RT Book, Section
A1 Paduch, Darius A.
A1 Schlegel, Peter N.
A1 Bergadá, Ignacio
A1 Rey, Rodolfo A.
A2 Sarafoglou, Kyriakie
A2 Hoffmann, Georg F.
A2 Roth, Karl S.
SR Print(0)
ID 1140321405
T1 Male Hypogonadism
T2 Pediatric Endocrinology and Inborn Errors of Metabolism, 2e
YR 2017
FD 2017
PB McGraw-Hill Education
PP New York, NY
SN 9780071773140
LK accesspediatrics.mhmedical.com/content.aspx?aid=1140321405
RD 2024/04/24
AB Normal  testicular  function  is  necessary  for  external  genital  development  and  function,  diverse  psychosexual  dimorphic  features,  normal  muscle,  and  bone  structure*.  Depending  on  age  and  developmental  stage,  underlying  defects  may  have  variable  phenotypic  presentations.  For  example,  deletion  of  the  AZF  region  of  the  Y  chromosome  will  result  in  spermatogenic  failure  during  puberty  and  in  adulthood,  but  has  no  effect  on  normal  childhood  development  and  timing  or  progression  of  puberty.  Most  defects  in  Leydig  cell,  Sertoli  cell,  or  germ  cell  function  may  have  subtle  but  variable  presentation  from  fetal  period  to  adolescence.  Thus,  it  is  helpful  to  consider  hypogonadism  as  disorder  of  specific  cell  populations  like  Leydig  cells,  germ  cells,  or  Sertoli  cells,  remembering  that  close  and  tight  interactions  between  Sertoli  and  germ  cells  exist  and  are  critical  in  normal  testicular  function1  (Table  38-1).  A  broader  definition  of  hypogonadism,  applicable  to  males  from  fetal  life  to  adulthood,  requires  a  comprehensive  consideration  of  the  physiology  of  the  hypothalamo-pituitary-testicular  axis  and  its  disturbances  along  development.  In  this  chapter,  we  address  male  hypogonadism  based  on  the  pathophysiology  of  the  hypothalamo-pituitary-testicular  axis  in  different  periods  of  life.