Epidemiology


Etiology

  • Associated with advanced maternal age

Pathophysiology

  • 47,XXY (rarely 48,XXXY or 48,XXYY)
    • Presence of a Barr body (inactivated X chromosome)
  • Testicular dysgenesis leads to:
    • Seminiferous tubules dysgenesis → loss of Sertoli cells → ↓ inhibin B → ↑ FSH
    • Leydig cell dysfunction → ↓ testosterone → ↑ LH
  • Both ↑ LH and ↑ FSH lead to increased conversion of testosterone to estrogen.

Clinical features

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  • Eunuchoid growth pattern: tall, slim stature with long extremities (Growth plate closure is delayed )
  • Gynecomastia
  • Testicular atrophy
  • Possible developmental delay
    • Neurocognitive dysfunction (impaired executive function and memory, decreased intelligence)
  • Associated disorders

Diagnostics


Treatment