17-Hydroxyprogesterone
The 17-hydroxyprogesterone test measures serum 17-OHP, a steroid intermediate that accumulates in 21-hydroxylase deficiency, the most common form of congenital adrenal hyperplasia. It is the first-line biochemical test for diagnosing classic and non-classic CAH, distinguishing it from other causes of virilisation and hyperandrogenism, with borderline values prompting cosyntropin stimulation for…
1
Biomarkers
Blood (serum)
Sample
2–5 business days
Turnaround
Preferred
Fasting
What is the 17-OHP test?
The 17-Hydroxyprogesterone test quantifies serum 17-OHP, a steroid intermediate that accumulates when 21-hydroxylase is deficient. It is ordered principally to diagnose congenital adrenal hyperplasia, the commonest form of which is 21-hydroxylase deficiency, and to distinguish it from other causes of virilisation or premature adrenarche in children and hyperandrogenism in adults. Classic CAH presents in the neonatal period with ambiguous genitalia in genetic females or salt-wasting crisis in both sexes; non-classic CAH may be silent until adolescence or adulthood, when it mimics polycystic ovary syndrome with hirsutism, oligomenorrhoea, and acne. Basal 17-OHP measurement is the first-line biochemical test, and a markedly elevated result in the right clinical context is diagnostic. Borderline or moderately raised values require a cosyntropin stimulation test, in which a post-ACTH 17-OHP above a defined threshold confirms non-classic CAH. The test is also a component of newborn bloodspot screening in many regions, though specificity is lower in premature and stressed neonates, generating false positives that must be resolved with follow-up sampling.
What does the 17-OHP test measure?
17-Hydroxyprogesterone is a C21 steroid hormone intermediate in the adrenal and gonadal synthesis pathways. It is produced when progesterone undergoes 17α-hydroxylation by CYP17A1, the rate-limiting step before cleavage to dehydroepiandrosterone and androstenedione. In the adrenal cortex, 21-hydroxylase (CYP21A2) converts 17-OHP to 11-deoxycortisol, the penultimate step toward cortisol; deficiency of this enzyme causes 17-OHP to accumulate dramatically. Ovarian production follows the luteal rise in progesterone, so 17-OHP peaks mid-cycle and again in the luteal phase in cycling women.
Measurement of 17-OHP is the biochemical cornerstone of screening and diagnosing congenital adrenal hyperplasia due to 21-hydroxylase deficiency, which accounts for over 90% of CAH cases. Markedly elevated basal values confirm classic CAH in symptomatic neonates or children; moderate elevations prompt an ACTH stimulation test to detect non-classic forms that present with signs of androgen excess in adolescence or adulthood. The test is also included in newborn screening programmes in many jurisdictions, where a very high value triggers confirmatory testing.
Why is the 17-OHP test ordered?
- Diagnostic evaluation of newborns with ambiguous genitalia, to distinguish virilising CAH from other intersex conditions
- Investigation of salt-wasting adrenal crisis or hypoglycaemia in infancy, where both cortisol and mineralocorticoid synthesis may be impaired
- Work-up of premature adrenarche or accelerated growth and bone age in prepubertal children
- Evaluation of adolescent or adult women with hirsutism, severe acne, oligomenorrhoea, or infertility, to screen for non-classic CAH before or alongside PCOS work-up
- Follow-up of a positive newborn screen, typically repeated after the first week of life to reduce false positives from neonatal stress
- Monitoring adequacy of glucocorticoid replacement in known CAH, though timing and target ranges differ from diagnostic use
- Assessment of suspected ovarian or adrenal androgen-secreting tumours, where 17-OHP may be modestly raised but other androgens are typically more informative
Sample collection and turnaround
Sample type
Blood (serum)
Fasting required
Preferred
Collection method
Venipuncture at patient service centre
Turnaround
2–5 business days
Collection notes
Phlebotomy at the laboratory draw site (Quest or Access Medical Laboratories). For diagnostic evaluation of suspected non-classic CAH in adult women, collect in the early follicular phase (days 3–5) or at least note the menstrual cycle day. Morning fasting sampling improves consistency and reduces confounding from diurnal variation. Neonates: if following up a positive newborn screen, defer repeat venous sampling until after the first week of life to allow stress-related elevation to resolve.
Specimen requirements
Minimum 0.5 mL serum. Separate promptly and refrigerate or freeze if there will be a delay; steroid hormones are generally stable when stored appropriately. Note the assay platform (immunoassay vs LC-MS/MS) if available, as specificity differs.
What can affect 17-OHP results?
17-OHP rises in parallel with progesterone in the luteal phase; ideally sample in the early follicular phase or note the cycle day to avoid misinterpreting a physiological peak as pathology.
Neonatal stress activates the adrenal axis and transiently raises 17-OHP, contributing to false positives in newborn screening; repeat sampling after recovery improves specificity.
Many immunoassays cross-react with other steroids (17α-hydroxypregnenolone, progesterone metabolites), especially when 17-OHP is in the normal-to-mildly elevated range; liquid chromatography–tandem mass spectrometry is the gold standard for precision.
High-dose progesterone or certain progestins may be metabolised to compounds that cross-react in immunoassays, occasionally raising measured 17-OHP artifactually.
Adrenal steroid secretion follows a circadian rhythm, peaking in the morning; fasting morning sampling improves consistency, particularly when monitoring replacement therapy.
Exogenous glucocorticoids suppress ACTH and adrenal androgen production; oestrogen-containing contraceptives may lower free androgens and modestly affect steroid intermediates through hepatic binding-globulin changes.
What do 17-OHP results mean?
Elevated
Markedly elevated basal 17-OHP (typically >1000–1500 ng/dL) is diagnostic of classic 21-hydroxylase deficiency CAH. Moderate elevations (200–1000 ng/dL) in an adult woman with hyperandrogenism raise suspicion for non-classic CAH and should be followed by a cosyntropin stimulation test; a stimulated value >1000–1500 ng/dL confirms the diagnosis. Mild elevations may also be seen in heterozygous carriers, PCOS, or ovarian/adrenal tumours, so interpretation requires correlation with DHEA-S, testosterone, and imaging where indicated.
Normal
A basal 17-OHP in the low-normal range effectively excludes classic CAH and makes non-classic CAH unlikely when sampled in the follicular phase or fasting state. A normal result does not rule out other causes of hyperandrogenism, so additional investigation guided by the clinical picture is often warranted.
Reduced
Low 17-OHP is not clinically significant in isolation and may reflect assay variation or suppression by exogenous glucocorticoids. It does not exclude other causes of adrenal insufficiency, where cortisol and ACTH are the primary markers.
Note: Interpretation is heavily context-dependent: age, sex, menstrual phase, assay method, and timing all matter. Newborn values are elevated and decline over the first week; sampling too early or in a stressed neonate generates false positives. Immunoassay results in the intermediate range should be confirmed by LC-MS/MS or an ACTH stimulation test. Serial monitoring in treated CAH aims for a balance — too low suggests over-replacement and growth suppression, too high indicates under-replacement and ongoing virilisation.
Frequently asked questions
17-Hydroxyprogesterone is a steroid hormone intermediate in cortisol synthesis. When 21-hydroxylase — the enzyme that converts it to cortisol — is deficient, 17-OHP accumulates in the blood, making it the key diagnostic marker for congenital adrenal hyperplasia.
How to access the 17-OHP test
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Published: October 7, 2026
Last reviewed: October 7, 2026
- Speiser PW, et al. Endocrine Society clinical practice guideline: congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency. J Clin Endocrinol Metab. (2018)
- Carmina E, et al. Non-classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency revisited: an update with a special focus on adolescent and adult women. Hum Reprod Update. (2020)
- Brosnan PG, et al. Current controversies in late-onset congenital adrenal hyperplasia. Curr Opin Endocrinol Diabetes Obes. (2010)
- El-Maouche D, et al. Longitudinal assessment of illnesses, stress, and menses on short-term serum 17-hydroxyprogesterone variability in women with congenital adrenal hyperplasia. J Clin Endocrinol Metab. (2018)
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.
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