What could be causing my testicular atrophy with normal sperm count, slightly elevated Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH) levels, and no evidence of infection or inflammation?

Testicular Atrophy with Normal Sperm Count and Borderline Elevated Gonadotropins

Your FSH and LH levels are in the upper-normal range, suggesting mild compensated testicular dysfunction, but your excellent sperm count indicates preserved spermatogenesis despite the testicular size reduction. 1

Understanding Your Hormone Profile

Your hormonal pattern reveals important information about testicular function:

• FSH at 10 IU/L (upper normal range) indicates your pituitary is working harder to maintain sperm production, which typically occurs when the testes have some degree of dysfunction but are still producing sperm adequately. 1, 2

• LH at 7.2 IU/L (also upper-normal) shows your Leydig cells require more stimulation to maintain testosterone production, but the fact that they're responding suggests functional testosterone synthesis. 1

• The combination of borderline elevated FSH with normal sperm count is reassuring - FSH levels between 7.6-10 IU/L typically indicate impaired but not absent spermatogenesis, and your excellent sperm parameters confirm this. 1, 2

Why Your Testicles Are Getting Smaller

Several mechanisms could explain progressive testicular atrophy despite maintained sperm production:

• Primary testicular dysfunction with compensatory pituitary response - Your elevated gonadotropins suggest the testes are becoming less responsive, requiring more FSH/LH stimulation to maintain function. The testicular tissue may be gradually declining even as remaining functional tissue produces adequate sperm. 1, 3

• The 3mm varicocele, though "non-clinical," may still contribute to progressive testicular damage through chronic venous congestion and elevated testicular temperature, even if it doesn't meet surgical criteria. 2

• Intratesticular testosterone levels (50-100 times higher than serum) maintain spermatogenesis independently of testicular size, which explains why you can have shrinking testes but preserved sperm production. 4, 5

Essential Next Steps

Immediate Diagnostic Workup

• Measure total testosterone and SHBG to calculate free testosterone and determine if Leydig cell function is truly adequate despite the elevated LH. 1, 2

• Check serum prolactin to exclude hyperprolactinemia, which can disrupt gonadotropin secretion and contribute to testicular dysfunction. 1, 2

• Obtain thyroid function tests (TSH, free T4) as thyroid disorders commonly affect reproductive hormones and can cause testicular atrophy. 1, 2

• Repeat semen analysis in 3-6 months to establish whether sperm parameters are stable or declining, as single analyses can be misleading due to natural variability. 4, 2

Address Reversible Factors

• Optimize metabolic health - Weight loss and metabolic optimization can normalize gonadotropins and improve testosterone levels if obesity or metabolic stress is present. 2

• Evaluate for medications or substances that interfere with testosterone production or hypothalamic-pituitary axis function. 2

• Correct any thyroid dysfunction, as even subtle thyroid abnormalities can significantly affect testicular function and SHBG levels. 2

Fertility Preservation Considerations

Given your borderline hormonal profile and progressive testicular atrophy, strongly consider sperm cryopreservation now while parameters are excellent:

• Men with elevated FSH and testicular atrophy are at risk for progressive spermatogenic failure, and once azoospermia develops, even microsurgical testicular sperm extraction only achieves 40-50% retrieval rates. 4, 2

• Collect at least 2-3 ejaculates for cryopreservation to provide backup samples, as sperm concentration and motility decrease after freezing, though DNA integrity is preserved. 4

• Your current excellent sperm count (described as "very good") makes this the optimal time for preservation before potential future decline. 1, 4

Critical Management Pitfalls to Avoid

• Never start testosterone therapy if you desire current or future fertility - exogenous testosterone will completely suppress spermatogenesis through negative feedback on the hypothalamus and pituitary, potentially causing azoospermia that takes months to years to recover. 1, 2, 5

• Do not assume your fertility is secure based on current sperm count alone - the combination of borderline elevated FSH, elevated LH, and progressive testicular atrophy suggests ongoing testicular dysfunction that may worsen over time. 1, 4

• Do not delay genetic testing if future semen analyses show severe oligospermia (<5 million/mL) - karyotype analysis and Y-chromosome microdeletion testing would then be mandatory to guide prognosis and treatment options. 1, 2

Monitoring Strategy

• Repeat complete hormonal panel (FSH, LH, testosterone, SHBG, prolactin, thyroid function) in 3-6 months after addressing any reversible metabolic or thyroid factors. 1, 2

• Annual semen analysis to monitor for declining parameters, with more frequent testing if deterioration is detected. 4, 2

• Physical examination every 6-12 months to assess testicular volume progression and evaluate for varicocele changes. 2

Long-Term Health Implications

• Men with abnormal semen parameters have higher rates of testicular cancer and increased mortality compared to fertile men, making ongoing surveillance important beyond fertility concerns. 4

• Infertile men have more comorbidities compared to fertile controls, so this evaluation serves as important overall health screening. 4