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DOI 10.1590/s0004-27302008000500023

Медицинская библиотека · Arquivos brasileiros de endocrinologia e metabologia · 2008

[The influence of estrogen and progestogen replacement on growth hormone activity in women with hypopituitarism].

Isotton Ana Lúcia, Wender Maria Celeste O, Czepielewski Mauro A

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Аннотация

Treatment of hypogonadotropic hypogonadism in adult women with hypopituitarism can include a wide range of estrogen and progestogen treatment alternatives and oral administration is the route of least cost and greatest patient comfort. The oral estrogen route has a major impact on the growth hormone-insulin-like growth factor I (GH/IGF-1) axis. Oral estrogen therapy, when given concurrently with GH to patients with hypopituitarism, antagonizes the biological effects of GH treatment and aggravates the abnormalities of body composition and the metabolism in general. It is presumed that oral estrogen suppresses the secretion/production of IGF-1 by a hepatic first-pass mechanism, resulting in increased GH secretion by means of suppressing the IGF-1 negative feedback that is present in healthy women. This is clinically manifested in reduced lean body mass, increased fat mass, an atherogenic lipid profile and damage to psychological well-being. Some studies have indicated that progestogens with androgenic actions reverse the effect of reduced serum IGF-1 levels that is induced by the oral estrogens. Neutral progestogens do not exert this effect, however the stronger the androgenic potentialis, the more the effect of reduced IGF-1 will be reversed. This bibliographical review will deal with the clinical aspects of estrogen and progestogen replacement in women with hypopituitarism, their interactions with other hormone deficiencies and the impact of estrogen treatment on the metabolic actions of GH.

Для цитирования: Isotton Ana Lúcia, Wender Maria Celeste O, Czepielewski Mauro A. [The influence of estrogen and progestogen replacement on growth hormone activity in women with hypopituitarism].. Arquivos brasileiros de endocrinologia e metabologia. 2008. DOI: 10.1590/s0004-27302008000500023.

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