Kits
17 OH-Progesterone ELISA
Kits
Description
17-Hydroxyprogesterone (17OH Progesterone or 17αOHP
or 17-OHP) is a C-21 steroid hormone produced
in the adrenal gland and gonads, during the synthesis
of glucocorticoids and sex steroids. It is derived from
progesterone via 17-hydroxylase, a P450c17 enzyme,
or from 17-hydroxypregnenolone via 3β-hydroxysteroid
dehydrogenase/∆5-4 isomerase. 17OH progesterone is
a precursor of cortisol that accumulates in the case of
adrenal 21-hydroxylase deficiency and decreased after
replacement therapy with cortisol. High values are
found in congenital adrenal hyperplasia.
17-OHP has no defined physiologic role except as a
precursor molecule.
Serum 17-OHP levels are age-dependent, with peak
levels observed during fetal life and the immediate
postnatal period. During the first week of life, serum 17
-OHP levels fall ~50-fold as compared to cord blood
values. A small transient increase occurs in male
infants 30-60 days postnatally. Levels for both sexes
remain at constant low levels during childhood, and
then progressively increase during puberty reaching
adult levels of ~100 ng/dL (~3.03 nmol/L). As with
cortisol, serum 17-OHP levels normally have an
ACTH-dependent diurnal variation, with peak levels in
the morning and a nadir at night. In addition, ovarian
production of 17-OHP increases during the luteal
phase of the menstrual cycle.
17-hydroxyprogesterone is a natural progestin and in
pregnancy increases in the third trimester primarily
due to fetal adrenal production.
Normal levels are 3-90 ng/dl in children, and in
women, 15-70 ng/dl prior to ovulation, and 35-290
ng/dl during the luteal phase.
Measurements of levels of 17-hydroxyprogesterone
are useful in the evaluation of patients with suspected
congenital adrenal hyperplasia as the typical enzymes
that are defective, namely 21-hydroxylase and 11βhydroxilase,
lead to a build-up of 17-OHP. In contrast,
the rare patient with 17α-hydroxylase deficiency will
have very low or undetectable levels of 17-OHP.
Elevated serum 17-OHP levels at baseline and/or after
ACTH stimulation have also been reported in other
forms of adrenal hyperplasia.
or 17-OHP) is a C-21 steroid hormone produced
in the adrenal gland and gonads, during the synthesis
of glucocorticoids and sex steroids. It is derived from
progesterone via 17-hydroxylase, a P450c17 enzyme,
or from 17-hydroxypregnenolone via 3β-hydroxysteroid
dehydrogenase/∆5-4 isomerase. 17OH progesterone is
a precursor of cortisol that accumulates in the case of
adrenal 21-hydroxylase deficiency and decreased after
replacement therapy with cortisol. High values are
found in congenital adrenal hyperplasia.
17-OHP has no defined physiologic role except as a
precursor molecule.
Serum 17-OHP levels are age-dependent, with peak
levels observed during fetal life and the immediate
postnatal period. During the first week of life, serum 17
-OHP levels fall ~50-fold as compared to cord blood
values. A small transient increase occurs in male
infants 30-60 days postnatally. Levels for both sexes
remain at constant low levels during childhood, and
then progressively increase during puberty reaching
adult levels of ~100 ng/dL (~3.03 nmol/L). As with
cortisol, serum 17-OHP levels normally have an
ACTH-dependent diurnal variation, with peak levels in
the morning and a nadir at night. In addition, ovarian
production of 17-OHP increases during the luteal
phase of the menstrual cycle.
17-hydroxyprogesterone is a natural progestin and in
pregnancy increases in the third trimester primarily
due to fetal adrenal production.
Normal levels are 3-90 ng/dl in children, and in
women, 15-70 ng/dl prior to ovulation, and 35-290
ng/dl during the luteal phase.
Measurements of levels of 17-hydroxyprogesterone
are useful in the evaluation of patients with suspected
congenital adrenal hyperplasia as the typical enzymes
that are defective, namely 21-hydroxylase and 11βhydroxilase,
lead to a build-up of 17-OHP. In contrast,
the rare patient with 17α-hydroxylase deficiency will
have very low or undetectable levels of 17-OHP.
Elevated serum 17-OHP levels at baseline and/or after
ACTH stimulation have also been reported in other
forms of adrenal hyperplasia.