CPT Test code: 82670
|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.|
|Causes for Rejection:||Citrate plasma specimen; improper labeling|
|Reference Interval:||Adult male: 7.6-42.6 pg/mL
• Follicular: 12.5-166.0 pg/mL
• Ovulation: 85.8-498.0 pg/mL
• Luteal: 43.8-211.0 pg/mL
• Postmenopausal: <6.0-54.7 pg/mL
• First trimester: 215.0 to >4300.0 pg/mL
Children (1-10 years):
• Male: <6.0-20.0 pg/mL
• Female: 6.0-27.0 pg/mL
Note: The results displayed above were obtained with the Roche ECLIA methodology.
|Use:||This estradiol assay is designed for the investigation of fertility of women of reproductive age and for the support of in vitro fertilization.|
|Limitations:||Estradiol levels tend to fluctuate dramatically during the perimenopausal transition.1 There is significant overlap of the expected range in menopausal women with values observed during normal menstrual cycles. Estradiol results obtained with different assay methods cannot be used interchangeably in serial testing. To monitor a patient’s serial results, it is best to ensure that the same methodology is used each time the test is performed.
In patients receiving therapy with high biotin doses (ie, >5 mg/day), no sample should be taken until at least eight hours after the last biotin administration.2 As with all tests containing monoclonal mouse antibodies, erroneous findings may be obtained from samples taken from patients who have been treated with monoclonal mouse antibodies or who have received them for diagnostic purposes.2 In rare cases, interference due to extremely high titers of antibodies to streptavidin and ruthenium can occur.2 The test contains additives, which minimize these effects.
|Additional Information:||Estradiol is the primary reproductive hormone in nonpregnant women.3,4 This steroid hormone plays an important role in normal fetal development and in the development of secondary sexual characteristics in females. Estradiol influences the maturation and maintenance of the uterus during the normal menstrual cycle. Levels of estradiol steadily increase during the follicular phase of the menstrual cycle in association with the growth and development of the ovarian follicle. As the follicular phase proceeds, estradiol exerts a negative feedback control on the pituitary, resulting in a drop in FSH levels. Near the end of the follicular phase, there is a dramatic increase in estradiol levels. At this point, the feedback of estradiol on the hypothalamus becomes positive and produces the midcycle surge of LH which immediately precedes ovulation. After ovulation, estradiol levels initially fall abruptly, but then increase as the corpus luteum forms. At the end of the cycle, levels fall off in anticipation of the initiation of the next follicular phase. During pregnancy, the placenta produces estradiol. Estradiol levels are generally low in menopause due to diminished ovarian production.
A small amount of estradiol is produced by the male testes.3,4 Elevated levels in males can lead to gynecomastia. Increased estradiol levels in males may be caused by increased body fat, resulting in enhanced peripheral aromatization of androgens. Levels in men can also be increased by excessive use of marijuana, alcohol, or prescribed drugs, including phenothiazines and spironolactone. Estradiol levels can also be dramatically elevated in germ cell tumors and tumors of a number of glands in both men and women.
Estradiol levels are routinely used to monitor ovulation induction to stimulate follicle development in patients being treated by assisted reproductive techniques.4 Estradiol levels can be used to calibrate the exogenous gonadotropin administration and have been found to correlate with follicle size. The pattern of estradiol secretion during the cycle can be used to predict the outcome of the ART protocol.5
|Footnotes:||1. Burger HG. Diagnostic role of follicle-stimulating hormone (FSH) measurements during the menopausal transition−An analysis of FSH, oestradiol and inhibin. Eur J Endocrinol. 1994; 130(1):38-42.PubMed 8124478
2. Estradiol on Elecsys 1010/2010 and Modular Analytics E170, package insert 2007-09, V 13, Indianapolis, Ind: Roche Diagnostics; 2007.
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. Wheeler MJ. Infertility. In: , Wild D, ed. The Immunoassay Handbook. Stockton Press, 1994, 366-378.
5. Hugues JN, Cedrin-Durnerin I. Endocrine characteristics of ART cycles. In: Dardner DK, Weissman A, Howles CM, et al, eds. Textbook of Assisted Reproductive Techniques, Laboratory and Clinical Perspectives.Martin Dunitz Ltd; 2001: 459-472.
|References:||Kiel DP, Baron JA, Plymate SR, et al. Sex hormones and lipoproteins in men. Am J Med. 1989; 87(1):35-39. PubMed 2787120
Pont A, Goldman ES, Sugar AM, et al. Ketoconazole-induced increase in estradiol-testosterone ratio. Probable explanation for gynecomastia. Arch Intern Med. 1985; 145(8):1429-1431. PubMed 4040740
Segal KR, Dunaif A, Gutin B, et al. Body composition, not body weight, is related to cardiovascular disease risk factors and sex hormone levels in men. J Clin Invest. 1987; 80(4):1050-1055. PubMed 3654969
Stewart MO, Whittaker PG, Persson B, et al. A longitudinal study of circulating progesterone, oestradiol, hCG and hPL during pregnancy in type 1 diabetic mothers. Br J Obstet Gynaecol. 1989; 96(4):415-423. PubMed 2751954
Studd J, Savvas M, Waston N, et al. The relationship between plasma estradiol and the increase in bone density in postmenopausal women after treatment with subcutaneous hormone implants. Am J Obstet Gynecol. 1990; 163(5 Pt 1):1474-1479.PubMed 2240090