Hormonal
control of development of testis and spermatogenesis and final maturation of sec spermatocytes in
testis??
During
the first two trimesters of intrauterine life, fetal sex steroid production is
driven by maternal human chorionic gonadotropin (hCG). The HPG axis is
activated around the third trimester and remains active for the first 6-months
of neonatal life.
This
so-called mini-puberty is a developmental window that has profound effects on
future potential for fertility. In early puberty, GnRH secretion is reactivated
first at night and then night and day. Pulsatile GnRH stimulates both LH and
FSH, which induce maturation of the seminiferous tubules and Leydig cells.
But Congenital
hypogonadotropic hypogonadism (CHH) results from GnRH deficiency and resultant
NOA(Nonobstructive azoospermia) . Men with Congenital hypogonadotropic
hypogonadism (CHH) lack the
mini-pubertal and pubertal periods
of Sertoli Cell proliferation and thus present with prepubertal testes
(<4mL) and low inhibin serum levels --reflecting diminished SC(Sertoli
cell) numbers.
Medl
TR ? Ans: To induce full maturation of the testes, GnRH-deficient patients can
be treated with either pulsatile GnRH, hCG or combined gonadotropin therapy
(FSH+hCG). Fertility outcomes with each of these regimens are highly variable.
Recently, few randomized, open label treatment study addressed the question of
whether a sequential treatment
with FSH alone prior to LH and FSH (via GnRH pump) could enhance
fertility outcomes.
All
men receiving the sequential treatment developed sperm in the ejaculate,
AS
such few large, multicenter clinical
trial is needed to definitively prove the optimal treatment approach for severe
CHH.
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