Testosterone, Total, Serum
Testosterone, Total, Serum
    
Number
004226
CPT
84403
Related Information
  • Follicle-Stimulating Hormone (FSH), Serum
  • Luteinizing Hormone (LH), Serum
  • Special Instructions
    State patient's age and sex on the request form.
    Specimen
    Serum
    Volume
    0.8 mL
    Minimum Volume
    0.3 mL (Note: This volume does not allow for repeat testing.)
    Container
    Red-top tube or gel-barrier tube
    Collection
    If a red-top tube is used, transfer separated serum to a plastic transport tube.
    Storage Instructions
    Refrigerate
    Causes for Rejection
    Plasma specimen
    Reference Interval
    See table.1,2,3
    Testosterone, Total, Serum


    Age Male
    (ng/dL) 
    Female
    (ng/dL) 
    1-5 mo 1-177 1-10 
    6-11 mo 1-10 1-10 
    1-5 y 0-10 0-10 
    6-7 y 0-20 0-10 
    8-10 y 0-25 0-30 
    11-12 y 0-350 0-50 
    13-15 y 15-500 0-50 
    Adults 241-827 14-76 
    Tanner Stage 
    2-23 2-10 
    II 5-70 5-30 
    III 15-280 10-30 
    IV 105-545 15-40 
    265-800 10-40 
    Use
    Indicator of 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 (eg, Sertoli-Leydig cell tumor), tumors of the adrenal cortices, and congenital adrenal hyperplasia (high values)
    Methodology
    Immunochemiluminometric assay (ICMA)
    Additional Information
    Testosterone is the principal androgen in men.4,5 The production of testosterone by the male testes is stimulated by luteinizing hormone, LH, which is produced by the pituitary. LH secretion is, in turn, inhibited through a negative feedback loop by increased concentrations of testosterone and its metabolites. Most of the testosterone in males is produced by the Leydig cells of the testes and is secreted into the seminiferous tubule, where it is complexed to a protein made by the Sertoli cells. This results in the high local levels of testosterone that are required for normal sperm production.

    Diminished testosterone production is one of many potential causes of infertility in males.5,6 Low testosterone concentrations can be caused by testicular failure (primary hypogonadism) or inadequate stimulation by pituitary gonadotropins (secondary hypogonadism). Since men with hypogonadism often have high SHBG levels, the measurement of free or bioavailable testosterone has been advocated when total testosterone levels are normal in men with symptoms of androgen deficiency.6 Significant physiological changes occur in men as they age, in part due to a gradual decline in testosterone levels.7,8 It is generally accepted that the principal cause of this age-related decrease in testosterone production is testicular failure, although diminished gonadotropin production may play a role.9 By 75 years of age, the average male testosterone drops to 65% of average level in young adults. “Andropause” is a term that has been used to refer to the constellation of symptoms associated with the age-related decline in testosterone production in men.9,10

    Much smaller amounts of testosterone and dihydrotestosterone are produced in women than in men.4,5 Weaker adrenal androgens and ovarian precursor molecules including androstenedione, DHEA, and DHEA sulfate can have significant androgenic effects in women. The ovary and adrenal glands produce some testosterone but the majority of the testosterone in women is derived from the peripheral conversion of other steroids. Often, the first sign of testosterone excess in women is the development of male pattern hair growth, which is referred to as hirsutism.5,11,12 It should be noted that some women experience hair growth similar to that caused by increased testosterone due to racial or genetic causes and not due to excessive androgens. Measurement of the testosterone may help to distinguish racial or genetic causes of hirsutism from the abnormal pathology, particularly in women with mixed ethnic backgrounds. Women with more excessive testosterone levels may also experience virilization, with symptoms including increased muscle mass, redistribution of body fat, enlargement of the clitoris, deepening of the voice, and acne and increased perspiration. These women can also suffer from androgenic alopecia, the female equivalent of male pattern baldness.

    Many women with slowly progressive androgenic symptoms are diagnosed as having polycystic ovary syndrome (PCOS).12,13,14 PCOS is relatively common, affecting approximately 6% of women of reproductive age.4 Women with this complex syndrome experience symptoms of androgen excess associated with menstrual abnormalities and infertility. Most women with the syndrome have polycystic ovaries that can be detected by ultrasonography although this finding is not essential for diagnosis.5,6,11 Chronic anovulation experienced by patients with PCOS increases their risk of developing endometrial cancer. Women with PCOS are often overweight and are likely to suffer from insulin resistance putting them at increased risk for developing type 2 diabetes mellitus.4,13 Obesity and insulin resistance can result in acanthosis nigricans, a skin condition that is characterized by hyperpigmented, velvety plaques of body folds.4 Lipid abnormalities, including decreased high-density lipoprotein cholesterol levels and elevated triglyceride levels as well as impaired fibrinolysis, are seen in women with PCOS.13 Cardiovascular disease is more prevalent and women with PCOS have a significantly increased risk for myocardial infarction.13

    Footnotes
    1. Soldin SJ and Hicks JM, eds, Pediatric Reference Ranges, Washington, DC: AACC Press, 1995, 124.
    2. Meites S, Buffone GJ, Cheng MH, et al, eds, Pediatric Clinical Chemistry, Reference (Normal) Values, 3rd ed, Washington, DC: AACC Press, 1989, 247.
    3. Tietz NW, ed, Clinical Guide to Laboratory Tests, 3rd ed, Philadelphia, PA: WB Saunders Co, 1995, 578.
    4. Ismail AA, Astley P, Burr WA, et al, “The Role of Testosterone Measurement in the Investigation of Androgen Disorders,” Ann Clin Biochem, 1986, 23(Pt 2):113-34 (review).
    5. Gronowski AM and Landau-Levine M, “Reproductive Endocrine Function,” Tietz Textbook of Clinical Chemistry, 3rd ed, Burtis CA and Ashwood ER, eds, Philadelphia, PA: WB Saunders Co, 1999, 1601-41.
    6. Petak SM, Baskin HJ, Bergman DA, et al, “AACE Clinical Practice Guidelines for the Evaluation and Treatment of Hypogonadism in Adult Male Patients,” Endocrinol Pract, 1996, 2:440-53.
    7. Leifke E, Gorenoi V, Wichers C, et al, “Age-Related Changes of Serum Sex Hormones, Insulin-Like Growth Factor-1 and Sex-Hormone Binding Globulin Levels in Men: Cross-Sectional Data From a Healthy Male Cohort,” Clin Endocrinol, 2000, 53(6):689-95.
    8. Basaria S and Dobs AS, “Hypogonadism and Androgen Replacement Therapy in Elderly Men,” Am J Med, 2001, 110(7):563-72 (review).
    9. Bain J, “Andropause. Testosterone Replacement Therapy for Aging Men,” Can Fam Physician, 2001, 47:91-7 (review).
    10. Bhasin S, Bagatell CJ, Bremner WJ, et al, “Issues in Testosterone Replacement in Older Men,” J Clin Endocrinol Metab, 1998, 83(10):3435-48.
    11. Ehrmann DA, Barnes RB, and Rosenfield RL, “Hyperandrogenism, Hirsutism, and Polycystic Ovary Syndrome,” Endocrinology, 4th ed, DeGroot LJ and Jameson JL, eds, Philadelphia, PA: WB Saunders Co, 2001, 2122-37.
    12. Barth JH, “Investigations in the Assessment and Management of Patients With Hirsutism,” Curr Opin Obstet Gynecol, 1997, 9(3):187-92 (review).
    13. Hunter MH and Sterrett JJ, “Polycystic Ovary Syndrome: It's Not Just Infertility,” Am Fam Physician, 2000, 62(5):1079-88, 1090 (review).
    14. Lobo RA and Carmina E, “The Importance of Diagnosing the Polycystic Ovary Syndrome,” Ann Intern Med, 2000, 132(12):989-93
    References

    Catrou PG and Beeler MF, “Disorders of Gonadal and Fetoplacental Function,” Interpretations in Clinical Chemistry, 2nd ed, Chicago, IL: American Society of Clinical Pathologists, 1983, 76-82.

    Ruutiainen K, Sannikka E, Santti R, et al, “Salivary Testosterone in Hirsutism: Correlations With Serum Testosterone and the Degree of Hair Growth,” J Clin Endocrinol Metab, 1987, 64(5):1015-20.

    Wheeler JE and Rudy FR, “The Testis, Paratesticular Structures, and Male External Genitalia,” Principles and Practice of Surgical Pathology, 2nd ed, Volume 2, Silverberg SG, ed, New York, NY: Churchill Livingstone, 1990, 1531-85.


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