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Testosterone, Total, Women, Children, and Hypogonadal Males, LC/MS-MS
This assay provides the sensitivity and specificity required for the assessment of the low testosterone levels found in women, children, adolescents, and hypogonadal men.1
Drugs, including androgens and steroids, can decrease testosterone levels. Men with advanced prostate cancer often receive drugs that lower testosterone levels. Women receiving estrogen may have increased testosterone levels. Anticonvulsants, barbiturates, and clomiphene can cause testosterone levels to rise.
This test was developed and its performance characteristics determined by LabCorp. It has not been cleared or approved by the Food and Drug Administration.
Liquid chromatography/tandem mass spectrometry (LC/MS-MS)
premature (26 to 28 weeks) day 4
premature (31 to 35 weeks) day 4
1 to 7 months: Levels decrease rapidly the first week to 20.0−50.0 ng/dL, then increase to 60.0−400.0 ng/dL (mean = 190.0) between 20 to 60 days. Levels then decline to prepubertal range levels of <2.5−10.0 by seven months.
premature (26 to 28 weeks) day 4
premature (31 to 35 weeks) day 4
1 to 7 months: Levels decrease during the first month to <10.0 and remain there until puberty.
male (1 to 10 years)
female (1 to 9 years)
9.8 to 14.5
10.7 to 15.4
11.8 to 16.2
12.8 to 17.3
9.2 to 13.7
10.0 to 14.4
10.7 to 15.6
11.8 to 18.6
Testosterone is the principal androgen in men.2,3 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.3,4 Low testosterone concentrations can be caused by testicular failure (primary hypogonadism) or inadequate stimulation by pituitary gonadotropins (secondary hypogonadism). Several congenital conditions (ie, Klinefelter syndrome, Kallmann syndrome, Prader-Willi syndrome) can result in decreased testosterone production. Testosterone can also be diminished as the result of testicular damage caused by alcoholism, physical injury, viral diseases (eg, mumps), and in certain malignancies.
The adult male reference range for testosterone was established by Travison and coworkers through an epidemiologic study that included men from different geographic regions of the United States and Europe.5 Testosterone measurment was harmonized to the Center for Disease Control reference method.5 The reference population included only men younger than 40 years of age who had a BMI less than 30.
Significant physiological changes occur in men as they age, in part due to a gradual decline in testosterone levels.6,7 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.8 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 age-related decline in testosterone production in men.8.9 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.4
Much smaller amounts of testosterone and dihydrotestosterone are produced in women than in men.3,4 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.3,10,11 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 testosterone may help to distinguish racial or genetic causes of hirsutism from abnormal pathology, particularly in women with mixed ethnic backgrounds. Women with more excessive testosterone levels may also experience virilization with symptoms that include 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).11-14 PCOS is relatively common, affecting approximately 6% of women of reproductive age.2 Women with this complex syndrome experience symptoms of androgen excess associated with menstrual abnormalities and infertility. 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.2,12 Obesity and insulin resistance can result in acanthosis nigricans, a skin condition that is characterized by hyperpigmented, velvety plaques of body folds.2 Lipid abnormalities, including decreased high-density lipoprotein cholesterol levels and elevated triglyceride levels, as well as impaired fibrinolysis, are seen in women with PCOS.12,14 Cardiovascular disease is more prevalent, and women with PCOS have a significantly increased risk for myocardial infarction.12,14
0.6 mL (Note: This volume does not allow for repeat testing.)
Red-top tube or gel-barrier tube
Serum should be transferred from cells within one hour of collection and transferred to a plastic transport tube.
Causes for Rejection
Improper labeling; specimen drawn in citrate or ACD tube
State patient's age and sex on the test request form.
- 1. Rosner W, Auchus RJ, Azziz R, Sluss PM, Raff H. Utility, limitations, and pitfalls in measuring testosterone: An Endocrine Society position statement. J Clin Endocrinol Metab. 2007 Feb; 92(2):405-413.17090633
- 2. Ismail AA, Astley P, Burr WA, et al. The role of testosterone measurement in the investigation of androgen disorders. Ann Clin Biochem. 1986 Mar; 23(Pt 2):113-134.3532913
- 3. Gronowski AM, Landau-Levine M. Reproductive endocrine function. In: Burtis CA, Ashwood ER, eds. Tietz Textbook of Clinical Chemistry. 3rd ed. Philadelphia, Pa: WB Saunders Co;1999:1601-1641.
- 4. Petak SM, Baskin HJ, Bergman DA, Dickey RA, Nankin HR. AACE clinical practice guidelines for the evaluation and treatment of hypogonadism in adult male patients. Endocrine Pract. 1996 Nov-Dec; 2(6):440-453.
- 5. Travison TG, Vesper HW, Orwoll E, et al. Harmonized reference ranges for circulating testosterone levels in men of four cohort studies in the USA and Eroupe. J Clin Endocrinol Metab. 2017 (in press).
- 6. Leifke E, Gorenoi V, Wichers C, Von Zur Mühlen A, Von Büren E, Brabant G. 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 (Oxf). 2000 Dec; 53(6):689-695.11155090
- 7. Basaria S, Dobs AS. Hypogonadism and androgen replacement therapy in elderly men. Am J Med. 2001 May; 110(7):563-572.11343670
- 8. Bain J. Andropause. Testosterone replacement therapy for aging men. Can Fam Physician. 2001 Jan; 47:91-97.11212438
- 9. Bhasin S, Bagatell CJ, Bremner WJ, et al. Issues in testosterone replacement in older men. J Clin Endocrinol Metab. 1998 Oct; 83(10):3435-3448.9768643
- 10. Ehrmann DA, Barnes RB, Rosenfield RL. Hyperandrogenism, hirsutism, and polycystic ovary syndrome. In: DeGroot LJ, Jameson JL, eds. Endocrinology. 4th ed. Philadelphia, Pa: WB Saunders Co;2001: 2122-2137.
- 11. Barth JH. Investigations in the assessment and management of patients with hirsutism. Curr Opin Obstet Gynecol. 1997 Jun; 9(3):187-192.9263703
- 12. Hunter MH, Sterrett JJ. Polycystic ovary syndrome: It's not just infertility. Am Fam Physician. 2000 Sep 1; 62(5):1079-1088,1090.10997532
- 13. Lobo RA, Carmina E. The importance of diagnosing the polycystic ovary syndrome. Ann Intern Med. 2000 Jun 20; 132(12):989-993.10858183
- 14. Chang WY, Knochenhauer ES, Bartolucci AA, Azziz R. Phenotypic spectrum of polycystic ovary syndrome: Clinical and biochemical characterization of the three major clinical subgroups. Fetil Steril. 2005 Jun; 83(6):1717-1723.15950641
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|070001||Testosterone, Total, LC/MS||2986-8||070000||Testosterone, Total, LC/MS||ng/dL||2986-8|