Post Pubertal M to F Gender variant Adolescents: Comparison of British and Dutch Approaches

GIRES has compared the British and Dutch approaches to offering feminising hormones to adolescents with profound and persistent gender dysphoria who had male phenotype at birth and are at or beyond a late stage of pubertal development.

The British Approach

In the UK, the approach is based guidelines published by the British Society of Paediatric Endocrinolgy and Diabetes (BSPED) in 2004. BSPED’s approval was withdrawn in 2006. Nonetheless the clinicians at the UK’s sole treatment centre still follow them. The guidelines recommended that an adolescent should be left to experience his/her natural hormone environment until:

  1. Development of secondary sexual characteristics is complete
  2. Final height has been achieved
  3. Peak bone mass has been accrued (ideally)

After development of secondary sexual characteristics is complete, followed by a period of up to 15 months on the blocking medication, the authors of the BSPED Guidelines suggest 5-10 micrograms of ethinylestradiol per day for 6 months. However, their initial prescription is for 5 micrograms per day. The dose is increased to 15 then 20 micrograms over around 18 months. This is intended to mimic normal female puberty even though the adolescents now have fully masculinised bodies. Eventually, the patient might be put on what the clinicians say is an adult dose of 20–30 micrograms per day. They say that this is the normal dose of the oral contraceptive pill. It is not clear that it adequately feminises a fully masculine body.

The Dutch Approach

The adolescents cared for by the Dutch clinicians are mainly first seen before, or at an early stage of, puberty. For those confirmed as experiencing profound gender dysphoria that is highly likely to persist, hormone blocking medication is offered at a testicular volume of 6-8 ml to suspend puberty, thereby relieving immediate stress and providing more time for diagnosis. However, some adolescents are first seen at later stages of puberty or even after pubertal development is complete. These cases too are carefully screened and medication is administered to block endogenous sex hormones before feminising hormones are offered.

The opinion of the Dutch clinicians is that, for adolescents born with male phenotype who have already reached a late stage of pubertal development, 5μg ethinylestradiol is very low. For such adolescents, in contrast to the British approach, they do not undertake a slow initiation of puberty, but increase the dose of medication in relation to breast development. They do not use ethinylestradiol but 17 beta estradiol, the natural estrogen. For 17 beta estradiol they progressively increase the dose to 2mg per day which they say is an adult dose and comparable with 30-50μg ethinylestradiol. This is higher than the 20–30 μg offered by the British clinicians.

Monitoring breast development as a guide to dosage, rather than increasing it in pre-determined steps, accords with clinical experience of other conditions. In taking young girls through puberty, if you increase estrogens abruptly, they sometimes get uncomfortable breast development with an abnormal breast profile – characterised by increase in the areola, which gives a curious double hump. Whether the same would happen in an older breast is unclear. Although it is doubtful that quite the same caution would be warranted, careful monitoring seems appropriate.

The Dutch use of 17-beta estradiol seems warranted. The dose of ethinylestradiol necessary to feminise a transsexual adolescent, who has already completed full male puberty, may even be as high as 100μg daily. At such dosage levels there is reported to be a substantially greater thrombotic risk than in using 17-beta estradiol (reference below).

Reference

A. W. F. T. Toorians, M. C. L. G. D. Thomassen, S. Zweegman, E. J. P. Magdeleyns, G. Tans, L. J. G. Gooren and J. Rosing; Venous Thrombosis and Changes of Hemostatic Variables during Cross-Sex Hormone Treatment in Transsexual People; The Journal of Clinical Endocrinology & Metabolism; 2003;88(12);5723–5729

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