This test measures the amount of androstenedione in the blood. An androstenedione test is often performed after results of other tests, such as testosterone or 17-hydroxyprogesterone, are found to be abnormal.
Androstenedione is an endogenous androgen steroid hormone and intermediate in the biosynthesis of estrone and of testosterone from dehydroepiandrosterone (DHEA). It is closely related to androstenediol. Androstenedione has been found to possess some estrogenic activity, similarly to other DHEA metabolites. However, in contrast to androstenediol, its affinity for the estrogen receptors is very low.
DHEA is not androgenic per se, in that it does not bind to cellular androgen receptors like testosterone and DHT, but it is a precursor for androstenedione, which then converts to testosterone.
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Androstenedione is produced by the ovaries in women, the testicles in men, and by the adrenal glands in both.
Androstenedione is an androgen, one of several “male” sex hormones that are responsible for the onset of sexual differentiation in males and females and the development of secondary male physical characteristics such as a deep voice and facial hair. Though it is considered to be a “male” sex hormone, it is present in the blood of both men and women and is a precursor that can be converted by the body into more potent androgens, such as testosterone, or converted into the female hormone estrogen.
The pituitary hormone LH stimulates the release of androstenedione by the ovaries and testicles.
The pituitary hormone adrenocorticotropic hormone (ACTH) stimulates the release of androstenedione by the adrenal glands.
The level of androstenedione in the blood will vary during the day in a “diurnal pattern,” and it will vary during a woman’s menstrual cycle. Because of its origins, androstenedione can be useful as a marker of adrenal gland function, of androgen production, and of the function of the ovaries or testicles.
In premenopausal women about half of the androstenedione is derived from the ovaries and the other half from the adrenals. At menopause, most of the androstenedione derives from DHEA(S) produced by the adrenal glands. DHEA is synthesized in the adrenal glands and is rapidly sulfated to DHEA-sulfate (DHEAS) to extend its half-life in blood.
Androstenedione, the down-stream metabolite of DHEA, is further converted into testosterone and Epi-testosterone in near equal amounts in most individuals, or into estrone. More conversion to the estrogen, estrone, occurs in individuals with higher amounts of adipose (fat) tissue.
Low levels of these androgen precursors are associated with self-reported symptoms of low androgens. DHEA is commonly used as a supplement to raise testosterone levels in women. If low androgen symptoms persist, consider supplemental DHEA to raise testosterone levels, particularly if testosterone, or its down-stream and more potent metabolite DHT, are within mid range or lower.
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- Elevated androstenedione levels can cause symptoms or signs of hyperandrogenism in women.
- Significant elevations of androstenedione may be indicative of androgen-producing adrenal or gonadal tumors.
DHEA(S), as well as its down-stream metabolites, androstenedione and testosterone, is more commonly found to be elevated in women with insulin resistance and polycystic ovarian syndrome (PCOS). These individuals usually have higher levels of insulin and LH (LH/FSH ratio is usually > 2.5 in 75% of women with PCOS), which stimulates high adrenal synthesis of DHEA(S), and high ovarian synthesis of testosterone.
An excess level of androstenedione and other androgens can cause children to have sex organs that are not clearly male or female (ambiguous external genitalia), excess body hair (hirsutism), and abnormal menstrual periods in girls and precocious (early) puberty in girls and boys.
Adrenal tumors, ACTH-producing tumors, and adrenal hyperplasia can lead to the overproduction of androstenedione.
Women with polycystic ovary syndrome (PCOS) may have higher levels of androstenedione as well.
While elevated levels may not be noticed in adult men, they can lead to noticeable male physical characteristics (virilization) and a lack of monthly menstrual periods (amenorrhea) in females.
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ACE, Serum, Acetone, Blood, Activated Protein C Resistance, Ammonia, Plasma, ANA by IFA Rfx Titer/Pattern, ANA Direct, ANA Pattern, Androstenedione LCMS, Anti GAD 65 Antibodies, Anti-DNase B Strep Antibodies, Anti-histone Abs, Anti-intermyofibrillar, Anti-sarcolemma, Antiadrenal Antibodies, Quant, Antinuclear Antibodies, IFA, Antistreptolysin O Ab, B-Type Natriuretic Peptide, Babesia duncani WA1 IgG IFA, C difficile Toxins A+B, EIA, Carbon Monoxide, Blood, Cold Agglutinin Titer, Quant, Copper, RBC, Dehydroepiandrosterone (DHEA), Ethanol, Blood, F078-IgG Casein, F079-IgG Gluten, F2-Isoprostane/Creatinine, Fats, Neutral, Fats, Total, Folate, Hemolysate, Folate, RBC, G-6-PD, Quant, G6PD, Galectin-3, Hexagonal Phospholipid Neutral, Histamine Determination, Blood, Immune Complexes, C1q Binding, Interleukin-8, Serum, Isopropanol, Blood, K080-IgE Formaldehyde, Lactic Acid, Plasma, M-Spike, Manganese, Plasma, Manganese, RBC, Melanocyte-stimulating Hormone (MSH), Methanol, Blood, Mono Qual W/Rflx Qn, Neopterin, Serum, NT-proBNP, Platelet Neutralization, Propeptide Type I Collagen, Protein C-Functional, RNP Antibodies, Rubella Antibodies, IgG, Serotonin, Serum, Sirolimus (Rapamune), Blood, Strongyloides IgG Antibody, Testost., F+W Bound, Thyroxine Binding Globulin, Toxoplasma gondii Ab, IgG, Treponema pallidum Antibodies, Valproic Acid (Depakote), Serum, Varicella Zoster IgG, Vasoactive Intestinal Polypeptide (VIP), Plasma, Zinc Protoporphyrin (ZPP), ZnT8 Antibodies
