Do I have testicular failure given my elevated Follicle-Stimulating Hormone (FSH) level, testicular atrophy, low normal sperm count, and low testosterone level?

Assessment of Testicular Function with FSH 9.9 IU/L, Testicular Atrophy, Sperm Count 90 million/mL, and Testosterone 36 nmol/L

You do not have testicular failure—your sperm count of 90 million/mL far exceeds the WHO lower reference limit of 16 million/mL, and your testosterone level of 36 nmol/L (approximately 1040 ng/dL) is well above the normal range, indicating preserved testicular function despite mild FSH elevation and testicular atrophy. 1, 2

Understanding Your Hormone Profile

Your clinical picture represents compensated testicular function, not testicular failure. Here's why:

• Primary testicular failure presents with testosterone below normal range, FSH typically >7.6 IU/L (often much higher, frequently >15-20 IU/L), elevated LH, and reduced sperm counts or azoospermia 1, 2
• Your FSH of 9.9 IU/L is mildly elevated above the 7.6 IU/L threshold, but this level indicates some degree of testicular stress—not complete failure 1, 3
• Your testosterone of 36 nmol/L (≈1040 ng/dL) is in the high-normal to elevated range, which argues strongly against primary testicular failure 1
• Your sperm count of 90 million/mL is 5.6 times higher than the WHO reference limit, confirming active spermatogenesis 1, 2

What the Testicular Atrophy Means

The presence of testicular atrophy with preserved function creates an apparent paradox that requires explanation:

• Testicular atrophy typically indicates reduced seminiferous tubule mass, which should correlate with elevated FSH and impaired sperm production 1, 2
• However, your normal sperm count demonstrates that sufficient functional testicular tissue remains to maintain spermatogenesis 2
• The pituitary is compensating by producing slightly more FSH (9.9 IU/L) to maintain normal sperm output despite reduced testicular volume 1, 4
• This represents compensated testicular dysfunction—the testes are working harder (reflected by elevated FSH) but still producing normal results 2

Critical Distinction: Compensated vs. Decompensated Function

Compensated testicular function (your situation):

• Normal or high testosterone 2
• Mildly elevated FSH (typically 7.6-12 IU/L) 1, 3
• Normal sperm production 2
• Testicular atrophy may be present but function is preserved 2

Decompensated testicular failure (not your situation):

• Low testosterone (<10 nmol/L or <300 ng/dL) 1, 2
• Markedly elevated FSH (typically >15-20 IU/L) 1, 4
• Severe oligospermia or azoospermia 1, 2
• Small, atrophic testes with progressive dysfunction 2

Essential Next Steps

Immediate Diagnostic Workup

• Measure LH level to complete the hormonal picture—normal LH with your testosterone level would confirm compensated function rather than primary failure 1, 2
• Obtain complete semen analysis with at least two samples 2-3 months apart to confirm stable parameters including motility and morphology, not just concentration 1, 2
• Check SHBG and calculate free testosterone to ensure bioavailable testosterone is adequate despite any SHBG elevation 1, 2
• Evaluate thyroid function (TSH, free T4) as thyroid disorders can elevate FSH and affect spermatogenesis 1, 2
• Assess for varicocele on standing physical examination, as this is a reversible cause of testicular atrophy and elevated FSH 1

Genetic Testing Considerations

• Genetic testing is NOT indicated with your normal sperm count of 90 million/mL 2
• Karyotype and Y-chromosome microdeletion testing are only recommended when sperm concentration is <5 million/mL with elevated FSH 1, 2

Monitoring and Fertility Preservation

Follow-Up Protocol

• Repeat hormonal panel (FSH, LH, testosterone) in 6-12 months to establish whether FSH is stable or trending upward 2
• Repeat semen analysis in 6-12 months to confirm stable sperm parameters 2
• If FSH rises above 12 IU/L or sperm count drops below 20 million/mL on follow-up, consider sperm cryopreservation 1, 2

Addressing Reversible Factors

• Optimize metabolic health—weight loss and metabolic optimization can normalize gonadotropins in functional hypogonadism 1, 2
• Correct thyroid dysfunction if present, as this disrupts the hypothalamic-pituitary-gonadal axis 1, 2
• Evaluate and treat varicocele if present, as repair can improve testosterone levels, reduce FSH, and stabilize testicular volume 1

Critical Pitfall to Avoid

NEVER start testosterone therapy if you have any interest in current or future fertility. 2, 5, 6

• Exogenous testosterone completely suppresses FSH and LH through negative feedback on the hypothalamus and pituitary 2, 5, 6
• This eliminates intratesticular testosterone production (which is 50-100 times higher than serum levels and essential for spermatogenesis) and causes azoospermia 1, 6
• Recovery after stopping exogenous testosterone takes approximately 14 months for sperm output and 38 months for sperm motility 6
• Your current testosterone level of 36 nmol/L is already in the high-normal range—you do not need supplementation 2

Fertility Outlook

Your fertility prognosis is excellent:

• Sperm count of 90 million/mL places you well within the normal fertile range (WHO reference ≥16 million/mL) 1, 2
• Your total motile sperm count (assuming normal motility) likely exceeds the 10 million threshold associated with good natural conception rates 1
• The mildly elevated FSH indicates reduced testicular reserve but does not preclude natural conception with your current sperm parameters 1, 2
• Natural conception should be attempted for 12 months before considering assisted reproductive technology, assuming female partner has normal fertility 1