CEDIE   05498
CENTRO DE INVESTIGACIONES ENDOCRINOLOGICAS "DR. CESAR BERGADA"
Unidad Ejecutora - UE
artículos
Título:
Male hypogonadism: an extended classification based on a developmental, endocrine physiology-based approach
Autor/es:
REY R; GRINSPON R; GOTTLIEB S; PASQUALINI T; KNOBLOVITS P; ASZPIS S; PACENZA N; STEWART USHER J; BERGADA I; CAMPO S
Revista:
INTERNATIONAL JOURNAL OF ANDROLOGY
Editorial:
WILEY-BLACKWELL PUBLISHING, INC
Referencias:
Lugar: Londres; Año: 2012
ISSN:
0105-6263
Resumen:
Normal testicular physiology results from the integrated function of the tubular and interstitial compartments. Serum markers of interstitial tissue function are testosterone and insulin-like factor 3 (INSL3) levels, whereas tubular function can be assessed by sperm count, morphology and motility, and serum anti-Müllerian hormone (AMH) and inhibin B. The classical definition of male hypogonadism refers to testicular failure associated with androgen deficiency, without considering potential deficiencies in germ and Sertoli cells. Furthermore, nor does it consider the fact that low basal serum testosterone cannot be equated to hypogonadism in childhood, since Leydig cells are normally quiescent. A broader clinical definition of hypogonadism that could be applied to males in different periods of life requires a comprehensive consideration of the physiology of the hypothalamic-pituitary-testicular axis and its disturbances along development. Here we propose an extended classification of male hypogonadism based on the pathophysiology of the hypothalamic-pituitary-testicular axis in different periods of life. The clinical and biochemical features of male hypogonadism vary according to: a) the level of the hypothalamic-pituitary-testicular axis primarily affected: central, primary or combined; b) the testicular cell population initially impaired: whole testicular dysfunction or dissociated testicular dysfunction, and: c) the period of life when the gonadal function begins to fail: fetal-onset or postnatal-onset. The evaluation of basal testicular function in infancy and childhood relies mainly on the assessment of Sertoli cell markers (AMH and inhibin B). Hypergonadotropism should not be considered a sine qua non condition for the diagnosis of primary hypogonadism in childhood. Finally, the lack of elevation of gonadotropins in adolescents or adults with primary gonadal failure is indicative of a combined hypogonadism involving the gonads and the hypothalamic-pituitary axis.