Addition of recombinant follicle-stimulating hormone to human chorionic gonadotropin treatment in adolescents and young adults with hypogonadotropic hypogonadism promotes normal testicular growth and may promote early spermatogenesis

Zacharin, Margaret; Sabin, Matthew A.; Nair, Veena; Dagabdhao, Preeti

doi:10.1016/j.fertnstert.2012.06.022

Cited by 69 publications

(48 citation statements)

References 28 publications

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“…The only data on this topic have been produced by Sinisi et al (2010). They conducted a retrospective Yang et al (2012) 158 N/A 3 (1.9) 1 (0.6) Zacharin et al (2012) 19 N/A 1 (0.1) -…”

Section: Discussionmentioning

confidence: 99%

Factors affecting spermatogenesis upon gonadotropin‐replacement therapy: a meta‐analytic study

et al. 2014

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SUMMARYA meta-analysis was performed to systematically analyse the results of gonadotropin and GnRH therapy in inducing spermatogenesis in subjects with hypogonadotropic hypogonadism (HHG) and azoospermia. An extensive Medline and Embase search was performed including the following words: 'gonadotropins' or 'GnRH', 'infertility', 'hypogonadotropic', 'hypogonadism' and limited to studies in male humans. Overall, 44 and 16 studies were retrieved for gonadotropin and GnRH therapy, respectively. Of those, 43 and 16 considered the appearance of at least one spermatozoa in semen, whereas 26 and 10 considered sperm concentration upon gonadotropin and GnRH, respectively. The combination of the study results showed an overall success rate of 75% (69-81) and 75% (60-85) in achieving spermatogenesis, with a mean sperm concentration obtained of 5.92 (4.72-7.13) and 4.27 (1.80-6.74) million/ mL for gonadotropin and GnRH therapy, respectively. The results upon gonadotropin were significantly worse in studies involving only subjects with a pre-pubertal onset HHG, as compared with studies involving a mixed population of pre-and post-pubertal onset [68% (58-77) vs. 84% (76-89), p = 0.011 and 3.37 (2.25-4.49) vs. 12.94 (8.00-17.88) million/mL, p < 0.0001; for dichotomous and continuous data, respectively]. A similar effect was observed also upon GnRH. No difference in terms of successful achievement of spermatogenesis and sperm concentration was found for different FSH preparations. Previous use of testosterone replacement therapy (TRT) did not affect the results obtained with gonadotropins. Finally, a higher success rate was found for subjects with lower levels of gonadotropins at the baseline and for those using both human chorionic gonadotropin and FSH. Gonadotropin therapy, even with urinary derivatives, is a suitable option in inducing/restoring fertility in azoospermic HHG subjects. Gonadotropins appear to be more efficacious in subjects with a pure secondary nature (low gonadotropins) and a post-pubertal onset of the disorder, whereas previous TRT does not affect outcome.

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“…The only data on this topic have been produced by Sinisi et al (2010). They conducted a retrospective Yang et al (2012) 158 N/A 3 (1.9) 1 (0.6) Zacharin et al (2012) 19 N/A 1 (0.1) -…”

Section: Discussionmentioning

confidence: 99%

Factors affecting spermatogenesis upon gonadotropin‐replacement therapy: a meta‐analytic study

et al. 2014

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“…Induction of puberty in adolescent males with either hCG monotherapy or with combinational therapy of hCGC recombinant FSH (rFSH) may result in better testicular growth and improvement in potential fertility compared with treatment with testosterone therapy (59). If the patient has spontaneous onset of pubertal development one can start with hCG monotherapy; FSH can be added in cases where azoospermia persists after 6-12 months of treatment.…”

Section: Hypogonadotrophic Hypogonadismmentioning

confidence: 99%

“…Early induction of spermatogenesis may increase sperm production capacity and reduce the time required for appearance of sperm once fertility is desired. Monotherapy of hCG alone is at least theoretically less efficacious in the induction of spermatogenesis induction than combinational therapy of hCGCFSH (59,60). Rationale for the use of aromatase inhibitors in the induction of puberty in CDGP is to increase adult height.…”

Section: Hypogonadotrophic Hypogonadismmentioning

confidence: 99%

TRANSITION IN ENDOCRINOLOGY: Induction of puberty

Dunkel

Quinton

2014

European Journal of Endocrinology

112

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Puberty is the period during which we attain adult secondary sexual characteristics and reproductive capability. Its onset depends upon reactivation of pulsative GNRH, secretion from its relative quiescence during childhood, on the background of intact potential for pituitary-gonadal function. This review is intended: to highlight those current practices in diagnosis and management that are evidence based and those that are not; to help clinicians deal with areas of uncertainty with reference to physiologic first principles; by sign-posting relevant data arising from other patient groups with shared issues; to illustrate how recent scientific advances are (or should be) altering clinician perceptions of pubertal delay; and finally, to emphasise that the management of men and women presenting in advanced adult life with absent puberty cannot simply be extrapolated from paediatric practice. There is a broad spectrum of pubertal timing that varies among different populations, separated in time and space. Delayed puberty usually represents an extreme of the normal, a developmental pattern referred to as constitutional delay of growth and puberty (CDGP), but organic defects of the hypothalamo-pituitary-gonadal axis predisposing to hypogonadism may not always be initially distinguishable from it. CDGP and organic, or congenital hypogonadotrophic hypogonadism are both significantly more common in boys than girls. Moreover, around 1/3 of adults with organic hypogonadotrophic hypogonadism had evidence of partial puberty at presentation and, confusingly, some 5-10% of these subsequently may exhibit recovery of endogenous gonadotrophin secretion, including men with Kallmann syndrome. However, the distinction is crucial as expectative ('watch-and-wait') management is inappropriate in the context of hypogonadism. The probability of pubertal delay being caused by organic hypogonadism rises exponentially both with increasing age at presentation and the presence of associated 'red flag' clinical features. These 'red flags' comprise findings indicating lack of prior 'mini-puberty' (such as cryptorchidism or micropenis), or the presence of non-reproductive congenital defects known to be associated with specific hypogonadal syndromes, e.g. anosmia, deafness, mirror movements, renal agenesis, dental/digital anomalies, clefting or coloboma would be compatible with Kallmann (or perhaps CHARGE) syndrome. In children, interventions (whether in the form or treatment or simple reassurance) have been historically

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“…Different treatment protocols can be used. The typical gonadotro-pin regimen combines human chorionic gonadotropin (hCG) and FSH [28,29]. Adverse events are reduced high-density lipoprotein cholesterol, thromboembolism,osteoporosis, increased prostatic symptoms in males and increased cardiovascular risk [30].…”

Section: Discussionmentioning

confidence: 99%

Effect of Iron Overload on Gonadotrophins and Organ Sex Steroids in Pubertal Thalassemia Patients

2017

IJCRR

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Addition of recombinant follicle-stimulating hormone to human chorionic gonadotropin treatment in adolescents and young adults with hypogonadotropic hypogonadism promotes normal testicular growth and may promote early spermatogenesis

Cited by 69 publications

References 28 publications

Factors affecting spermatogenesis upon gonadotropin‐replacement therapy: a meta‐analytic study

Factors affecting spermatogenesis upon gonadotropin‐replacement therapy: a meta‐analytic study

TRANSITION IN ENDOCRINOLOGY: Induction of puberty

Effect of Iron Overload on Gonadotrophins and Organ Sex Steroids in Pubertal Thalassemia Patients

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