Androstenedione, Dehydroepiandrosterone, and Dehydroepiandrosterone Sulfate

Androstenedione (AD), Dehydroepiandrosterone (DHEA), and Dehydroepiandrosterone Sulfate ester (DHEA S) are known as Androstenediones (ADs). Androstenediones are precursors of Testosterone and Estrone. Androstenediones and are made in the gonads and the adrenal gland. Adrenocorticotropic Hormone (ACTH) stimulates the adrenal secretion of Androstenediones. The ADs are often elevated in cases of hirsutism and virilization.

 

In the female peripheral tissues and ovaries, androstenedione is converted into testosterone and estrogen. In females, 50% to 60% of testosterone is made in the peripheral tissues, 30% is produced in the adrenal gland, and 20% is produced in the ovary. In the adult woman, elevated levels of ADs can cause virilizing symptoms such as hirsutism, change in voice, and sterility. Children with congenital adrenal hyperplasia have enzyme defects in the synthesis of cortisol. ACTH secretion is stimulated by the lack of cortisol. As ACTH levels increase, production of ADs is stimulated, and levels increase. These hormones are converted into a relatively high level of testosterone by the peripheral tissues. In female children, pseudohermaphroditism results. In male children with similar congenital defects, precocious puberty will become obvious. This test is also used to assess delayed puberty.

 

Androstenedione and Dehydroepiandrosterone secretion is episodic and exhibits a diurnal variation similar to cortisol. Dehydroepiandrosterone Sulfate, on the other hand, does not show diurnal variation and is present in the serum at levels much higher than androstenedione or Dehydroepiandrosterone. Patients with polycystic ovary syndrome (Stein-Leventhal syndrome) have particularly elevated levels of androstenediones. DHEA S levels are particularly high in patients with adrenal carcinoma and to a lesser extent in patients with congenital adrenal hyperplasia and Cushing disease. Normal androstenedione levels are found in patients with Cushing syndrome caused by benign adrenal tumors.

 

It is preferred that the patient fast before drawing blood for the Androstenediones test. However, fasting is not necessary. Androstenediones are the highest around 7 AM; it is also preferred to draw blood around that time of the day.

 

 

 

Normal Androstenediones Levels

Males have higher Androstenediones Levels than females.

 

Normal Androstenedione Levels

Males: Between 0.6 and 2.7 ng/mL.

Females: Between 0.5 and 2.7 ng/mL.

 

 

Normal Dehydroepiandrosterone Levels

Males: Between 1 and 9.5 ng/mL.

Females: Between 0.4 and 3.7 ng/mL.

 

 

Normal Dehydroepiandrosterone Sulfate Levels

Males: between 280 and 640 mcg/dL.

Females: Between 65 and 380 mcg/dL.

 

 

 

Causes of Androstenediones False Indications

  • A radioactive scan performed 1 week before the test may invalidate the test results, if it is performed by radioimmunoassay.
  • Drugs that may increase levels of Androstenedione are Clomiphene, Corticotropin, and Metyrapone.
  • Steroids may decrease levels of Androstenedione.

 

 

 

Causes of High Androstenediones Levels

  • Adrenal Tumor: Some tumors make large amounts of Androstenediones, which is then converted by the ovaries and fatty tissue to testosterone and estrogen. The relatively high level of testosterone causes the virilizing signs.
  • Congenital Adrenal Hyperplasia: This disease is characterized by enzyme defects that prevent conversion of androstenediones to cortisol. Androstenediones levels are increased.
  • High Androstenediones Levels are associated with Ectopic ACTH-producing Tumors and Cushing Disease since Adrenocorticotropic Hormone (ACTH) stimulates the adrenal gland to make large amounts of hormones, including androstenediones. Cushing syndrome: Large amounts of hormones, including androstenediones, are made in the adrenal gland.
  • Stein-Leventhal Syndrome.
  • Ovarian Sex Cord Tumor.

 

 

 

Causes of Low Androstenediones Levels

  • Primary or Secondary Adrenal Insufficiency.
  • Ovarian Failure.
  • Oophorectomy.