INVESTIGADORES
BERGADÁ Ignacio
artículos
Título:
Spreading the clinical window for diagnosing fetal-onset hypogonadism in boys
Autor/es:
GRINSPON RP; LORETI N; BRASLAVSKY D; VALERI C; SCHTEINGART, H; BALLERINI MG; BEDECARRAS PATRICIA; AMBAO V; GOTTLIEB S; ROPELATO, M.G.; BERGADÁ I; CAMPO SM; REY RA
Revista:
Frontiers in Endocrinology
Editorial:
Lausanne
Referencias:
Año: 2014
Resumen:
In early fetal development, the testis secretes ? independent of pituitary gonadotropins ?
androgens and anti-Müllerian hormone (AMH) that are essential for male sex differentiation.
In the second half of fetal life, the hypothalamic?pituitary axis gains control of testicular
hormone secretion. Follicle-stimulating hormone (FSH) controls Sertoli cell proliferation,
responsible for testis volume increase and AMH and inhibin B secretion, whereas luteinizing
hormone (LH) regulates Leydig cell androgen and INSL3 secretion, involved in the
growth and trophism of male external genitalia and in testis descent.This differential regulation
of testicular function between early and late fetal periods underlies the distinct clinical
presentations of fetal-onset hypogonadism in the newborn male: primary hypogonadism
results in ambiguous or female genitalia when early fetal-onset, whereas it becomes clinically
undistinguishable from central hypogonadism when established later in fetal life. The
assessment of the hypothalamic?pituitary?gonadal axis in male has classically relied on
the measurement of gonadotropin and testosterone levels in serum. These hormone levels
normally decline 3?6 months after birth, thus constraining the clinical evaluation window
for diagnosing male hypogonadism. The advent of new markers of gonadal function has
spread this clinical window beyond the first 6 months of life. In this review, we discuss the
advantages and limitations of old and new markers used for the functional assessment of
the hypothalamic?pituitary?testicular axis in boys suspected of fetal-onset hypogonadism.