INVESTIGADORES
BERGADÁ Ignacio
artículos
Título:
Sertori cell markers in the diagnosis of paediatric male hypogonadism
Autor/es:
GRINSPON RP; LORETI N; BRASLAVSKY D; BEDECARRAS PATRICIA; AMBAO V; GOTTLIEB S; BERGADÁ I; CAMPO SM; REY RA
Revista:
JOURNAL OF PEDIATRIC ENDOCRINOLOGY AND METABOLISM
Editorial:
Walter de Gruyter GmbH & Co. KG
Referencias:
Año: 2012 p. 3 - 11
ISSN:
2191-0251
Resumen:
During childhood, the pituitary-testicular axis is partially
dormant: testosterone secretion decreases following a drop
in luteinising hormone levels; follicle-stimulating hormone
(FSH) levels also go down. Conversely, Sertoli cells are most
active, as revealed by the circulating levels of anti-M ü llerian
hormone (AMH) and inhibin B. Therefore, hypogonadism
can best be evidenced, without stimulation tests, if Sertoli cell
function is assessed. Serum AMH is high from fetal life until
mid-puberty. Testicular AMH production increases in response
to FSH and is potently inhibited by androgens. Inhibin B is
high in the fi rst years of life, then decreases partially while
remaining clearly higher than in females, and increases again
at puberty. Serum AMH and inhibin B are undetectable in
anorchid patients. In primary or central hypogonadism affecting
the whole gonad established in fetal life or childhood, all
testicular markers are low. Conversely, when hypogonadism
only affects Leydig cells, serum AMH and inhibin B are normal.
In males of pubertal age with central hypogonadism,
AMH and inhibin B are low. Treatment with FSH provokes
an increase in serum levels of both Sertoli cell markers,
whereas human chorionic gonadotrophin (hCG) administration
increases testosterone levels. In conclusion, measurement
of serum AMH and inhibin B is helpful in assessing testicular
function, without need for stimulation tests, and orientates the
aetiological diagnosis of paediatric male hypogonadism.