DHT (Dihydrotestosterone)
The DHT test measures serum dihydrotestosterone, the most potent endogenous androgen, synthesised from testosterone by 5α-reductase. Ordered to investigate under-virilisation with normal testosterone (5α-reductase deficiency), clarify androgen sources in hirsutism or virilisation, and assess peripheral androgen metabolism, DHT is not part of routine androgen work-up but answers specific…
1
Biomarkers
Blood (serum)
Sample
5–7 business days
Turnaround
No
Fasting
What is the DHT test?
The DHT test quantifies serum dihydrotestosterone, the most potent naturally occurring androgen, formed from testosterone by 5α-reductase in peripheral tissues. Because DHT circulates at roughly one-tenth the concentration of testosterone and closely parallels it in most conditions, direct measurement is not part of routine androgen work-up. Instead, practitioners order DHT to investigate discordance between phenotype and testosterone — a virilised or under-virilised patient whose testosterone does not explain the clinical picture — or to confirm a rare enzyme defect. DHT is indispensable in the differential diagnosis of disorders of sex development when a 46,XY infant presents with ambiguous or female-appearing genitalia despite a testosterone response to stimulation, the hallmark of 5α-reductase type 2 deficiency. In adults it is occasionally ordered to clarify the androgen source in a woman with hirsutism or virilisation when total and free testosterone are borderline, or to assess peripheral androgen metabolism in men with signs of hyperandrogenism but unremarkable testosterone. Monitoring DHT during 5α-reductase inhibitor treatment is not routine but may be requested when clinical response is uncertain.
What does the DHT test measure?
Dihydrotestosterone is synthesised from testosterone by 5α-reductase, predominantly the type 2 isoform in reproductive tissues and the type 1 isoform in skin and liver. DHT binds the androgen receptor with three- to five-fold greater affinity than testosterone and dissociates more slowly, making it the most potent endogenous androgen. In utero it drives male external genital differentiation; at puberty it mediates growth of the prostate, scrotum, and body hair, and deepening of the voice. In adults DHT governs prostate growth, male-pattern hair distribution, and sebaceous gland activity, but contributes minimally to muscle anabolism or libido, which are largely testosterone-dependent.
Serum DHT measurement is reserved for specific diagnostic questions: confirming 5α-reductase deficiency in a phenotypically under-virilised male with normal or elevated testosterone, evaluating hirsutism or virilisation in women when testosterone is equivocal, monitoring 5α-reductase inhibitor therapy in selected cases, and investigating precocious puberty when an autonomous androgen source is suspected. DHT adds little to routine androgen assessment because its concentration tracks testosterone in most conditions, and direct measurement is technically demanding.
Why is the DHT test ordered?
- Investigation of a 46,XY newborn or infant with under-virilisation (ambiguous genitalia, microphallus, or perineal hypospadias) and a normal or elevated testosterone-to-DHT ratio, to confirm 5α-reductase type 2 deficiency
- Evaluation of a woman with hirsutism, acne, or virilisation when total and free testosterone are equivocal or normal, to assess peripheral androgen production
- Work-up of male precocious puberty when an autonomous source of potent androgen is suspected and testosterone alone does not clarify the picture
- Assessment of a man with signs of hyperandrogenism — severe acne, marked androgenic alopecia, or prostatic symptoms — in whom testosterone is unremarkable, to investigate elevated peripheral conversion
- Confirmation of biochemical response in patients taking finasteride or dutasteride for benign prostatic hyperplasia or androgenic alopecia, when clinical response is ambiguous
- Research or specialised protocols examining androgen metabolism, 5α-reductase activity, or the impact of therapies that modulate peripheral androgen synthesis
- Paediatric endocrinology evaluation of delayed puberty or atypical virilisation where enzyme defects in androgen synthesis or metabolism are considered
Sample collection and turnaround
Sample type
Blood (serum)
Fasting required
No
Collection method
Venipuncture at patient service centre
Turnaround
5–7 business days
Collection notes
Phlebotomy required. Morning collection (before 10:00) is preferred to capture peak diurnal androgen concentrations and ensure comparability with reference data. Document any 5α-reductase inhibitor use, as finasteride and dutasteride profoundly lower DHT. Specimen is referred to Access Medical Laboratories.
Specimen requirements
Minimum 1.0 mL serum in a red-top or gel separator tube. Separate serum from cells within two hours and freeze if not analysed promptly; DHT is stable frozen at −20°C for weeks. Verify specimen handling and shipping requirements with Access Medical Laboratories.
What can affect DHT results?
These drugs inhibit conversion of testosterone to DHT, lowering serum DHT by 60–90 per cent and raising testosterone slightly; the patient's medication history must be documented.
DHT follows the diurnal rhythm of testosterone, with higher morning concentrations, so timing of collection matters for serial comparisons; however DHT pulses are less pronounced than those of testosterone.
DHT circulates at low concentrations and immunoassays can suffer from cross-reactivity with testosterone and other androgens; liquid chromatography–tandem mass spectrometry is the preferred method but not universally available.
Hepatic synthesis of sex hormone-binding globulin and hepatic clearance of androgens can both be impaired, altering free and total DHT in unpredictable ways.
Adipose tissue expresses 5α-reductase type 1, potentially increasing peripheral DHT production, though serum concentrations do not always rise proportionately; SHBG is often low, raising free androgen fractions.
DHT concentrations are very low in childhood, rise sharply at puberty, remain stable through adulthood, and decline modestly with ageing in parallel with testosterone; age-appropriate reference intervals are essential.
What do DHT results mean?
Elevated
Elevated DHT in the context of normal or low testosterone suggests increased 5α-reductase activity, seen in some cases of idiopathic hirsutism, severe acne, early-onset androgenic alopecia, and rarely androgen-secreting tumours that produce DHT directly or its precursors. In women elevated DHT with borderline testosterone may clarify the androgen source driving virilisation. An elevated testosterone-to-DHT ratio is not physiological and usually indicates assay interference or a pre-analytical error.
Normal
A DHT concentration within the reference range, interpreted alongside testosterone, LH, and SHBG, suggests normal peripheral androgen metabolism. In most routine androgen disorders — hypogonadism, polycystic ovary syndrome, late-onset hypogonadism — DHT tracks testosterone and adds limited information.
Reduced
Low DHT with normal or elevated testosterone is the biochemical signature of 5α-reductase type 2 deficiency, confirmed by a testosterone-to-DHT ratio above 20–30 in infants or above 10–15 after hCG stimulation. Pharmacological reduction occurs with finasteride and dutasteride. Isolated low DHT without a clear cause may reflect assay variability or a pre-analytical issue, and correlation with clinical phenotype is essential.
Note: DHT is technically challenging to measure, circulates at low concentrations, and is prone to assay interference; mass spectrometry is preferred over immunoassay. The testosterone-to-DHT ratio is more informative than the absolute DHT in suspected enzyme deficiency. Results must be interpreted with the clinical phenotype, as DHT rarely clarifies diagnosis in isolation. Reference intervals are assay-specific, and Access Medical Laboratories' ranges should be verified.
Frequently asked questions
DHT circulates at about one-tenth the concentration of testosterone and tracks it closely in most conditions, so it adds limited information to routine hypogonadism or polycystic ovary syndrome work-up. It is ordered only when peripheral androgen metabolism or a rare enzyme defect is suspected.
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
- Bhasin S, et al. Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. (2018)
- Imperato-McGinley J, et al. Steroid 5α-reductase deficiency in man: an inherited form of male pseudohermaphroditism. Science. (1974)
- Andersson S, et al. Physiological role of 5α-reductase isoenzymes in androgen action. (Landmark description of tissue-specific isoenzyme distribution.) (1990)
- Azziz R, et al. Androgen excess in women: experience with over 1000 consecutive patients. J Clin Endocrinol Metab. (2004)
- Rosner W, et al. Position statement: utility, limitations, and pitfalls in measuring testosterone — an Endocrine Society position statement. J Clin Endocrinol Metab. (2007)
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.