In a male patient with low testosterone, normal luteinizing hormone (LH) and normal follicle‑stimulating hormone (FSH), and normal prolactin, is the cause primary testicular failure or secondary pituitary/hypothalamic hypogonadism?

Secondary (Pituitary/Hypothalamic) Hypogonadism

Your patient has secondary hypogonadism, not primary testicular failure. The combination of low testosterone (2.11 ng/mL) with inappropriately normal LH (6.1 mIU/mL) and FSH (3.39 mIU/mL) indicates a pituitary or hypothalamic problem rather than testicular dysfunction 1.

Diagnostic Reasoning

In primary testicular failure, the pituitary responds appropriately to low testosterone by markedly elevating LH and FSH above the normal range 2, 3. Your patient's gonadotropins are not elevated—they remain in the normal range despite severely low testosterone. This represents an inadequate pituitary response, which is the hallmark of secondary hypogonadism 1, 4.

Key Distinguishing Features:

• Primary hypogonadism (testicular): Low testosterone + High LH/FSH (typically >12-15 mIU/mL) 2, 3
• Secondary hypogonadism (pituitary/hypothalamic): Low testosterone + Low or inappropriately normal LH/FSH 1, 2, 4

The physiological negative feedback loop between testosterone and gonadotropins should drive LH and FSH significantly higher when testosterone is this low 5. The failure of your patient's pituitary to mount this response confirms central (secondary) hypogonadism 1, 4.

Required Additional Workup

Before proceeding with treatment, you must complete the evaluation for secondary hypogonadism:

• Repeat morning testosterone (8-10 AM) on a second occasion to confirm persistent low levels 1, 6
• Measure serum prolactin immediately to screen for hyperprolactinemia, which is a common reversible cause of secondary hypogonadism 1, 7, 4
• Check thyroid function (TSH, free T4) as thyroid disorders affect sex hormone metabolism and can contribute to hypogonadism 6, 4
• Consider pituitary MRI if prolactin is elevated or if other pituitary hormone deficiencies are suspected to evaluate for pituitary tumors, infiltrative disease, or structural abnormalities 1, 4
• Assess for reversible causes: obesity (increased aromatization of testosterone to estradiol suppresses LH), medications (opiates, corticosteroids), systemic illness, hemochromatosis (check iron saturation) 1, 6, 8

Common Pitfalls to Avoid

Do not assume normal-range LH/FSH means normal pituitary function when testosterone is low 1, 4. In the context of hypogonadism, "normal" gonadotropins are actually inappropriately low—the pituitary should be driving them much higher 5.

In obese men specifically, increased adipose tissue aromatizes testosterone to estradiol, which then suppresses pituitary LH secretion through negative feedback 1, 6. This creates a functional secondary hypogonadism that may improve with weight loss 6.

Treatment Considerations

• If fertility is desired, do NOT use testosterone replacement therapy, as it will further suppress LH/FSH and eliminate spermatogenesis 6, 2
• For fertility preservation, consider selective estrogen receptor modulators (SERMs) like clomiphene citrate to stimulate endogenous testosterone production 6
• Standard testosterone replacement is appropriate if fertility is not a concern and reversible causes have been addressed 1, 2
• Address underlying obesity through weight loss if present, as this can improve functional hypogonadism independent of hormonal therapy 1, 6