Article Text

Oestrogen treatment of tall stature
  1. C G D BROOK,
  2. R STANHOPE,
  3. M A PREECE,
  4. A AYNSLEY GREEN,
  5. P C HINDMARSH
  1. London Centre for Paediatric Endocrinology & Metabolism
  2. The University College
  3. London Hospitals NHS Trust
  4. The Middlesex Hospital
  5. Mortimer Street, London WIN BAA, UK

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    Editor,—We deplore the publication of a paper that lends credibility to a therapeutic regimen that is not only obsolete but also dangerous.1 High dose oestrogen treatment has an unacceptable incidence of side effects, which the authors record, and an unknown risk of thromboembolic problems2 and carcinoma of the breast, ovary, and uterus.

    The prevention of excessive adult stature is attained much more benignly by the induction of puberty using low doses of sex steroid at an age and height judged to achieve a satisfactory end point.

    Final height is determined by the height attained at onset of puberty,3 a constant amount of height (30 cm) being added to that height. This is why children with precocious puberty end up short; they have an insufficient amount of time to grow along the childhood curve of growth. For example, if a girl is not to exceed a final height of 180 cm, she needs to have started breast development (spontaneously or induced with low dose oestrogen) when she has attained a height of 150 cm. The only problem is if she is too young to induce puberty when she has attained this stature. This is a very rare situation, which is probably pathological. Exactly the same arithmetic applies to boys whose puberty can be induced with low dose testosterone.

    References

    Dr Weimann and Professor Böhles comment:

    We were particularly concerned about this harsh criticism because not all necessary points of view have been taken into consideration. Our paper is the result of a retrospective analysis of our data from 1985 to 1994. It describes our experience with high dose oestrogen treatment for the prevention of excessive adult stature, which has been used worldwide over the past 42 years. We were well aware of the risk of hypercoagulability. There was increased platelet aggregation in 60% of the 50 girls we examined. All other coagulation parameters such as activated prothrombin time, partial thromboplastin time, fibrinogen, and antithrombin III were normal. Platelet aggregation can easily be avoided with low dose aspirin supplementation. The risk of carcinoma of the breast, ovary, and uterus is a hypothetical speculation when natural oestrogens are used, as in our patients.

    The interesting approach of using low dose oestrogen in girls at risk of attaining excessive adult stature when they reach 150 cm may be theoretically better with respect to possible side effects; however, practically it may be applicable only in some patients because they usually present at a later age when they are deeply concerned about their possible final height. In our study the mean age and mean height at first presentation was 12.8 years and 175.5 cm. In addition, in most cases a height of 150 cm in girls above the 97th percentile is accompanied by a chronological age of less than 10 years, when an accurate adult height prediction is still difficult.

    We know of no sufficiently evaluated study on the efficacy of low dose oestrogen treatment for the prevention of excessive adult stature in girls. We were therefore very surprised that such critical emphasis has been placed by our colleagues on an unevaluated opinion.

    When patients present with a height above the 97th percentile and ongoing puberty, a decision has to be made, and reports about the experience with treatment regimens other than low dose oestrogens will be welcome. As we are counselling healthy young girls, the indication for treatment is always the result of a thorough appraisal of all known treatment risks, and the consequence of the psychological impact of an excessive final height.

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