Androstenedione Unit Converter
Androstenedione Unit Converter
Convert androstenedione between ng/dL, ng/mL, µg/L and nmol/L — and read it knowing that it is never interpreted alone, and that an immunoassay result and a mass spectrometry result on the same serum are not the same number.
Androstenedione converter
Mass ⇄ molarAndrostenedione 100 ng/dL in an adult woman
The conversion, and the hundred-fold step beside it
ng/dL = nmol/L ÷ 0.034915
because 0.034915 = 1 ng/dL (10⁻⁸ g/L) ÷ 286.41 g/mol, the molecular weight of androstenedione
- MW 286.41
- androst-4-ene-3,17-dione, C₁₉H₂₆O₂ — a C19 steroid with ketones at both C3 and C17, one aromatisation away from oestrone and one reduction away from testosterone
- ng/dL → nmol/L is ÷ 28.6
- a useful mental check: divide the ng/dL figure by roughly 29 to get nmol/L. 100 ng/dL is 3.49 nmol/L
- ng/mL = µg/L = ng/dL ÷ 100
- so 100 ng/dL is 1.00 ng/mL. A bare androstenedione of “1.0” on a report is almost certainly ng/mL, and reading it as ng/dL understates it a hundredfold
- the method matters more than the unit
- immunoassays for androstenedione cross-react with structurally similar steroids and show poor agreement with each other and with mass spectrometry, particularly at the low concentrations seen in children and in men. LC-MS/MS is the reference method and is what the intervals on this page were established on
Worked example
Androstenedione 100 ng/dL in an adult woman
100 ng/dL = 1.00 ng/mL = 1.00 µg/L — the hundred-fold step that catches people out
100 × 0.034915 = 3.49 nmol/L (3.4915 before rounding)
That is mid-interval: Mayo's adult female band of 30–200 ng/dL is 1.05–6.98 nmol/L
The same 3.49 nmol/L in an adult man is also normal (40–150 ng/dL, 1.40–5.24 nmol/L), and in a prepubertal child it would be well above the Tanner I limit of 51 ng/dL (1.78 nmol/L) and would need explaining
The caveat the number cannot show: run the identical serum on an immunoassay rather than LC-MS/MS and the reported value can differ by tens of per cent, enough to move a borderline result across the top of the interval
Where androstenedione sits, and what it is measured with
| Test | What it adds | Typical pattern in PCOS | Typical pattern in non-classic CAH |
|---|---|---|---|
| Androstenedione | An adrenal and gonadal precursor that is often the first androgen to rise, and the one least affected by SHBG because it is not strongly protein-bound | Raised in a substantial minority, sometimes with a normal testosterone | Raised, alongside 17-OHP |
| Total testosterone | The androgen with the clearest link to symptoms, but heavily SHBG-dependent | Mildly raised or high-normal | Mildly raised |
| 17-hydroxyprogesterone, early morning, follicular | The discriminator between the two diagnoses | Normal | Raised — the finding that changes the diagnosis |
| DHEA-sulfate | Adrenal-specific; a marked elevation points at the adrenal rather than the ovary | Normal or mildly raised | Normal or mildly raised |
| SHBG, with a free androgen index or calculated free testosterone | Converts a total testosterone into something interpretable | SHBG low, free androgen index raised | Variable |
Mayo Clinic Laboratories reference values, androstenedione by LC-MS/MS
| Group | ng/dL | nmol/L |
|---|---|---|
| Adult female | 30–200 | 1.05–6.98 |
| Adult male | 40–150 | 1.40–5.24 |
| Female, Tanner V | 80–240 | 2.79–8.38 |
| Male, Tanner V | 65–210 | 2.27–7.33 |
| Tanner I (prepubertal), either sex | <51 | <1.78 |
| Full term, 1 month – 1 year | <69 | <2.41 |
| Full term, 1–7 days | 20–290 | 0.70–10.1 |
| Premature, 31–35 weeks, day 4 | 80–446 | 2.79–15.6 |
Why two laboratories disagree about the same androstenedione
| Source of difference | Consequence |
|---|---|
| Immunoassay cross-reactivity — antibodies raised against a small steroid bind its close structural relatives | Immunoassay results run higher than LC-MS/MS in most comparisons, and the bias is not constant across the range |
| Poor performance at low concentrations | Children, men and suppressed patients are where the disagreement is worst, and where the clinical question often is |
| Different extraction and calibration between mass spectrometry laboratories | Even LC-MS/MS methods are not perfectly harmonised, although they agree far better with each other than immunoassays do |
| Interval transfer | A reference interval established on one platform applied to a result from another is the commonest practical error, and it produces both spurious abnormals and false reassurance |
A precursor, not an end product — and a measurement that depends on the method
Androstenedione is reported in nanograms per decilitre, in nanograms per millilitre and in nanomoles per litre. The molar conversion runs through its molecular weight of 286.41: one nanogram per decilitre is 0.034915 nanomoles per litre, so 100 ng/dL is 3.49 nmol/L. Nanograms per millilitre and micrograms per litre are identical to each other and a hundred times larger than nanograms per decilitre, which makes 100 ng/dL and 1.00 ng/mL the same result — a hundred-fold trap that is easy to fall into when a report gives a bare number.
Biochemically, androstenedione sits at a junction rather than an endpoint. It is a C19 steroid made by both the adrenal zona reticularis and the gonads, and it is the immediate precursor of testosterone by 17β-hydroxysteroid dehydrogenase and of oestrone by aromatase. That position explains most of its clinical uses. It rises in 21-hydroxylase deficiency because precursor accumulating behind the enzyme block is shunted into the androgen pathway, and it is one of the analytes used to judge whether glucocorticoid replacement in treated congenital adrenal hyperplasia is adequate without being excessive. It rises in polycystic ovary syndrome, sometimes as the only abnormal androgen in a woman whose total testosterone is unremarkable. And because adipose aromatase converts it to oestrone, it is the substrate behind the dominant oestrogen of the postmenopausal years.
It is not a test to order on its own. Androstenedione earns its place as one line in an androgen profile alongside total testosterone, sex hormone-binding globulin, DHEA-sulfate and — where the question is congenital adrenal hyperplasia — an early-morning follicular 17-hydroxyprogesterone. A raised androstenedione in a hirsute woman does not distinguish polycystic ovary syndrome from non-classic CAH; the 17-OHP does. A markedly raised androstenedione with rapidly progressive virilisation is a different problem again and points towards an androgen-secreting adrenal or ovarian tumour.
The other thing worth knowing before acting on a result is that androstenedione is a difficult analyte to measure well. Immunoassays raised against a small steroid cross-react with its structural relatives, agree poorly with one another, and are least reliable at the low concentrations found in children, in men and in suppressed patients — which is frequently where the clinical question lies. Liquid chromatography-tandem mass spectrometry is the reference method, it is what modern reference intervals including the ones on this page were established on, and the difference between methods on the same serum can be large enough to move a borderline result across the top of the interval. Where a result will change management, it should be a mass spectrometry result, read against that method’s interval, and serial values should stay on one assay.
Frequently asked questions
How do you convert androstenedione from ng/dL to nmol/L?
Multiply by 0.034915, which is one nanogram per decilitre divided by androstenedione’s molecular weight of 286.41 g/mol. So 100 ng/dL is 3.49 nmol/L, and dividing the ng/dL figure by roughly 29 gets you there in your head. To go back, divide by 0.034915. Nanograms per millilitre and micrograms per litre are the same as each other and are the ng/dL figure divided by 100.
Why is androstenedione measured with testosterone and 17-OHP rather than alone?
Because on its own it does not answer a clinical question. It is a precursor that both the adrenal and the gonad make, so a raised value tells you there is androgen excess without saying where it comes from. Total testosterone with SHBG tells you how much bioactive androgen there is; DHEA-sulfate points to an adrenal source; and an early-morning follicular 17-hydroxyprogesterone is what separates non-classic congenital adrenal hyperplasia from polycystic ovary syndrome. Androstenedione’s particular value in that panel is that it can be raised in a woman whose total testosterone is normal.
Does it matter whether androstenedione was measured by immunoassay or mass spectrometry?
Yes, materially. Immunoassays for androstenedione cross-react with structurally similar steroids, agree poorly with each other, and are least reliable at low concentrations — in children, in men and in patients on suppressive treatment. Liquid chromatography-tandem mass spectrometry is the reference method and is what current reference intervals, including Mayo’s, were established on. Results from the two approaches on the same serum can differ by enough to change the interpretation, so a reference interval from one method must not be applied to a result from the other, and serial monitoring should stay on one assay.
What raises androstenedione?
Polycystic ovary syndrome and congenital adrenal hyperplasia are the common causes. It is also raised in Cushing syndrome, in androgen-secreting adrenal and ovarian tumours — usually markedly, and with rapid virilisation — and physiologically through puberty, with the highest reference values at Tanner stage V. Exogenous androstenedione supplements raise it directly. Treated congenital adrenal hyperplasia is the one setting where it is followed serially, as a marker that the glucocorticoid dose is controlling adrenal androgen output.
What does a low androstenedione mean?
Usually not very much on its own. It falls in adrenal insufficiency, in hypogonadism, on glucocorticoid treatment and on the combined oral contraceptive, and it is deliberately suppressed in treated congenital adrenal hyperplasia — where a value below the reference interval, alongside a suppressed testosterone, is one of the signs that the steroid dose is higher than it needs to be. It is interpreted with cortisol, ACTH and the rest of the androgen profile rather than in isolation.
Related calculators
References
- Mayo Clinic Laboratories. Test ID: ANST — Androstenedione, Serum. Liquid chromatography-tandem mass spectrometry. Reference values: adult males 40–150 ng/dL; adult females 30–200 ng/dL; Tanner stage I <51 ng/dL.
- Handelsman DJ, Wartofsky L. Requirement for mass spectrometry sex steroid assays in the Journal of Clinical Endocrinology and Metabolism. J Clin Endocrinol Metab. 2013;98(10):3971–3973. doi:10.1210/jc.2013-3375
- Speiser PW, Arlt W, Auchus RJ, et al. Congenital Adrenal Hyperplasia Due to Steroid 21-Hydroxylase Deficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2018;103(11):4043–4088. doi:10.1210/jc.2018-01865
- Teede HJ, Tay CT, Laven J, et al. Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. J Clin Endocrinol Metab. 2023;108(10):2447–2469. doi:10.1210/clinem/dgad463
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.