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Interpretive Handbook

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Test 8141 :
Progesterone, Serum

Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

Sources of progesterone are the adrenal glands, corpus luteum, and placenta.

 

Adrenal Glands:

Progesterone synthesized in the adrenal glands is converted to other corticosteroids and androgens and, thus, is not a major contributor to circulating serum levels unless there is a progesterone-producing tumor present.

 

Corpus Luteum:

After ovulation, there is a significant rise in serum levels as the corpus luteum begins to produce progesterone in increasing amounts. This causes changes in the uterus, preparing it for implantation of a fertilized egg. If implantation occurs, the trophoblast begins to secrete human chorionic gonadotropin, which maintains the corpus luteum and its secretion of progesterone. If there is no implantation, the corpus luteum degenerates and circulating progesterone levels decrease rapidly, reaching follicular phase levels about 4 days before the next menstrual period.

 

Placenta:

By the end of the first trimester, the placenta becomes the primary secretor of progesterone.

Useful For Suggests clinical disorders or settings where the test may be helpful

Ascertaining whether ovulation occurred in a menstrual cycle

 

Evaluation of placental function in pregnancy

 

Workup of some patients with adrenal or testicular tumors

Interpretation Provides information to assist in interpretation of the test results

Ovulation results in a mid-cycle surge of luteinizing hormone (LH) followed by an increase in progesterone secretion, peaking between day 21 and 23. If no fertilization and implantation has occurred by then, supplying the corpus luteum with human chorionic gonadotropin-driven growth stimulus, progesterone secretion falls, ultimately triggering menstruation. A day 21 to 23 serum progesterone peak of 6.5 to 7 ng/mL is the minimal level considered consistent with ovulation. A level in excess of 18 ng/mL is considered conclusive proof of ovulation.

 

Placental insufficiency has been associated with low levels of LH and progesterone.

 

Levels of LH and progesterone may be increased in some adrenal or testicular tumors.

Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances

Assessment of the function of the corpus luteum requires correlation with the phase of the menstrual cycle.

 

In patients receiving therapy with high biotin doses (ie, >5 mg/day), no specimen should be drawn until at least 8 hours after the last biotin administration.

 

As with all tests containing monoclonal mouse antibodies, erroneous findings may be obtained from specimens drawn from patients who have been treated with monoclonal mouse antibodies or have received them for diagnostic purposes

 

In rare cases interference due to extremely high titers of antibodies to ruthenium and streptavidin can occur.

Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.

Males

Cord blood: 569-1,107 ng/mL*

0-23 months: 0.87-3.37 ng/mL*

2-9 years: <0.15 ng/mL*

10-17 years: adult levels are attained by puberty.*

> or =18 years: 0.20-1.40 ng/mL

Females

Cord blood: 569-1,107 ng/mL*

0-23 months: 0.87-3.37 ng/mL*

2-9 years: 0.20-0.24 ng/mL*

10-17 years: values increase through puberty and adolescence.*

Premenopausal

Follicular phase: 0.20-1.50 ng/mL

Ovulation phase: 0.80-3.00 ng/mL

Luteal phase: 1.70-27.00 ng/mL

Postmenopausal: <0.15-0.80 ng/mL

 

*Lippe BM, LaFranchi SH, Lavin N, et al: Serum 17-alpha-hydroxyprogesterone, progesterone, estradiol, and testosterone in the diagnosis and management of congenital adrenal hyperplasia. J Pediatr 1974;85:782-787

Clinical References Provides recommendations for further in-depth reading of a clinical nature

1. Lippe BM, LaFranchi SH, Lavin N, et al: Serum 17-alpha-hydroxyprogesterone, progesterone, estradiol, and testosterone in the diagnosis and management of congenital adrenal hyperplasia. J Pediatr 1974;85:782-787

2. Haymond S, Gronowski AM: In Tietz Textbook of Clinical Chemistry and Molecular Diagnostics, Fourth edition. Edited by CA Burtis, ER Ashwood, DE Bruns. St. Louis, Elsevier, Inc, 2006, pp 2097-2152


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