• An indicator of Lutenizing Hormone (LH) secretion and Leydig cell function. Evaluate gonadal and adrenal function. Helpful in the diagnosis of hypogonadism, hypopituitarism, Klinefelter syndrome and impotence (low values) in males, and hirsutism, anovulation, amenorrhea, and virilization in females, due to Stein-Leventhal syndrome, masculinizing tumors of ovary such as Sertoli-Leydig cell tumor, tumors of the adrenal cortex, and congenital adrenal hyperplasia (high values).

• Hirsutism in females is most commonly caused by anovulation and excessive ovarian androgen production. Adrenal causes are uncommon. Contemporary investigation for female hirsutism includes dehydroepiandrosterone sulfate, 17-hydroxyprogesterone, and testosterone. Testosterone is used in investigation of male precocious puberty. Male pseudohermaphroditism includes defective testosterone synthesis, androgen insensitivity syndromes, 5 alpha reductase deficiency, and testicular dysgenesis.

• Methodology Immunochemiluminometric (ICMA)

• Additional Information In males, testosterone may be normal or decreased in hypopituitarism, including selective gonadotropin deficiency (eg, Kallmann syndrome). It may be decreased with hepatic cirrhosis, estrogen therapy, and with severe obesity. Low testosterone and high LH are encountered with renal failure and in malnutrition. It is decreased with excessive alcohol intake. Testosterone is usually increased in precocious puberty, related to idiopathic or CNS lesion, or to adrenal tumors or congenital adrenal hyperplasia.

• Testosterone exists in serum both free and bound to albumin and to sex hormone binding globulin (SHBG) (testosterone binding globulin). Unbound (free) testosterone is the active moiety. Free as well as total testosterone can be measured. Usual testosterone assays measure both bound and unbound levels. In certain settings, total testosterone can be normal but free testosterone increased, or the reverse; then the total testosterone result is misleading.

• The major androgens of normal females include dehydroepiandrosterone (DHEA) and androstenedione, both weak androgens. Both are derived from adrenal glands as well as gonads, and can be converted to testosterone. About half of the testosterone in a female is derived from peripheral conversion of androstenedione.

• Lutenizing Hormone (LH) stimulates androgen production. Adrenalcorticotropic Hormone (ACTH) and Thyroid Stimulating Hormone (TSH) deficiencies are more likely the cause of secondary testicular failure than is an LH decrease. Low LH with low testosterone are evidence of a pituitary lesion.

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