17-Hydroxyprogesterone (17-OHP) Unit Converter
17-Hydroxyprogesterone (17-OHP) Unit Converter
Convert 17-OHP between ng/mL, ng/dL, µg/L and nmol/L — and read the result the way the screening analyte for congenital adrenal hyperplasia has to be read: early morning, in the follicular phase, and with a short Synacthen test rather than a repeat when it is borderline.
17-Hydroxyprogesterone (17-OHP) converter
Mass ⇄ molar17-OHP 0.5 ng/mL, drawn at 08:00 on day 4 of the cycle
The conversion, and the unit ladder around it
ng/mL = nmol/L ÷ 3.02599
because 3.02599 = 1 ng/mL (10⁻⁶ g/L) ÷ 330.47 g/mol, the molecular weight of 17-hydroxyprogesterone
- MW 330.47
- 17α-hydroxyprogesterone, C₂₁H₃₀O₃ — progesterone with a hydroxyl at C17, one step upstream of the 21-hydroxylase block
- ng/mL = µg/L
- numerically identical. A 17-OHP of 0.5 ng/mL is 0.5 µg/L, and nothing needs multiplying between them
- ng/dL = ng/mL × 100
- the commonest source of a hundred-fold error on this analyte, because North American laboratories report 17-OHP in ng/dL and most of the rest of the world in nmol/L. A Mayo interval of “<220 ng/dL" is <2.20 ng/mL, which is <6.66 nmol/L
- 6 nmol/L ≈ 200 ng/dL
- worth memorising, because it is the same threshold in the two units everyone uses. Two nanograms per millilitre is 200 ng/dL and 6.05 nmol/L, and that is the early-morning follicular screening cut-off for non-classic 21-hydroxylase deficiency
- what is being measured
- immunoassays for 17-OHP cross-react with other Δ4 and Δ5 steroids, notably 17-hydroxypregnenolone and the sulphated precursors that are abundant in newborns. LC-MS/MS does not, which is why confirmatory and second-tier newborn screening assays use it
Worked example
17-OHP 0.5 ng/mL, drawn at 08:00 on day 4 of the cycle
0.5 ng/mL = 0.50 µg/L = 50 ng/dL — the same concentration written three ways
0.5 × 3.02599 = 1.51 nmol/L (1.513 before rounding)
That sits comfortably inside Mayo's follicular interval of <80 ng/dL, which is <0.80 ng/mL and <2.42 nmol/L
Now take the threshold everyone quotes. A 17-OHP of 2.0 ng/mL is 200 ng/dL and 2.0 × 3.02599 = 6.05 nmol/L — the early-morning follicular value above which non-classic 21-hydroxylase deficiency has to be excluded by ACTH stimulation rather than assumed away
And the trap. The identical 0.5 ng/mL drawn at 16:00 on day 22 is uninformative: 17-OHP falls through the day with ACTH and the luteal interval runs to 2.85 ng/mL (8.6 nmol/L), so a normal afternoon or luteal result excludes nothing
Mayo Clinic Laboratories reference values, 17-OHP by LC-MS/MS
| Group | ng/dL (as published) | ng/mL | nmol/L |
|---|---|---|---|
| Female, follicular phase | <80 | <0.80 | <2.42 |
| Female, luteal phase | <285 | <2.85 | <8.62 |
| Female, postmenopausal | <51 | <0.51 | <1.54 |
| Adult male | <220 | <2.20 | <6.66 |
| Prepubertal male | <110 | <1.10 | <3.33 |
| Prepubertal female | <100 | <1.00 | <3.03 |
| Term infant, 0–28 days | <630 | <6.30 | <19.1 |
| Preterm infant | may exceed 630, uncommonly reaching 1,000 | may exceed 6.30 | may exceed 19.1 |
Getting the sample right, which decides whether the number means anything
| Requirement | Why | What happens if it is ignored |
|---|---|---|
| Early morning, ideally before 09:00 | 17-OHP is ACTH-driven and follows the cortisol rhythm, peaking in the early morning and falling through the day | An afternoon sample can be normal in a patient with non-classic CAH — a false reassurance rather than a false alarm |
| Follicular phase, days 2–5 | The corpus luteum makes 17-OHP in quantity, so the luteal interval is more than three times the follicular one | A luteal sample read against a follicular cut-off looks abnormal in a healthy woman; a luteal sample read against a luteal cut-off is too insensitive to screen with |
| Off glucocorticoids where the question is diagnosis | Exogenous steroid suppresses ACTH and with it 17-OHP | A suppressed result excludes nothing |
| Newborn screening: dried blood spot, usually day 5 | Timing is set to catch salt-wasting crises, which present in the second week | Sampling too early raises the false-positive rate further, because 17-OHP is high in the first 24–48 hours of life in normal babies too |
How a raised 17-OHP is actually resolved
| Basal early-morning follicular 17-OHP | Reading | Next step |
|---|---|---|
| Below about 2 ng/mL (200 ng/dL, 6 nmol/L) | Non-classic 21-hydroxylase deficiency is very unlikely | No further adrenal testing for this question |
| Between roughly 2 and 10 ng/mL (6–30 nmol/L) | Indeterminate — the range in which most non-classic CAH and most healthy people with a slightly high result both sit | Short Synacthen test: 250 µg tetracosactide, 17-OHP at 0 and 60 minutes. A stimulated 17-OHP above roughly 10 ng/mL (30 nmol/L) supports the diagnosis, and CYP21A2 genotyping confirms it. Repeating the random level does not resolve anything |
| Above about 10 ng/mL (30 nmol/L) basally | Strongly suggestive without stimulation | Genotyping; classic CAH presents earlier and much higher, typically hundreds of nmol/L |
| Newborn screen positive on a dried blood spot | Depends heavily on gestation and birth weight | Second-tier LC-MS/MS on the same spot, a serum 17-OHP, electrolytes, and clinical assessment for salt loss and virilisation — urgently, because a salt-wasting crisis is a neonatal emergency |
The analyte one enzyme block upstream, and why the timing decides the answer
17-hydroxyprogesterone is reported in nanograms per millilitre, in nanograms per decilitre and in nanomoles per litre, and the bridge between mass and molar units is its molecular weight of 330.47: one nanogram per millilitre is 3.02599 nanomoles per litre. Nanograms per millilitre and micrograms per litre are the same number, while nanograms per decilitre — the unit most North American laboratories report in — is a hundred times larger, so 2 ng/mL, 200 ng/dL and 6.05 nmol/L are one and the same result. That equivalence is worth holding on to, because 200 ng/dL and 6 nmol/L are the same widely quoted screening threshold written in the two conventions.
The reason the analyte is measured at all is 21-hydroxylase deficiency, which causes about 95% of congenital adrenal hyperplasia. The missing enzyme converts 17-hydroxyprogesterone to 11-deoxycortisol, so the substrate accumulates immediately behind the block while cortisol — and, in the salt-wasting form, aldosterone — cannot be made. Precursor is shunted into androgen synthesis instead, which is why the biochemical abnormality and the clinical picture of virilisation are two halves of the same process. Newborn screening programmes measure 17-OHP on a dried blood spot for exactly this reason, since a salt-wasting crisis in the second week of life is fatal if it is not anticipated.
Newborn screening also produces most of the false positives in the field, and they have a single dominant cause: preterm and sick babies have physiologically raised 17-hydroxyprogesterone. An immature adrenal cortex, a persistent foetal zone still making sulphated precursors, and the ACTH drive of illness all push the concentration up in an infant with entirely normal enzymes, and the immunoassays used for first-tier screening cross-react with those precursors. Programmes mitigate it with cut-offs stratified by gestational age or birth weight and with a second-tier mass spectrometry assay run on the same spot, but a positive screen in a 30-week baby remains far more likely to be prematurity than disease — which does not make it ignorable, because the babies who do have the salt-wasting form need treating within days.
Outside the neonatal period the number is only as good as the sample. 17-OHP is driven by ACTH and follows the cortisol rhythm, so it is highest in the early morning and can be unremarkable by the afternoon; and the corpus luteum secretes it, so the luteal reference interval is more than three times the follicular one. A random 17-OHP therefore has to be taken early in the morning and, in a menstruating woman, in the follicular phase, or it cannot exclude anything. When a properly taken basal level comes back borderline — roughly 2 to 10 ng/mL, or 6 to 30 nmol/L — the test that settles it is a short Synacthen test with 17-OHP measured 60 minutes after 250 µg of tetracosactide, followed where necessary by CYP21A2 genotyping. Repeating the random level is the one thing that does not help.
Frequently asked questions
How do you convert 17-OHP from ng/mL to nmol/L?
Multiply by 3.02599, which is one nanogram per millilitre divided by 17-hydroxyprogesterone’s molecular weight of 330.47 g/mol. So 0.5 ng/mL is 1.51 nmol/L and 2 ng/mL is 6.05 nmol/L. Divide by the same factor to go back. Micrograms per litre are identical to nanograms per millilitre, and nanograms per decilitre are a hundred times larger — 2 ng/mL is 200 ng/dL.
Why must a 17-OHP be taken early in the morning and in the follicular phase?
Because it is both diurnal and cycle-dependent. 17-OHP is secreted under ACTH drive and follows the cortisol rhythm, peaking in the early morning and falling substantially by the afternoon, so a late sample can be normal in someone who has non-classic congenital adrenal hyperplasia. It is also made by the corpus luteum, and the luteal reference interval — under 2.85 ng/mL on Mayo’s LC-MS/MS assay — is more than three times the follicular one of under 0.80 ng/mL. A sample drawn in the wrong half of the cycle read against a follicular cut-off looks abnormal in a healthy woman.
What causes a false-positive newborn screening result for congenital adrenal hyperplasia?
Prematurity, above everything else, with low birth weight and acute illness close behind. Preterm and sick babies have physiologically raised 17-hydroxyprogesterone from an immature adrenal cortex, a persisting foetal zone producing sulphated steroid precursors, and stress-driven ACTH, and the immunoassays used for first-tier dried blood spot screening cross-react with those precursors. Mayo note that preterm infants may exceed 630 ng/dL and uncommonly reach 1,000, against a term-infant reference of under 630. Screening programmes use gestation- or weight-stratified cut-offs and a second-tier mass spectrometry assay on the same blood spot to reduce it.
My 17-OHP is borderline. Should it just be repeated?
Not as the next step. A borderline basal 17-OHP — very roughly 2 to 10 ng/mL, or 6 to 30 nmol/L, on a properly timed early-morning follicular sample — is the range in which non-classic 21-hydroxylase deficiency and normality overlap, and repeating a random level mostly reproduces the ambiguity. The test that resolves it is a short Synacthen (ACTH stimulation) test: 250 µg of tetracosactide with 17-OHP measured at baseline and 60 minutes. A stimulated value above about 10 ng/mL (30 nmol/L) supports the diagnosis, and CYP21A2 genotyping confirms it.
Is 17-OHP a test of adrenal function like cortisol?
No. Cortisol tells you whether the adrenal cortex is producing enough glucocorticoid; 17-OHP tells you whether a specific enzymatic step is blocked, by measuring the substrate that piles up behind it. The two are usually measured together — in classic 21-hydroxylase deficiency the 17-OHP is very high and the cortisol inappropriately low — and the same short Synacthen test can answer both questions from one set of samples.
Related calculators
References
- Mayo Clinic Laboratories. Test ID: OHPG — 17-Hydroxyprogesterone, Serum. Liquid chromatography-tandem mass spectrometry. Reference values: adult males <220 ng/dL; females follicular <80 ng/dL, luteal <285 ng/dL, postmenopausal <51 ng/dL; term infants 0–28 days <630 ng/dL; preterm infants may exceed 630 ng/dL.
- 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
- Held PK, Bird IM, Heather NL. Newborn Screening for Congenital Adrenal Hyperplasia: Review of Factors Affecting Screening Accuracy. Int J Neonatal Screen. 2020;6(3):67. doi:10.3390/ijns6030067
- White PC, Speiser PW. Congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Endocr Rev. 2000;21(3):245–291. doi:10.1210/edrv.21.3.0398
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