Male Reproductive Endocrinology and Hormone Testing
Core concepts
Understand the hypothalamic-pituitary-gonadal axis: GnRH pulses drive LH and FSH; LH stimulates Leydig cell testosterone production; FSH supports Sertoli cell function and spermatogenesis. Know the patterns: primary hypogonadism (low testosterone, high LH/FSH), secondary hypogonadism (low testosterone, low or inappropriately normal gonadotropins), and the distinction between total and free testosterone (SHBG, albumin binding). Recognize hyperprolactinemia, thyroid dysfunction, and exogenous androgen use as causes of suppressed spermatogenesis. Know assay pitfalls: immunoassay variability, diurnal testosterone rhythm (morning sampling), biotin interference, and the need for confirmatory testing.
Traps
Questions often present a low testosterone with normal gonadotropins and expect you to recognize secondary hypogonadism or androgen abuse rather than primary failure. Another trap: interpreting a single testosterone value without morning timing or repeat confirmation. Watch for confusion between FSH as a marker of spermatogenesis (elevated in Sertoli cell dysfunction) and LH as a marker of Leydig cell function. Also remember that exogenous testosterone suppresses LH/FSH and reduces intratesticular testosterone, impairing fertility-a common clinical reasoning trap.
Worked example / rule of thumb
A man with low libido, testosterone 180 ng/dL, LH 1.0 IU/L, FSH 1.2 IU/L: gonadotropins are inappropriately low, indicating secondary hypogonadism (or exogenous androgen use). Rule of thumb: draw testosterone in the morning, confirm abnormal results on a second sample, and always interpret testosterone together with LH and FSH rather than in isolation.