How do You initiate Oestrogen Therapy in a Girl Who has Not Undergone Puberty?

Peter C. Hindmarsh

Disclosures

Clin Endocrinol. 2009;71(1):7-10. 

In This Article

Pubertal Induction in Special Situations

Consideration needs to be given to the underlying condition which is being treated. In girls with Turner syndrome, there is often associated obesity, insulin insensitivity, adverse lipid profile and high blood pressure/hypertension.[16,17] Given this constellation of features along with a likely adverse coagulopathy profile then care in choosing long-term HRT is essential. The aim in this situation must be to use HRT with a profile that minimizes any impact on this already adverse cardiometabolic profile.

In patients with secondary gonadal failure and associated anterior pituitary hormone deficiencies, consideration of the interaction of the induction and maintenance programme on substitution of the deficient hormones is needed. Oestrogens themselves will alter cortisol and thyroid binding globulin concentrations but it is relatively unusual to have to alter replacement doses of hydrocortisone and thyroxine although ongoing monitoring should be undertaken.

Interaction of GH and oestrogen is perhaps more important. GH and oestrogen contribute 50% each to the magnitude of the pubertal growth spurt. This means that GH dosing needs to be optimized so that a normal pubertal growth spurt is engendered. The secretion of GH during puberty doubles;[18] studies that have attempted to mimic this in the therapeutic setting have not yielded many differences from the standard dosing.[19] Nonetheless, frequent growth monitoring (3–4 monthly) should be undertaken to ensure the spurt is maximized. The corollary of this is that in anyone undergoing pubertal induction a poor pubertal growth response should alert the clinician to the possibility of associated GH deficiency.

Prior to the commencement of therapy the clinician should obtain a history of thrombotic episodes which may lead to consideration of a more physiological approach using pulsatile subcutaneous GnRH therapy. Family history of breast/gynaecological malignancy may be of concern. At this stage there are no data on risks of malignancy in those undergoing pubertal induction and maintenance of secondary sexual characteristics using oestrogen preparations. Nor are these data likely to be forthcoming given the sample size that would be required to tease out these particular effects. At best we can only quote risks from studies of the oral contraceptive pill. In contrast, however, to the general population these risks, which are relatively small, have to be offset against the long-term effects of osteoporosis. Whether oestrogen therapy in the pubertal induction population will protect from the premature development of cardiovascular disease is unclear. Postmenopausal data would argue against although with these studies, there was a suggestion of benefit for those starting HRT immediately postmenopausal.[20] Further, there is evidence for endothelial dysfunction in young women with premature ovarian failure prior to hormone replacement and improvement on therapy.[21] On balance, the health risk of osteoporosis outweighs the small increase in breast cancer risk with some evidence to argue the case for an effect on surrogate markers of cardiovascular disease.

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