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Androstenedione, ACTH Stimulation

CPT: 82157(x2)
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Synonyms

  • 17-Dione (Two Specimens)
  • δ4-Androstene, 3

Special Instructions

Draw blood for baseline androstenedione. Inject cosyntropin 250 μg IM or IV (if IV, dilute cosyntropin in 2 to 5 mL of sterile saline and inject over two minutes). Draw blood for stimulated androstenedione 60 minutes after.


Expected Turnaround Time

4 - 6 days


Related Information


Related Documents

For more information, please view the literature below.

Adrenal Steroid Response to ACTH: Pediatrics


Specimen Requirements


Specimen

Serum


Volume

1 mL (each specimen)


Minimum Volume

0.5 mL (each specimen) (Note: This volume does not allow for repeat testing.)


Container

Red-top tube. Do not use a gel-barrier tube. The use of gel-barrier tubes is not recommended due to slow absorption of the steroid by the gel. Depending on the specimen volume and specimen time, the decrease in androstenedione level due to absorption may be clinically significant.


Collection

Transfer separated serum to a plastic transport tube. Note: Label each tube with the patient's name, collection time, and date. Submit specimens simultaneously on the same test request form.


Storage Instructions

Refrigerate.


Stability Requirements

Temperature

Period

Room temperature

14 days

Refrigerated

14 days

Frozen

14 days

Freeze/thaw cycles

Stable x2


Causes for Rejection

Gross hemolysis; lipemia; gel-barrier tube


Test Details


Use

This test may involve significant risk and should be performed only by qualified personnel who are familiar with the test and who have taken adequate precautions to protect the safety of the patient. Every effort has been made to ensure accuracy in these recommendations, but clinicians must use their judgement and refer to specific pharmaceutical resources to determine appropriate drug dosages for their patients.


Methodology

Liquid chromatography/tandem mass spectrometry (LC/MS-MS)


Additional Information

Androstenedione (also known as 4-androstenedione and δ4-androstenedione) is a 19-carbon steroid hormone produced in the adrenal glands and the gonads that is the common precursor in the biochemical pathway that produces the androgen testosterone and the estrogens estrone and estradiol.1-7 Androstenedione has approximately one tenth of the androgenic potency of testosterone.1 Androstenedione is synthesized by means of two biochemical pathways. The predominant pathway involves conversion of 17-hydroxypregnenolone to dehydroepiandrosterone (DHEA) catalyzed by the enzyme 17,20-lyase, with subsequent conversion of DHEA to androstenedione catalyzed by the enzyme 3-β-hydroxysteroid dehydrogenase. A secondary pathway for androstenedione production involves conversion of 17-hydroxyprogesterone to androstenedione directly by 17,20-lyase. 17,20-lyase is required for both pathways of androstenedione synthesis.

The production of adrenal androstenedione is controlled by ACTH, whereas production of gonadal androstenedione is governed by the gonadotropins, luteinizing hormone (LH), and follicle stimulating hormone (FSH). Androstenedione produced in the adrenal gland of both men and women is further converted to testosterone by the enzyme 17-β-hydroxysteroid dehydrogenase.1 In women, androstenedione produced by theca cells of the ovary is converted to estrogen by the enzyme aromatase in the granulosa cells of the ovary.5 Androstenedione secreted into the plasma by either the adrenal or ovary can be converted to testosterone and estrogens by the same enzymes in peripheral tissues. Androstenedione, largely of ovarian origin, is the only circulating androgen that is higher in premenopausal women than in men.1 After menopause, androstenedione production is about halved, primarily due to the reduction of the steroid secreted by the ovary. Nevertheless, androstenedione is the principal steroid produced by the postmenopausal ovary.

Congenital adrenal hyperplasia (CAH) is a family of disorders caused by defects in one of the enzymes of the adrenal steroidogenic pathway.1,3,6 The most common form of CAH results from mutations in the gene that codes for the 21-hydroxylase enzyme.1,3,6 Patients with CAH develop varying degrees of glucocorticoid and mineralocorticoid deficiency due to the inability to produce cortisol and aldosterone, respectively.1,3,6 Diminished cortisol levels cause an increase in pituitary adrenocorticotrophic hormone (ACTH) secretion due to a lack of negative feedback. The resultant high levels of ACTH lead to adrenal hyperplasia and dramatically increased production of adrenal steroids proximal to the enzyme block.1,3,6 These steroids (progesterone and 17-hydroxyprogesterone) are shunted into the adrenal androgen pathway that leads to increased concentrations of dehydroepiandrosterone and androstenedione.1,3,6 These weakly androgenic steroids are then peripherally converted to testosterone that produces the androgenic symptoms frequently associated with CAH.1,3,6

The diagnosis and therapeutic monitoring of CAH is based on clinical parameters and the measurement of the concentrations of adrenal steroid products and their metabolites.1,3,6 Recent clinical guidelines have recommended the use of 17-hydroxyprogesterone (17OHP) as the primary marker for diagnosis and monitoring of CAH.6 Other steroid products--including androstenedione and testosterone--can provide additional clinical information in some circumstances.3,6,8-11 There is generally a good correlation between 17OHP, androstenedione, and testosterone concentrations in a single blood sample, suggesting these hormone concentrations are all under similar influences.9 Random serum steroid levels in CAH patients tend to fluctuate with time of day and timing relative to glucocorticoid administration.3 For this reason, samples for a given patient should be collected at a consistent time before the administration of the morning glucocorticoid dose.3

Polycystic ovary syndrome (PCOS) is a syndrome of ovarian dysfunction characterized by hyperandrogenism, menstrual irregularities, and polycystic ovaries.9,12 PCOS is associated with an increased risk of diabetes and cardiovascular disease.1 The measurement of circulating androstenedione levels has been applied to the diagnosis of PCOS in several studies.6,12-14


Footnotes

1. ACOG Committee on Practice Bulletins-Gynecology. ACOG Practice Bulletin N° 108: Polycystic Ovary Syndrome. Obstet Gynecol. 2009; 114(4):936-949. 19888063
2. Azziz R, Carmina E, Dewailly D, et al. Position Statement Criteria for Defining Polycystic Ovary Syndrome as Predominantly Hyperandrogenic Syndrome: An Androgen Excess Society Guideline. J Clin Endocrinol Metab. 2006; 91(11)4237-4245. 16940456
3. Dauber A, Kellogg M, Majzoub JA. Monitoring of therapy in congenital adrenal hyperplasia. Clin Chem. 2010; 56(8):1245-1251. 20558634
4. Demers LM, Whitley RJ. Function of the adrenal cortex. In: Burtis AC, Ashwood ER, eds. Tietz Textbook of Clinical Chemistry. 3rd ed. Philadelphia, Pa: WB Sanders Co;1999:1530-1569.
5. Longcope C. Adrenal and gonadal androgen secretion in normal females. Clin Endocrinol Metab. 1986; 15(2):213-228. 3013468
6. Merke DP. Approach to the adult with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. J Clin Endocrinol Metab. 2008; 93(3):653-660. 18326005
7. Speiser, PW, Azziz R, Baskin LS, et al. Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2010; 95(9):4133-4160. 20823466
8. Cavallo A, Corn C, Bryan GT, et al. The use of plasma androstenedione in monitoring therapy of patients with congenital adrenal hyperplasia. J Pediatr. 1979; 95(1):33-37. 480011
9. Hughes IA, Winter JS. The relationships between serum concentrations of 17OH-progesterone and other serum and urinary steroids in patients with congenital adrenal hyperplasia. J Clin Endocrinol Metab. 1978; 46(1):98-104. 752027
10. Korth-Schutz S, Virdis R, Saenger P, et al. Serum androgens as a continuing index of adequacy of treatment of congenital adrenal hyperplasia. J Clin Endocrinol Metab. 1978; 46(3):452-458. 156192
11. Lee PA, Urban MD, Gutal JP, et al. Plasma progesterone, 17-hydroxyprogesterone, androstenedione, and testosterone in prepubertal, pubertal and adult subjects with congenital virilizing adrenal hyperplasia as indicators of adrenal suppression. Horm Res. 1980; 13(6):347-357. 7196877
12. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod. 2004; 19(1):41-47. 14711538
13. Knochenhauer ES, Key TJ, Kahsar-Miller M, et al. Prevalence of the polycystic ovary syndrome in unselected black and white women of the southeastern United States: A prospective study. J Clin Endocrinol Metab. 1998 Sep; 83(9):3078-3082. 9745406
14. Laven JS, Imani B, Eijkemans MJ, et al. New approach to polycystic ovary syndrome and other forms of anovulatory infertility. Obstet Gynecol Surv. 2002; 57(11):755-767. 12447098

LOINC® Map

Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
140758 Androstenedione, ACTH Stimul. 140759 Andros Baseline ng/dL 24407-9
140758 Androstenedione, ACTH Stimul. 140760 Andros Stimulated ng/dL 13857-8
140758 Androstenedione, ACTH Stimul. 140795 ACTH (2) n/a

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