Development of Suprarenal Glands
Development of Suprarenal Glands
The cortex and medulla of the suprarenal (adrenal) glands have
different originsThe cortex develops from mesoderm and the medulla
differentiates from neural crest cellsThe cortex is first indicated
during the sixth week by an aggregation for mesenchymal cells on
each side, between the root of the dorsal mesentery and the
developing gonadThe cells that form the fetal cortex are derived
from the mesothelium lining the posterior abdominal wall
The cells that form the medulla are derived from an adjacent
sympathetic ganglion, which is derived from neural crest
cellsInitially the neural crest cells form a mass on the medial
side of the fetal cortexAs they are surrounded by the fetal cortex,
these cells differentiate into the secretory cells of the
suprarenal medullaLater more mesenchymal cells arise from the
mesothelium and enclose the fetal cortex
These cells give rise to the permanent cortexDifferentiation of
the characteristic suprarenal cortical zones begins during the late
fetal periodThe zona glomerulosa and zona fasciculata are present
at birth , but the zona reticularis is not recognizable until the
end of the third yearThe suprarenal glands of the human fetus are
10 to 20 times larger than the adult glands relative to body
weight, and are large compared with the kidneys
These large glands result from the extensive size of the fetal
cortexThe suprarenal medulla remains relatively small until after
birthThe suprarenal glands rapidly become smaller as the fetal
cortex regresses during the first yearThe glands lose about
one-third of their weight during the first 2 or 3 weeks after birth
and do not regain their original weight until the end of the second
year
Congenital Adrenal HyperplasiaAn abnormal increase in the cells
of the suprarenal cortex results in excessive androgen production
during the fetal periodIn females this usually causes
masculinization of the external genitalia and enlargment of the
clitoris Affected male infants have normal external genitalia and
may go undetected in early infancyLater in childhood in both sexes,
androgen excess leads to rapid growth and accelerated skeletal
maturation
The androgenital syndrome associated with congenital adrenal
hyperplasia (CAH) manifests itself in various clinical forms that
can be correlated with enzymatic deficiencies of cortisol
biosynthesisCAH is a group of autosomal recessive disorders that
result in virilization of female fetusesCAH is caused by a
genetically determined mutation in the cytochrome p450c21-steroid
21-hydroxylase gene, which causes a deficiency of suprarenal
cortical enzymes that are necessary for the biosynthesis of various
steroid hormonesThe reduced hormone ouput results in an increased
release of adrenocorticotropic hormone (ACTH), which causes adrenal
hyperplasia and overproduction of androgens by the hyperplastic
suprarenal glands
