ESPE Abstracts (2016) 86 P-P1-357

Changes in Adrenal Steroids During Puberty Suppression and Cross Sex Hormone Treatment in Gender Dysphoric Adolescents

Sebastian Schagena,b, Paul Lustenhouwerb & Sabine Hannemab


aVU University Medical Centre, Amsterdam, The Netherlands; bLeiden University Medical Centre, Leiden, The Netherlands


Background: Current guidelines recommend that gender dysphoric adolescents be treated with puberty suppression using gonadotropin releasing hormone analogues (GnRHa) followed by cross sex hormones. However limited data are available on the safety and side effects of this treatment. In adults changes in adrenal steroids have been observed during cross sex hormone treatment.

Objective and hypotheses: We aimed to investigate the effect of GnRHa and cross sex hormones on adrenal steroid levels in gender dysphoric adolescents.

Method: 54 male-to-females (MtFs) and 73 female-to-males (FtM) were treated with triptorelin 3.75 mg i.m. every 4 weeks and from the age of 16 years testosterone or 17beta-oestradiol was added at increasing doses. Serum DHEA-S and androstenedione levels were measured every 6 months.

Results: Baseline androstenedione was above the reference range in 5/67 FtMs and in none of the MtFs. All individuals had baseline DHEA-S within the reference range. During GnRHa treatment DHEA-S increased in FtMs, but in those aged 12–14 years at start DHEA-S levels after 2 years of treatment were comparable to baseline levels of those aged 14–16 at start. During cross sex hormone treatment DHEA-S levels did not change in either sex. Androstenedione decreased during GnRHa treatment in FtMs whereas levels in MtFs did not change. Testosterone treatment induced a rise in androstenedione in FtMs whereas oestradiol treatment in MtFs had no effect.

Conclusion: The increase of DHEA-S during GnRHa treatment in FtMs may be physiologic and unrelated to treatment or could imply stimulation of adrenal activity by GnRHa treatment. However, androstenedione levels decreased, probably due to decreased ovarian androstenedione production. The increase in androstenedione during testosterone treatment might be caused by direct conversion or alternatively through an effect on adrenal steroidogenesis although DHEA-S did not change. The clinical implications of the changes that were observed are still unclear.

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