG preserves testicular

function and prevents testicular atrophy

(104)

. Treatment

with hCG is known to increase testicular volume, based on

studies in patients with hypogonadotropic hypogonadism

(105, 106)

. Furthermore, AAS users typically self-administer

hCG at low doses, such as 250-500 IU subcutaneously or

intramuscularly daily or every other day for several weeks to-

ward the end of long cycles and through the

rst few weeks of

their post-cycle regimen (

Table 2

). SERMs may be equally

cacious for the prevention of AAS-induced testicular atro-

phy, although quality comparative studies are not available.

hCG may be added to the protocol if response to primary

SERM treatment is inadequate.

Management of polycythemia.

Supraphysiologic levels of

plasma androgens stimulate erythropoietin production in a

dose-dependent manner and may lead to clinically signi

cant

secondary polycythemia

(107, 108)

. The increase in plasma

viscosity

may

contributing

factor

adverse

cardiovascular events in AAS users, especially in those

patients with preexisting coronary risk factors

(109)

;

however, this potential relationship has not been de

nitely

demonstrated by meta-analysis

(108)

. Nevertheless, correc-

tion of severe polycythemia in AAS users should be attempted

by phlebotomy. However, ultimately the discontinuation of

AAS and a restoration of normal endogenous hormone levels

are paramount for reducing the patient's risk for potential

polycythemia-associated complications.

DISCUSSION

Recently, a retrospective database review of 6,033 hypogona-

dal men found ASIH to be a common cause of profound

hypogonadism (T

50 ng/dL)

(16)

. Even more surprising, it

was found that as many as one out of

ve men who were be-

ing treated for symptomatic hypogonadism had previously

used AAS

(16)

. These important new data identify ASIH as a

concerning and preventable cause of hypogonadism, espe-

cially in younger hypogonadal men. Despite being the only

class of U.S. Drug Enforcement Administration scheduled

drugs for which the Diagnostic and Statistical Manual of

Mental Disorders does not recognize a dependence syndrome,

expert psychiatrists now appreciate AAS dependence as a

valid diagnostic entity

(31)

. The primary goal of counseling

patients with ASIH should be to deter future and potentially

harmful use of nonprescribed AAS. Understanding the pa-

tient's motivations for use can help to deliver the most effec-

tive counseling and may identify treatable pathologies such

as primary hypogonadism, delayed puberty, or psychopathol-

ogy, all of which could be safely addressed through medically

supervised treatment strategies.

Symptomatic hypogonadism is common after completion

of an AAS cycle

(16)

. After a complete endocrine and meta-

bolic assessment, management strategies for hypogonadism

include use of transient TRT, SERMs, and hCG. Responses

may be quite variable, depending on speci

c characteristics

of AAS use. Recognition of the speci

c details of the user's

AAS cycle is important for their subsequent medical manage-

ment. Use of AIs may be more problematic in light of recent

evidence suggesting that their use may lead to potential sex-

ual side effects

(94)

For the treatment of acute gynecomastia, tamoxifen

should be used as the SERM for the recovery protocol. hCG

may exacerbate or cause gynecomastia in patients with

ASIH. Erectile dysfunction may be effectively managed

with a temporary course of short- or long-acting PDE5i

while the HPG axis recovers function. Likewise, symptoms

of decreased libido will likely improve gradually as endoge-

nous T production returns to the patient's baseline levels.

Management strategies for male infertility secondary to

ASIH should parallel strategies for correction of the underly-

ing hypogonadal state, and hCG should be included in the

recovery protocol for these patients. Normal spermatogenesis

is likely to be achieved as the ITT concentration improves.

Treatment with hCG may be of bene

t for patients with

infertility secondary to ASIH.

Acknowledgments:

The authors thank Heather Bass, Ph.D.,

for making this paper possible.

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