Testis and epididymis
General
Gonadotropin deficiency

Author: Turki Al-Hussain, M.D. (see Authors page)

Revised: 4 April 2017, last major update August 2012

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PubMed Search: Testis and epididymis Gonadotropin deficiency

Cite this page: Gonadotropin deficiency. PathologyOutlines.com website. http://pathologyoutlines.com/topic/testisgonadotropin.html. Accessed December 12th, 2017.
Definition / general
  • For normal function, require intact axis of GnRH to FSH / LH
  • Prepubertal:
    • Delayed puberty: failure of adolescent development by age 16
    • Deficiency if gonadotropins were never secreted normally
    • Most patients with associated syndromes have major congenital anomalies
    • Kallmann syndrome: young adults / teenagers with prepubertal testes, anosmia / hyposmia (loss / reduction in sense of smell), cleft lip / palate, color blindness, short fourth metacarpals, low LH, FSH and testesterone
    • LH mutation preventing binding to receptor: high LH, normal FSH, low testosterone, no Leydig cells, maturation arrest
  • Postpubertal:
    • Selective LH deficiency: normal FSH, active spermatogenesis with normal tubules, low LH and testosterone, low semen volume, reduced / absent Leydig cells
    • Selective FSH deficiency: normal LH, normal testosterone, variable sperm counts, low FSH, infertile with hypospermatogenesis, spermatogenesis with germ cell aplasia and incomplete maturation arrest
Etiology
  • Postpubertal:
    • Pituitary or hypothalamic trauma, surgery, tumor, radiation, androgens / estrogens
Treatment
  • Prepubertal:
    • Exogenous FSH and LH produce normal appearing and functioning testes
  • Postpubertal:
    • FSH and LH produce normal appearing and functioning testes
Microscopic (histologic) description
  • Prepubertal
    • Testis resembles that in prepubertal child - small tubules without lumina, prepubertal Sertoli cells, scattered spermatogonia
    • No recognizable Leydig cells
  • Postpubertal:
    • Histology progresses from incomplete to complete maturation arrest, germ cell hypoplasia, germ cell aplasia, sclerotic tubules; tubules have thick / fibrotic walls, may have loss of Leydig cells
    • High dose estrogens for sex change patients cause immature Sertoli cells, germ cell hypoplasia and Leydig cell atrophy
    • Low dose estrogens for prostate adenocarcinoma cause maturation arrest and partial Leydig cell atrophy