Dihydrotestosterone (DHT) Test
The DHT test measures serum dihydrotestosterone, the most potent endogenous androgen synthesised from testosterone by 5α-reductase in peripheral tissues. It is ordered to evaluate suspected 5α-reductase deficiency in undervirilised males, to monitor suppression during finasteride or dutasteride therapy, and to clarify androgen metabolism in hirsutism or alopecia when testosterone does not fully…
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Biomarkers
Blood (serum)
Sample
3–5 business days
Turnaround
No
Fasting
What is the DHT test?
The Dihydrotestosterone (DHT) Test measures the circulating concentration of the most potent endogenous androgen, synthesised from testosterone by 5α-reductase in peripheral tissues. Because DHT is produced locally in skin, prostate, and other target organs, its serum level represents only a small fraction of tissue activity, yet measurement is invaluable when enzyme defects, inhibitor therapy, or tissue-specific androgen effects are in question. Practitioners order DHT to investigate undervirilisation in male infants and adolescents when 5α-reductase deficiency is suspected, to monitor suppression during finasteride or dutasteride therapy for benign prostatic hyperplasia or androgenic alopecia, and to clarify the androgen milieu in adults with hirsutism or hair loss whose total and free testosterone do not fully account for the clinical picture. The test is not part of routine androgen screening; it is reserved for situations in which testosterone-to-DHT conversion is clinically relevant.
What does the DHT test measure?
Dihydrotestosterone is synthesised from testosterone by 5α-reductase in androgen-responsive tissues including the prostate, skin, and hair follicles. It is the most potent naturally occurring androgen, binding the androgen receptor with three to five times greater affinity than testosterone and dissociating more slowly. Peripheral tissues generate DHT locally, and although circulating concentrations are only a fraction of testosterone, intracellular DHT drives many virilisation effects in utero, secondary sexual development at puberty, and androgenic phenomena such as male-pattern hair loss and prostatic growth throughout life.
Serum DHT is ordered to evaluate disorders of androgen metabolism and action. In paediatrics it aids the work-up of ambiguous genitalia and suspected 5α-reductase deficiency, a rare condition in which testosterone is normal but DHT synthesis is impaired, resulting in undervirilisation. In adults DHT measurement can clarify testosterone-to-DHT conversion in the context of prostatic disease, guide monitoring of 5α-reductase inhibitor therapy (finasteride, dutasteride), and occasionally help interpret hirsutism or alopecia when testosterone and free androgen index are near normal.
Why is the DHT test ordered?
- Evaluation of undervirilisation, micropenis, or ambiguous genitalia in male infants when 5α-reductase deficiency is suspected, typically alongside testosterone and genetic studies
- Work-up of delayed or incomplete pubertal virilisation in adolescent males with normal testosterone but clinical features suggesting impaired androgen action
- Baseline and monitoring of patients treated with 5α-reductase inhibitors (finasteride, dutasteride) for benign prostatic hyperplasia or androgenic alopecia, to confirm target-enzyme suppression
- Investigation of hirsutism in women when testosterone, DHEA-S, and androstenedione are normal or only mildly elevated, to explore peripheral androgen metabolism
- Clarification of androgenic alopecia mechanisms in men whose testosterone is in the low-normal range but tissue androgen effects appear pronounced
- Assessment of androgen metabolism in the context of polycystic ovary syndrome or suspected peripheral androgen excess, interpreted with other androgens
- Research or specialist endocrinology settings evaluating the testosterone-to-DHT ratio in androgen-sensitive conditions such as prostatic disease
Sample collection and turnaround
Sample type
Blood (serum)
Fasting required
No
Collection method
Venipuncture at patient service centre
Turnaround
3–5 business days
Collection notes
Phlebotomy via Quest. Morning collection (0700–1000 h) is preferred to capture peak androgen secretion and minimise diurnal variation. Record the patient's age, sex, pubertal status, and any androgen or 5α-reductase inhibitor therapy on the requisition.
Specimen requirements
Minimum 1 mL serum in a gel separator tube. Separate from cells within two hours; DHT is stable refrigerated for up to one week or frozen for longer storage. Note the assay method (immunoassay versus liquid chromatography–mass spectrometry) for interpretation.
What can affect DHT results?
Finasteride and dutasteride competitively inhibit 5α-reductase isoenzymes, blocking conversion of testosterone to DHT and lowering serum DHT; this is the therapeutic mechanism and expected during treatment.
DHT follows diurnal variation loosely parallel to testosterone. Exogenous testosterone raises DHT through peripheral conversion; collect morning specimens and note any androgen therapy.
DHT rises sharply at puberty and declines modestly with ageing in parallel with testosterone. Interpretation requires age- and Tanner-stage-appropriate reference ranges.
Adipose tissue aromatises testosterone to oestradiol, lowering substrate for DHT synthesis, yet peripheral 5α-reductase may be upregulated in metabolic syndrome; the net effect on serum DHT is context-dependent.
DHT is conjugated and cleared hepatically; severe liver disease or renal dysfunction can alter androgen metabolism and binding protein concentrations, complicating interpretation.
DHT circulates at low concentrations, so immunoassay cross-reactivity with other steroids can occur; liquid chromatography–tandem mass spectrometry offers superior specificity for low-level measurements.
What do DHT results mean?
Elevated
Elevated DHT in males may reflect increased peripheral 5α-reductase activity, sometimes seen with exogenous testosterone or anabolic steroid use. In females elevated DHT accompanies severe hyperandrogenism, certain virilising tumours, or states of enhanced peripheral androgen conversion. Isolated DHT elevation without commensurate testosterone rise is uncommon and warrants repeat measurement and comprehensive androgen profiling.
Normal
A normal DHT with appropriate testosterone indicates intact peripheral conversion. In the context of 5α-reductase inhibitor therapy a 'normal' result may reflect inadequate suppression, depending on therapeutic goals. In hirsutism or alopecia a normal serum DHT does not exclude enhanced local tissue conversion or androgen-receptor sensitivity.
Reduced
Low DHT in the setting of normal or elevated testosterone suggests 5α-reductase deficiency (typically type 2 deficiency in genetic males, presenting with undervirilisation) or pharmacologic inhibition. Low DHT with low testosterone simply reflects low substrate and does not point to an enzyme defect. In women very low DHT is not clinically significant unless androgen deficiency is suspected.
Note: Serum DHT represents only a fraction of tissue DHT production, so the result must be interpreted in conjunction with testosterone, sex hormone–binding globulin, clinical findings, and the testosterone-to-DHT ratio when enzyme defects are considered. DHT measured by immunoassay can be affected by cross-reactivity; liquid chromatography–mass spectrometry is preferred when precision at low concentrations matters. Reference ranges are assay-, age-, and sex-specific.
Frequently asked questions
Testosterone is the primary circulating androgen produced by the testes and adrenals, while DHT is synthesised from testosterone by 5α-reductase in peripheral tissues. DHT binds the androgen receptor with three to five times greater affinity and drives many tissue-specific effects including prostatic growth and male-pattern hair loss.
How to access the DHT test
The DHT reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.
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Published: October 7, 2026
Last reviewed: October 7, 2026
- Wilson JD, et al. The role of 5α-reductase in androgen physiology. Endocrine Reviews. (1993)
- Imperato-McGinley J, et al. Steroid 5α-reductase deficiency in man: an inherited form of male pseudohermaphroditism. Science. (1974)
- Traish AM, et al. 5α-reductase inhibitors in andrology: clinical applications, mechanisms, and therapeutic implications. Journal of Andrology. (2011)
- Kaufman KD, et al. Finasteride in the treatment of men with androgenetic alopecia. Journal of the American Academy of Dermatology. (1998)
- Roehrborn CG, et al. AUA guideline on the management of benign prostatic hyperplasia. (2021)
This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.