17-Hydroxypregnenolone, Mass Spectrometry (Endocrine Sciences)

Serum or plasma. frozen

1 mL

0.3 mL adult; 0.1 mL pediatric (Note: This volume does not allow for repeat testing.)

Red-top tube, gel-barrier tube, or lavender-top (EDTA) tube

High-pressure liquid chromatography/tandem mass spectrometry (LC/MS-MS)

• Premature (26 to 28 weeks): day 4: 375−3559 ng/dL

• Premature (31 to 35 weeks): day 4: 64−2380 ng/dL

• 3 days: 10−829 ng/dL

• 1 to 5 months: 36−763 ng/dL

• 6 to 11 months: 42−540 ng/dL

• 12 to 23 months: 14−207 ng/dL

• 24 months to 5 years: 10−103 ng/dL

• 6 to 9 years: 10−186 ng/dL

• Pubertal: 44−235 ng/dL

• Adults: 53−357 ng/dL

In humans, the adrenal glands and the gonads produce steroid hormones.^1,2 The formation of pregnenolone from cholesterol is the first step in steroidogenesis. Steroidogenesis continues along two paths from pregnenolone. 17-Hydroxypregnenolone is produced from pregnenolone through the enzymatic action of 17-α-hydroxylase (17α-H). 3-β-hydroxysteroid dehydrogenase (3β-HSD) mediates the conversion of 17-hydroxypregnenolone to 17-hydroxyprogesterone. Alternatively, the enzyme 17,20 lyase can convert 17-hydroxypregnenolone to dehydroepiandrosterone (DHEA). 17α-H and 17,20 lyase activity are both mediated by a single microsomal cytochrome P450 complex.

17-hydroxypregnenelone levels have been shown to remain in the normal range in patients with Cushing.³ Levels can be suppressed with dexamethasone inhibition and increased with exogenous ACTH stimulation.³ Levels during the follicular phase of the menstrual cycle tend to be higher than during the luteal phase.³ 17-hydroxypregnenelone levels have been shown to be elevated in patients with idiopathic hirsutism.⁴