In a male patient with Klinefelter syndrome (47,XXY), the characteristic hormonal profile is:

• A Low FSH, low LH, low testosterone (hypogonadotropic hypogonadism)
• B High FSH, high LH, low testosterone (hypergonadotropic hypogonadism due to primary gonadal failure) ✓
• C High FSH, normal LH, normal testosterone (isolated Sertoli cell failure)
• D Normal FSH, normal LH, high testosterone (androgen resistance with reflex hypergonadotropism)

Explanation

Klinefelter syndrome (47,XXY) causes primary testicular failure due to progressive seminiferous tubule fibrosis and Leydig cell dysfunction. Both Sertoli cells (producing inhibin B, which suppresses FSH) and Leydig cells (producing testosterone, which suppresses LH via negative feedback) fail. The result is hypergonadotropic hypogonadism: elevated FSH (due to loss of inhibin B and reduced Sertoli cell mass) and elevated LH (due to low testosterone), with low testosterone. Azoospermia is invariable due to seminiferous tubule failure. This pattern — high FSH + high LH + low testosterone — is the classic hormonal fingerprint of primary hypogonadism (testicular failure) as distinguished from hypogonadotropic hypogonadism (low FSH/LH + low testosterone).

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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