After 4 weeks of treatment with TRT and/or a SERM,

repeated hormone panels should be obtained. If the patient

has had either a poor gonadotropin response or a poor T

response, the authors commence a 4-week course of hCG

(1,000

–

3,000 IU, 3 times per week) while continuing daily

treatment with a SERM at the initial starting dose

(66

–

69)

patient

develops

gynecomastia

while

hCG,

tamoxifen (10 mg b.i.d.) or anastrazole may be commenced.

After 8 weeks of hCG and adjunctive treatment, hormone

levels should once again be assessed. At this point, if the

total serum T remains low and the patient continues to be

symptomatic, primary testicular failure is likely

(46)

. These

patients will require a longer duration of TRT to avoid

permanent ASIH. If appropriately increased serum T and

gonadotropin levels are observed, the SERM may be

reduced to 50% of its starting dose at 10 weeks of treatment

and continued through weeks 12

–

16 or until target serum T

level is achieved

(70)

(

Fig. 2

). Recovery of hormonal

function may be limited in men with testicular failure, and

close monitoring is recommended.

Management of gynecomastia.

Gynecomastia, or painful

breast enlargement, is a common and distressing complica-

tion of AAS use occurring in as many as one-half of all users

(71)

. Partially due to an imbalance of T/E

signaling in breast

tissue

(72)

, symptoms may arise in the post-cycle period

because of profound ASIH or administration of hCG (and sub-

sequent elevations in E

secondary to aromatization) along

with a systemwide decline of endogenous androgen

signaling. Alternatively, it may occur while on-cycle, depend-

ing on the relative anabolic-to-androgenic effects as well as

any progestin-like effects of medications used. AAS com-

pounds that are susceptible to aromatization are more likely

to cause gynecomastia

(72)

. Finasteride, used by as many as

10% of AAS users for alopecia

(17)

, may potentiate this effect

and should be discontinued in ASIH users with gynecomastia

(73

–

76)

. Herbal supplements such as tribulus terrestris and

saw palmetto extract have no proven bene

t and might

cause worsening gynecomastia. As such, AAS users should

be advised to discontinue these supplements

(77, 78)

. The

use of hCG has been reported in

40% of AAS users

(17)

and may cause, or exacerbate, gynecomastia

(72)

Symptom duration is likely the best prognostic indicator

for response to therapy

(72, 79, 80)

with acutely tender

gynecomastia

being

the

most

amenable

medical

treatment. Gynecomastia that has persisted for

1 year is

more likely to involve signi

cant

brosis and typically

responds poorly to drug therapy

(72, 80

–

82)

. In such

nonpainful chronic cases, surgical treatment is the best

option for cosmetic improvement

(73, 83, 84)

. Although

large trials are lacking, tamoxifen appears to be the most

safe and effective agent for the medical management of

AAS-associated gynecomastia

(63, 81, 82, 85

–

87)

. Because

tamoxifen

has

been

used

effectively

increase

gonadotropin secretion and restart the HPG axis in the

setting of ASIH as well as idiopathic hypogondotropic

hypogonadism

(15,

–

93)

the

authors

recommend

tamoxifen for the medical treatment of ASIH with

concomitant AAS-associated gynecomastia (

Fig. 2

Evidence that AIs are effective in the treatment of gy-

necomastia exists, and the authors have used them previously

with good success and minimal side effects. However, Finkel-

stein et al.

(94)

recently reported

ndings suggesting that sup-

pression of circulating estrogen levels with AIs decreases

libido, worsens erectile dysfunction, and increases percentage

body fat in men with a chemically repressed HPG axis despite

the administration of TRT. Given that men with symptomatic

FIGURE 2

Suggested treatment algorithm for symptomatic anabolic-androgenic steroid

–

induced hypogonadism (ASIH). SERM

selective estrogen receptor

modulator; TRT

testosterone replacement therapy.

Rahnema. Anabolic steroid

–

induced hypogonadism. Fertil Steril 2014.

VOL. 101 NO. 5 / MAY 2014

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Fertility and Sterility®