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Hormones Add-On: Androstenedione

The androstenedione test measures serum concentration of a precursor androgen synthesised in the adrenal cortex and gonads. It helps localise androgen excess to adrenal or ovarian sources in the work-up of hirsutism, PCOS, congenital adrenal hyperplasia, and androgen-secreting tumours, and is interpreted alongside testosterone, DHEA-S, and 17-hydroxyprogesterone.

1

Biomarkers

Blood (serum)

Sample

5–7 business days

Turnaround

No

Fasting

What is the Androstenedione test?

The Androstenedione test measures serum concentration of a precursor androgen synthesised in both the adrenal cortex and the gonads. Practitioners order it as part of the diagnostic algorithm for androgen excess, where its role is to help localise the source of hyperandrogenism rather than to provide a stand-alone diagnosis. Because androstenedione sits upstream of testosterone and is produced in both adrenal and gonadal compartments, an isolated elevation can point towards adrenal pathology (congenital adrenal hyperplasia, adrenal tumours) or ovarian hyperandrogenism (polycystic ovary syndrome, ovarian tumours), while normal levels help exclude certain diagnoses. It is rarely ordered in isolation; androstenedione is interpreted alongside total and free testosterone, DHEA-S, 17-hydroxyprogesterone, sex hormone-binding globulin, and, when relevant, ACTH stimulation or pelvic imaging. The test is most useful in women with suspected PCOS or adrenal androgen excess and in paediatric patients being evaluated for premature adrenarche or non-classic congenital adrenal hyperplasia. In men, androstenedione adds less diagnostic value because testosterone is a more direct marker of clinically relevant androgen status.

What does the Androstenedione test measure?

1
A4(Androstenedione)
Range: Adult male approximately 40–190 ng/dL; adult female 30–200 ng/dL (follicular phase). Paediatric and pubertal ranges vary markedly.Optimal: Optimal levels are context-dependent. In the evaluation of hyperandrogenism, lower values within the reference range are typical; in women with PCOS, values are often elevated but may still fall within the laboratory reference interval, so trends and pattern recognition matter more than a single threshold.ng/dL / nmol/L

Androstenedione is a 19-carbon steroid produced in the adrenal cortex (zona reticularis) and the gonads (ovarian theca cells, testicular Leydig cells). It is a key intermediate in the synthesis of both androgens and oestrogens, converted to testosterone by 17β-hydroxysteroid dehydrogenase and to oestrone by aromatase. In adult men the adrenal contributes the majority of circulating androstenedione, whereas in premenopausal women the ovary and adrenal contribute roughly equally, with a mid-cycle ovarian peak. After menopause the adrenal becomes the dominant source of peripheral androgen substrates, as androstenedione is converted in adipose and other peripheral tissues to oestrone.

Androstenedione is measured to localise androgen excess — elevations suggest adrenal androgen overproduction (congenital adrenal hyperplasia, androgen-secreting adrenal tumours), ovarian hyperandrogenism (polycystic ovary syndrome, ovarian tumours), or, less commonly, exogenous androgen precursor use. In the work-up of hirsutism and virilisation it is less sensitive than testosterone or DHEA-S alone but adds diagnostic discrimination when evaluated alongside them. In paediatric endocrinology it assists in the diagnosis of premature adrenarche and non-classic congenital adrenal hyperplasia.

Why is the Androstenedione test ordered?

  • Work-up of hirsutism, acne, or androgenic alopecia in women when total testosterone and DHEA-S alone do not fully explain the clinical picture
  • Evaluation of suspected polycystic ovary syndrome, interpreted with LH, FSH, testosterone, and metabolic markers
  • Investigation of suspected androgen-secreting adrenal or ovarian tumours, especially when DHEA-S or imaging findings raise concern
  • Diagnostic assessment of suspected non-classic congenital adrenal hyperplasia, alongside 17-hydroxyprogesterone and, if indicated, ACTH stimulation testing
  • Evaluation of virilisation or ambiguous genitalia in the paediatric or adolescent patient, as part of a comprehensive adrenal and gonadal hormone panel
  • Premature adrenarche work-up in children with early development of pubic hair and body odour, to assess adrenal androgen production
  • Monitoring androgen suppression in patients treated for hyperandrogenic disorders, though testosterone and DHEA-S are more commonly followed
  • Investigation of suspected exogenous androgen precursor or performance-enhancing supplement use, where androstenedione may be present as a prohormone

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; specimen is sent to Genova for processing. In cycling women, follicular-phase (early cycle, days 3–5) sampling is preferred for baseline assessment; note menstrual-cycle day and hormonal contraceptive use on the requisition. Morning sampling is standard but not strictly required outside research protocols. Avoid collection shortly after vigorous exercise or acute stress, which may transiently affect adrenal androgen output.

Specimen requirements

Minimum 1 mL serum (gel separator acceptable). Separate from cells promptly and freeze if storage before dispatch exceeds 24 hours; androstenedione is stable frozen. Note whether the assay is immunoassay or LC-MS/MS, as methodology affects comparability.

What can affect Androstenedione results?

variableMenstrual cycle phase

Androstenedione rises at mid-cycle due to ovarian secretion during the LH surge; follicular-phase sampling is preferred for baseline assessment, though laboratories often provide phase-specific intervals.

variableTime of day

Androstenedione shows modest diurnal variation, paralleling cortisol and DHEA-S but less pronounced; morning sampling is standard but not always critical outside research protocols.

elevatesObesity and insulin resistance

Hyperinsulinaemia and increased ovarian and adrenal androgen synthesis in PCOS can raise androstenedione; peripheral aromatisation also increases, altering the androgen-to-oestrogen ratio.

reducesOral contraceptives and anti-androgen medications

Combined oral contraceptives suppress gonadotrophin drive and increase SHBG, lowering free and total androgen precursors; spironolactone and other anti-androgens do not directly suppress androstenedione but reduce target-tissue effects.

elevatesExogenous androgen or prohormone supplementation

Over-the-counter prohormone supplements may contain androstenedione or related precursors, raising serum levels and confounding the diagnostic evaluation; a detailed supplement history is essential.

variableAge and pubertal status

Androstenedione rises during adrenarche (typically age 6–8) and again at puberty; paediatric interpretation requires age- and Tanner-stage-specific reference data, and adult reference ranges do not apply.

What do Androstenedione results mean?

Elevated

Androstenedione elevation suggests androgen excess localised to the adrenal (congenital adrenal hyperplasia, androgen-secreting adrenal adenoma or carcinoma), the ovary (PCOS, ovarian hyperthecosis, androgen-secreting ovarian tumour), or, less commonly, exogenous prohormone use. Marked elevation (>800 ng/dL) raises suspicion for a virilising tumour and warrants urgent imaging and specialist referral. Modest elevations are common in PCOS, where they are interpreted with total testosterone, DHEA-S, LH:FSH ratio, and metabolic markers. In children, elevated androstenedione with raised 17-hydroxyprogesterone points towards non-classic 21-hydroxylase deficiency and may prompt ACTH stimulation testing.

Normal

A normal androstenedione does not exclude androgen excess — testosterone and DHEA-S may be elevated while androstenedione remains within the reference interval, particularly in mild PCOS or when the ovarian component predominates. Androstenedione is one piece of a multi-analyte androgen panel and should never be used in isolation to rule out hyperandrogenism.

Reduced

Low androstenedione is uncommon and usually not clinically significant in isolation. It may be seen in adrenal insufficiency (interpreted with cortisol, ACTH, and DHEA-S), hypogonadism, or in patients on anti-androgen therapy or combined oral contraceptives. In postmenopausal women, very low levels can reflect exhaustion of adrenal androgen reserve, though peripheral conversion pathways mean that oestrone may still be measurable.

Note: Androstenedione must be interpreted in the context of the patient's sex, age, menstrual phase, and pubertal status, and alongside other androgens (testosterone, free testosterone, DHEA-S), 17-hydroxyprogesterone, and SHBG. Assay methodology (immunoassay versus LC-MS/MS) affects accuracy, particularly at low concentrations; LC-MS/MS is preferred for research and paediatric applications. Reference intervals are laboratory- and platform-specific, and serial monitoring should use the same performing laboratory.

Frequently asked questions

Androstenedione is a precursor androgen converted to testosterone by 17β-hydroxysteroid dehydrogenase. Testosterone is the more potent, clinically relevant androgen; androstenedione is measured to help localise androgen excess to adrenal versus ovarian sources rather than as a direct marker of androgenic activity.

How to access the Androstenedione test

The Androstenedione 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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About this page

Published: October 7, 2026

Last reviewed: October 7, 2026

References:
  1. Teede HJ, et al. Recommendations from the 2023 international evidence-based guideline for the assessment and management of polycystic ovary syndrome. J Clin Endocrinol Metab. (2023)
  2. Speiser PW, et al. Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. (2018)
  3. Carmina E, Lobo RA. Use of fasting blood to assess the prevalence of insulin resistance in women with polycystic ovary syndrome. Fertil Steril. (2004)
  4. Speiser PW, White PC. Congenital adrenal hyperplasia. N Engl J Med. (2003)
  5. Azziz R, et al. Androgen excess in women: experience with over 1000 consecutive patients. J Clin Endocrinol Metab. (2004)

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.