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Hormonal Assessment

Hormonal assessment helps evaluate erectile dysfunction, reduced libido, suspected hypogonadism and selected fertility problems. Baseline hematocrit and prostate assessment become relevant when testosterone treatment is being considered. PSA requires attention to medications and hormone exposure, particularly 5-alpha-reductase inhibitors and feminizing therapy.[1][2][4]

Testosterone & Gonadotropin Panel​

AUA uses total testosterone <300 ng/dL on two separate early-morning measurements, together with compatible symptoms or signs. The Endocrine Society recommends morning fasting sampling[12]; AUA does not insist on fasting.[1] Avoid diagnosing from a single sample during acute illness, and use an accurate assay and clinically appropriate timing.[1][12]

Indications in the Reconstructive Population​

ScenarioRationale
Erectile dysfunction (any etiology)The AUA ED guideline recommends morning total testosterone in every man with ED ; a PDE5i may be more effective combined with testosterone when deficiency is confirmed[2]
Prostate-cancer survivorshipConfirm deficiency, then review the cancer history and PSA course with the oncology team when discussing TRT; the 2018 AUA guideline rates evidence insufficient to quantify benefit and risk after prostate cancer .[1] In a 2026 phase 2 randomized trial, 136 men (68 per arm; 125 completed) with symptomatic hypogonadism, organ-confined Gleason 3+3 or 3+4 cancer, and undetectable PSA for at least two years after prostatectomy received 12 weeks of testosterone or placebo; testosterone increased sexual activity and desire, erectile function did not change, and no biochemical recurrence occurred in either arm.[17]
Post-radiation, post-pelvic-trauma, spinal-cord injuryEvaluate testosterone deficiency when indicated, then use LH to distinguish primary testicular from secondary hypothalamic-pituitary hypogonadism; incorporate the result into rehabilitation planning.[1]
Pre-IPP counselingAddress libido, endocrine symptoms and expectations; routine pretreatment with testosterone has not been established as a way to improve every implant outcome
Decreased libido / fatigue / loss of morning erectionsStandard symptom cluster for AUA evaluation

Conditions Warranting Testosterone Measurement Even Without Symptoms​

The AUA 2018 Testosterone Deficiency Guideline states that clinicians should consider measuring total testosterone in the following conditions even without symptoms or signs :[1]

  • Unexplained anemia
  • Bone-density loss / osteoporosis
  • Diabetes mellitus
  • Chemotherapy exposure
  • Testicular radiation
  • HIV / AIDS
  • Chronic narcotic / opioid use
  • Infertility
  • Pituitary dysfunction
  • Chronic corticosteroid use

Consider reversible contributors, reproductive goals and whether the result will change care.[6]

Reflex Labs When Total T Is Low​

When total T returns <300 ng/dL on confirmatory testing, the next-step labs distinguish primary from secondary hypogonadism and identify treatable secondary causes:[1][5][6]

  • LH. Elevated in primary (testicular) hypogonadism; low or normal in secondary (hypothalamic-pituitary)
  • FSH. Adds infertility-axis information; elevated FSH with normal LH suggests Sertoli-cell dysfunction
  • Iron studies. In secondary hypogonadism, measure iron saturation or ferritin to assess iron overload.[12]
  • Prolactin. Order when testosterone is low and LH is low or low-normal; repeat an elevated prolactin result. Men with total testosterone <150 ng/dL and low or low-normal LH should undergo pituitary MRI regardless of prolactin because a nonsecreting adenoma may be present; prolactinoma is a treatable cause of secondary hypogonadism.[1] In a retrospective cohort of 141 men with mild hyperprolactinemia (15.1–50.0 ng/mL) and hypogonadal symptoms who underwent pituitary MRI, a ratio of prolactin in ng/mL to total testosterone in ng/dL of 0.10, combined with a prolactin cutoff of 25 ng/mL, identified pituitary abnormalities with 90% sensitivity and 48% specificity.[15]
  • Estradiol. Measure before testosterone therapy when breast symptoms or gynecomastia are present .[1]
  • SHBG and free testosterone. Useful when total T is borderline or altered SHBG is suspected. Low SHBG (for example with obesity or type 2 diabetes) can lower total T while free T remains normal. High SHBG (for example with aging, HIV or estrogen exposure) can leave total T normal or high despite low free T. Use equilibrium dialysis or a validated calculation from total T, SHBG and albumin; direct analog free-T immunoassays are unreliable.[12]

Hematocrit — Baseline AND On-Therapy​

AUA recommends baseline hemoglobin and hematocrit and follow-up during treatment:[1]

  • Baseline Hct >50%: consider withholding testosterone initiation until the cause is formally investigated.[1]
  • On-treatment Hct ≥54%: intervene.[1] With high testosterone levels, dose adjustment is generally first; other patterns may require free-T and SHBG assessment and hematology input.
  • During stable treatment, check hematocrit every 6–12 months or sooner according to prior values and clinical circumstances; early follow-up depends on formulation and the treatment plan.
  • The Endocrine Society 2018 guideline sets a lower baseline concern: hematocrit above 48% (above 50% at altitude) is a relative contraindication, and it recommends against starting testosterone with elevated hematocrit. It measures hematocrit at baseline, at 3 to 6 months and then annually, and stops therapy above 54% until the hematocrit falls, evaluates for hypoxia and sleep apnea, and restarts at a reduced dose.[12]

In the TRAVERSE randomized trial (n = 5,246; hypogonadal men with, or at high risk for, cardiovascular disease), testosterone was non-inferior to placebo for major adverse cardiovascular events.[7] Atrial fibrillation, pulmonary embolism and acute kidney injury were more frequent with testosterone and are discussed with the patient.[7] In the TRAVERSE fracture subtrial, among 5,204 men with symptomatic hypogonadism and cardiovascular disease or elevated cardiovascular risk, clinical fractures occurred in 91/2,601 (3.50%) testosterone recipients versus 64/2,603 (2.46%) placebo recipients over a median 3.19 years (HR 1.43, 95% CI 1.04–1.97).[16]

PSA in the Reconstructive Practice​

PSA screening starts with shared decision-making .[3] The AUA/SUO guideline states that clinicians may offer a baseline PSA at 45 to 50 years , should offer screening from 40 to 45 years to people at increased risk , and should offer regular screening every 2 to 4 years at 50 to 69 years .[3] Clinicians may personalize the interval .[3] The 2026 amendment updates imaging, biomarkers, biopsy techniques and ASAP management.[3][18]

When We Order PSA​

  • Pre-TRT baseline in men over 40, recommended by AUA 2018 before starting testosterone therapy to exclude prostate cancer [1]
  • On-TRT surveillance. Agree on prostate monitoring before treatment. The Endocrine Society recommends urologic consultation for a confirmed PSA rise >1.4 ng/mL above baseline in the first 12 months, a confirmed PSA >4.0 ng/mL, or a prostatic abnormality on digital rectal examination.[12] Thereafter, use an age-, risk- and history-appropriate screening schedule.[1][12]
  • Post-radical prostatectomy biochemical-recurrence surveillance. PSA is the primary tool; the threshold for biochemical recurrence is ≥0.2 ng/mL confirmed
  • Age- or risk-appropriate screening or cancer follow-up, including when relevant to prosthetic counseling; avoid a PSA panel solely because an implant is planned

Reconstruction-Specific Interpretation Caveats​

5-Alpha-Reductase Inhibitors​

5-ARIs suppress PSA. For finasteride 5 mg, labeling describes an approximately 50% reduction within six months, establishing a new baseline after at least six months, and doubling an isolated value for comparison with untreated reference ranges. Any confirmed rise from the on-treatment nadir merits evaluation, including adherence and other causes, even if the absolute value is within an untreated reference range.[13]

The doubling rule is an approximation affected by duration and individual response. Marks et al. was a review. It proposed a ≥0.3 ng/mL rise from nadir as an alternative trigger in dutasteride-treated men (71% sensitivity, 60% specificity); this is not a mandate for immediate biopsy after any single 0.3 rise.[9]

In a VA cohort of 80,875 men with prostate cancer, prediagnostic 5-ARI use was associated with a longer interval from first adjusted elevated PSA to diagnosis (median 3.6 vs 1.4 years among those with a known prostate biopsy date) and with higher prostate cancer-specific mortality (subdistribution HR 1.39, 95% CI 1.27 to 1.52). The finding shows why PSA suppression must be accounted for.[10] See 5-Alpha-Reductase Inhibitors.

Gender-Affirming Estrogen Therapy​

Estrogen-based GAHT, orchidectomy or both, can markedly lower PSA in people who retain a prostate. No validated PSA screening or biopsy threshold has been established for this population; neither 4.0 ng/mL nor an invented 0.1 ng/mL cutoff should provide automatic reassurance or trigger biopsy.[4][11]

Hall et al.'s 2025 systematic review included four studies (290 participants) and concluded that the data cannot support clinical recommendations or PSA thresholds. Consider symptoms, hereditary risk, hormone exposure and confirmed trends relative to an appropriate on-treatment baseline. Comparative rates of aggressive cancer are unavailable from case reports; discuss testing individually.[11] See Gender-Affirming Hormone Therapy.

Transient Elevations​

The AUA/SUO guideline advises repeating a newly elevated PSA before a secondary biomarker, imaging or biopsy . Retesting is timed around recent retention, infection, catheterization, biopsy or cystoscopy. A symptomatic infection is treated as an infection.[3]

Endocrine Evaluation in Male Infertility​

Evaluate both partners and interpret semen analysis with history and examination. AUA/ASRM recommends FSH and testosterone in infertile men with impaired libido, erectile dysfunction, oligozoospermia or azoospermia, atrophic testes or other evidence of hormonal abnormality .[14] LH and prolactin follow the hormonal pattern.[8][14]

The AUA/ASRM guideline (2020, amended 2024) sets separate genetic-testing thresholds for primary infertility with elevated FSH, testicular atrophy or a diagnosis of impaired sperm production:[14]

  • Karyotype for azoospermia or sperm concentration <5 million/mL .[14]
  • Y-chromosome microdeletion analysis for azoospermia or concentration ≤1 million/mL .[14]

Do not apply these production-failure criteria automatically to obstructive azoospermia. Suspected congenital absence of the vas deferens or idiopathic obstruction calls for a different genetic evaluation. Exogenous testosterone suppresses spermatogenesis, and the guideline states that clinicians should not prescribe testosterone monotherapy to a man interested in current or future fertility .[14]

See Also​

References​

1. Mulhall JP, Trost LW, Brannigan RE, et al. "Evaluation and management of testosterone deficiency: AUA guideline." J Urol. 2018;200(2):423-432. doi:10.1016/j.juro.2018.03.115

2. Burnett AL, Nehra A, Breau RH, et al. "Erectile dysfunction: AUA guideline." J Urol. 2018;200(3):633-641. doi:10.1016/j.juro.2018.05.004

3. Wei JT, Barocas D, Carlsson S, et al. "Early detection of prostate cancer: AUA/SUO guideline part I — prostate cancer screening." J Urol. 2023;210(1):46-53. doi:10.1097/JU.0000000000003491

4. Nik-Ahd F, Jarjour A, Figueiredo J, et al. "Prostate-specific antigen screening in transgender patients." Eur Urol. 2023;83(1):48-54. doi:10.1016/j.eururo.2022.09.007

5. Heidelbaugh JJ, Belakovskiy A. "Testosterone replacement therapy for male hypogonadism." Am Fam Physician. 2024;109(6):543-549. https://www.aafp.org/afp/2024/0600/testosterone-replacement-therapy-male-hypogonadism

6. De Silva NL, Papanikolaou N, Grossmann M, et al. "Male hypogonadism: pathogenesis, diagnosis, and management." Lancet Diabetes Endocrinol. 2024;12(10):761-774. doi:10.1016/S2213-8587(24)00199-2

7. Lincoff AM, Bhasin S, Flevaris P, et al. "Cardiovascular safety of testosterone-replacement therapy (TRAVERSE)." N Engl J Med. 2023;389(2):107-117. doi:10.1056/NEJMoa2215025

8. Agarwal A, Baskaran S, Parekh N, et al. "Male infertility." Lancet. 2021;397(10271):319-333. doi:10.1016/S0140-6736(20)32667-2

9. Marks LS, Andriole GL, Fitzpatrick JM, et al. "The interpretation of serum prostate specific antigen in men receiving 5alpha-reductase inhibitors: a review and clinical recommendations." J Urol. 2006;176(3):868-874. doi:10.1016/j.juro.2006.04.024

10. Sarkar RR, Parsons JK, Bryant AK, et al. "Association of treatment with 5α-reductase inhibitors with time to diagnosis and mortality in prostate cancer." JAMA Intern Med. 2019;179(6):812-819. doi:10.1001/jamainternmed.2019.0280

11. Hall R, Ball R, Bancroft E, Eeles R, Berner AM. "Systematic review of PSA reference intervals in the gender diverse population with prostates." BJU Int. 2025;136(4):568-577. doi:10.1111/bju.16825

12. Bhasin S, Brito JP, Cunningham GR, et al. "Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline." J Clin Endocrinol Metab. 2018;103:1715–1744. doi:10.1210/jc.2018-00229.

13. Finasteride 5 mg tablets. Prescribing information, section 5.1: Effects on PSA. DailyMed.

14. AUA/ASRM. Diagnosis and Treatment of Infertility in Men (2020; amended 2024). Full guideline.

15. Naelitz B, Shah A, Nowacki AS, et al. Prolactin-to-Testosterone Ratio Predicts Pituitary Abnormalities in Mildly Hyperprolactinemic Men with Symptoms of Hypogonadism. J Urol. 2021;205(3):871-878. doi:10.1097/JU.0000000000001431

16. Snyder PJ, Bauer DC, Ellenberg SS, et al. "Testosterone Treatment and Fractures in Men with Hypogonadism." N Engl J Med. 2024;390(3):203-211. doi:10.1056/NEJMoa2308836

17. Bhasin S, Burnett AL, Gagliano-Jucá T, et al. "Testosterone Treatment in Prostate Cancer Survivors With Hypogonadism: A Randomized Clinical Trial." JAMA Intern Med. 2026;186(7):805-814. doi:10.1001/jamainternmed.2026.1343

18. Lin DW, Carlsson S, Filson CP, et al. "Updates to Early Detection of Prostate Cancer: AUA/SUO Guideline (2026)." J Urol. 2026;215(5):491-501. doi:10.1097/JU.0000000000004995.