Bilateral Testicular Atrophy: Causes and Mumps as a Potential Etiology
Mumps orchitis is a well-documented cause of testicular atrophy, but it typically presents with acute painful symptoms during the infection, making painless bilateral atrophy without prior symptoms unlikely to be mumps-related. 1, 2
Understanding Mumps-Related Testicular Atrophy
Clinical Presentation of Mumps Orchitis
- Mumps orchitis occurs in 5-37% of postpubertal males with mumps infection, with bilateral involvement in 16-65% of affected patients 3
- The condition presents with acute painful testicular swelling during active mumps infection—not as silent, painless atrophy discovered later 1, 2
- Testicular atrophy develops 25-230 days (mean 95.9 days) after the acute orchitis episode, resulting in 23-55% volume reduction (mean final volume 6.3 mL) 1
- On ultrasound, mumps-related atrophic testes show characteristic oblong shape, heterogeneous hypoechoic appearance with multiple hyperechoic islands, and decreased vascularity 1
Why Painless Bilateral Atrophy Is Unlikely to Be Mumps
The key issue is that mumps orchitis is not asymptomatic. Patients experience severe testicular pain, swelling, fever, and systemic symptoms during the acute infection phase. 1, 3, 4 If you had bilateral mumps orchitis, you would have known about it—the pain and swelling are impossible to miss. The atrophy comes later as a sequela, not as the presenting finding. 1, 2
More Likely Causes of Painless Bilateral Testicular Atrophy
Primary Testicular Dysfunction (Hypergonadotropic Hypogonadism)
- Klinefelter syndrome (47,XXY)—the most common genetic cause of primary testicular failure 5
- History of bilateral cryptorchidism (undescended testes), especially if uncorrected or corrected late 5, 6
- Myotonic dystrophy (types I and II) 5
- Prior chemotherapy or pelvic/testicular radiation 5
- Autoimmune orchitis—can be bilateral and relatively painless 5
- Sickle cell disease with repeated vaso-occlusive episodes 5
Secondary Testicular Dysfunction (Hypogonadotropic Hypogonadism)
- Chronic opioid use—suppresses GnRH secretion leading to testicular atrophy 5
- Anabolic steroid or exogenous testosterone use—causes complete suppression of spermatogenesis and testicular atrophy that can persist for months to years after discontinuation 5, 6
- Hyperprolactinemia from pituitary adenoma or medications 5
- Kallmann syndrome or idiopathic hypogonadotropic hypogonadism 5
Systemic Conditions
- Type 2 diabetes mellitus/metabolic syndrome—associated with functional hypogonadism 5
- Chronic liver disease (cirrhosis) 5
- Chronic kidney disease 5
- HIV infection 5
Recommended Diagnostic Workup
Immediate Laboratory Evaluation
- Morning serum FSH, LH, and total testosterone (drawn 08:00-10:00h on two separate occasions) to distinguish primary from secondary hypogonadism 6
- Karyotype testing if FSH is elevated and testicular volume <12 mL to screen for Klinefelter syndrome 6
- Prolactin level to exclude hyperprolactinemia 5
- Complete metabolic panel including liver and kidney function 7
- Semen analysis to assess fertility potential 6
Imaging Studies
- Scrotal ultrasound with Doppler to confirm testicular volume (<12 mL is definitively atrophic), assess for masses, evaluate testicular architecture, and rule out malignancy 6, 7, 1
- Testicular volumes <12 mL are associated with impaired spermatogenesis and increased risk (≥34%) of intratubular germ cell neoplasia in men under 30-40 years, especially with history of cryptorchidism 5, 6
Historical Red Flags to Elicit
- History of undescended testes (cryptorchidism)—dramatically increases both atrophy and cancer risk 5, 6
- Medication history: anabolic steroids, testosterone, opioids, glucocorticoids 5
- Prior chemotherapy or radiation 5
- Family history of Klinefelter syndrome or hypogonadism 5
- Symptoms of systemic disease: diabetes, liver disease, chronic infections 5
Cancer Risk Considerations
When to Consider Testicular Biopsy
- Age <30-40 years with testicular volume <12 mL carries ≥34% risk of intratubular germ cell neoplasia (TIN) if testicular cancer develops 5, 6
- History of cryptorchidism plus volume <12 mL mandates close surveillance and consideration of biopsy 5, 6
- If TIN is left untreated, 70% progress to invasive testicular cancer within 7 years 5, 6
- Two patients in a historical cohort of 132 men with mumps orchitis-related atrophy subsequently developed testicular neoplasms 2
Surveillance Recommendations
- Teach testicular self-examination given increased cancer risk with atrophic testes 6
- Urology referral if palpable mass develops, rapid further atrophy occurs, or if age <30 years with volume <12 mL and cryptorchidism history 6
- Serum tumor markers (AFP, β-HCG, LDH) if any solid mass is detected on ultrasound 7
Fertility Implications and Management
Fertility Assessment
- Testicular volume <12 mL strongly correlates with impaired spermatogenesis, reduced total sperm count, and decreased sperm concentration 6
- Semen analysis every 6-12 months to detect early decline in sperm parameters 6
- Sperm banking discussion should occur before any surgical intervention or testosterone replacement therapy 7
Critical Caveat About Testosterone Therapy
- Never initiate testosterone replacement without first clarifying fertility intentions—exogenous testosterone completely suppresses spermatogenesis through negative feedback and causes azoospermia that can take months to years to recover 6
Common Pitfalls to Avoid
- Do not assume mumps without a clear history of acute painful orchitis during a mumps infection 1, 3, 4
- Do not dismiss bilateral atrophy as benign without imaging and tumor markers, especially in younger men 7
- Do not use the traditional ellipsoid formula (0.52 coefficient) for testicular volume calculation—it systematically underestimates volume by 20-30%; use the Lambert formula (0.71 coefficient) instead 6
- Do not fail to screen for Klinefelter syndrome in men with small testes and elevated FSH 6
- Do not start testosterone therapy without documenting baseline fertility status and discussing sperm banking 6, 7