Page 154 - Remedial Andrology

10.5.3.3 Primary Hypogonadism
There is no substantial evidence that gonadotrophin therapy has any beneficial effect in the presence of
classical testicular failure. Likewise, there are no data to support the use of other hormonal treatments
(including SERMs or AIs) in the case of primary hypogonadism to improve spermatogenesis [79, 1815].

10.5.3.4 Idiopathic Male Factor Infertility
There is some evidence that FSH treatment increases sperm parameters in idiopathic oligozoospermic men
with FSH levels within the normal range (generally 1.5 – 8 mIU/mL) [1816]. It has also been reported that FSH
may improve sperm DNA fragmentation rates as well as ameliorating AMH and inhibin levels [1817-1820].
High-dose FSH therapy is more effective in achieving a testicular response than lower doses are [1821].
A Cochrane systematic review including six RCTs with 456 participants, different treatment protocols and
follow-up periods concluded that FSH treatment resulted in higher live-birth and pregnancy rates compared
with placebo or no treatment. However, no significant difference among groups was observed when ICSI or
IUI were considered [1822]. In a more recent meta-analysis including 15 trials with > 1,200 patients, similar
findings after FSH treatment were observed in terms of both spontaneous pregnancies and pregnancies after
ART [1823]. A further study showed that in azoospermic men undergoing TESE-ICSI there were improved
SRRs and higher pregnancy and fertilisation rates in men treated with FSH compared to untreated men [1824].
In men with NOA, combination hCG/FSH therapy was shown to increase SRR in only one study [1825]. Human
Chorionic Gonadotrophin alone prior to TESE in NOA has not been found to have any benefit on SRRs [1826].

10.5.3.5 Anabolic Steroid Abuse
Oligospermia or azoospermia as a result of anabolic abuse should be treated initially by withdrawal of the
anabolic steroid. There is no common indication for treating this disorder; the management is based on case
reports and clinical experience. Usually, adequate sperm numbers and quality will improve over a six to twelve
month period. If after this interval the condition persists, then hCG without or in combination with FSH as an
alternative to clomiphene can be used to try and stimulate spermatogenesis [1827].

10.5.3.6 Recommendations for treatment of male infertility with hormonal therapy

Recommendations Strength rating
Hypogonadotropic hypogonadism (secondary hypogonadism), including congenital Strong
causes, should be treated with combined human chorionic gonadotropin (hCG) and follicle-
stimulating hormone (FSH) (recombinant FSH; highly purified FSH) or pulsed Gonadotropin-
releasing hormone (GnRH) via pump therapy to stimulate spermatogenesis.
In men with hypogonadotropic hypogonadism, induce spermatogenesis by an effective Strong
drug therapy (hCG; human menopausal gonadotropins; recombinant FSH; highly purified
FSH).
The use of GnRH therapy is more expensive and does not offer any advantages when Strong
compared to gonadotropins for the treatment of hypogonadotropic hypogonadism.
In men with idiopathic oligozoospermia and FSH values within the normal range, FSH Weak
treatment may ameliorate spermatogenesis outcomes.
No conclusive recommendations can be given on the use of high-dose FSH in men with Weak
idiopathic infertility and prior (m)TESE and therefore cannot be routinely advocated.
Do not use testosterone therapy for the treatment of male infertility. Strong
Provide testosterone therapy for symptomatic patients with primary and secondary Strong
hypogonadism who are not considering parenthood.
In the presence of hyperprolactinaemia, dopamine agonist therapy may improve Weak
spermatogenesis.

10.6 Invasive Male Infertility Management
10.6.1 Obstructive azoospermia
Obstructive azoospermia is the absence of spermatozoa in the sediment of a centrifuged sample of ejaculate
due to obstruction [1828]. Obstructive azoospermia is less common than NOA and occurs in 20-40% of
men with azoospermia [1829, 1830]. Men with OA usually have normal FSH, testes of normal size and
epididymal enlargement [1831]. Of clinical relevance, men with late maturation arrest may present with normal
gonadotropins and testicular size and may be only distinguished from those with OA at the time of surgical
exploration. The vas deferens may be absent bilaterally (CBAVD) or unilaterally (CUAVD). Obstruction in primary
infertile men is more frequently present at the epididymal level.

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