Progesterone 

Progesterone 

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Progesterone is produced in the luteal phase of the cycle. For the change from the luteal back to the follicular phase, progesterone decreases gonadotrophin-releasing hormone (GnRH) pulse frequency to suppress gonadotropin release and reset the hypothalamic-pituitary-gonadal axis. The mechanism of action of progesterone-containing contraceptives is to suppress GnRH.

Progesterone decreases endometrial proliferation and develops secretory endometrium. The abrupt decline in progesterone toward the end of the cycle causes the onset of menstruation. The effect of estrogen causing endometrial hyperplasia is necessary prior to the effect of progesterone on the endometrium for the normal menstrual pattern. Progesterone causes the endocervical glands to secrete a scant viscid material that decreases penetration of the cervix by sperm. By suppressing menstruation and uterine contractility, progesterone helps to maintain pregnancy.

See the list below:

Age 5-9 years: 0.6 ng/mL

Age 10-13 years: 10.2 ng/mL

Age 14-17 years: 11.9 ng/mL

Early follicular: 0.6 ng/mL

Late follicular: 14.5 ng/mL

Luteal: 31.4 ng/mL

Mid-cycle: 16.1 ng/mL

Postmenopausal: 0.2 ng/mL

See the list below:

Age 5-9 years: 0.7 ng/mL

Age 10-13 years: 1.2 ng/mL

Age 14-17 years: < 0.8 ng/mL

Age 18-29 years: 0.3 ng/mL

Age 30 and older: 0.2 ng/mL [1]

Progesterone is decreased in the following: [2]

Amenorrhea

Threatened abortion

Fetal death

Toxemia of pregnancy

Gonadal agenesis

Progesterone is increased in the following:

Luteal phase of the menstrual cycle

Luteal cysts ovary; origin tumors

Adrenal tumors

Congenital adrenal hyperplasia (21 hydroxylase, 17 hydroxylase and 11beta hydroxylase) [2]

Molar pregnancy

See the list below:

Collection: Tiger-top tube. [3] Specimen should be frozen at -20°C. It is preferable to use early morning specimen. [1]

Progesterone is produced in the luteal phase of the cycle. For the change from the luteal back to the follicular phase, progesterone decreases gonadotrophin-releasing hormone (GnRH) pulse frequency to suppress gonadotropin release and reset the hypothalamic-pituitary-gonadal axis. The mechanism of action of progesterone-containing contraceptives is to suppress GnRH.

Progesterone decreases endometrial proliferation and develops secretory endometrium. The abrupt decline in progesterone toward the end of the cycle causes the onset of menstruation. The effect of estrogen causing endometrial hyperplasia is necessary prior to the effect of progesterone on the endometrium for the normal menstrual pattern. Progesterone causes the endocervical glands to secrete a scant viscid material that decreases penetration of the cervix by sperm. By suppressing menstruation and uterine contractility, progesterone helps to maintain pregnancy.

Due to the effect of progesterone, a peak (transient) of mitotic activity occurs in the luteal phase but falls to its nadir in the follicular phase. However, continued exposure to progesterone causes decrease in the growth of the epithelial cells. Even though controlled studies with only progesterone have not been performed, progesterone may be responsible for the heightened risk of breast cancer associated with estrogen-progesterone use (hormone replacement) in postmenopausal women. [4, 5, 6]

The rise in basal body temperature of 0.6°C (1°F) is due to progesterone, although the exact mechanism of action remains unknown. Additionally, progesterone increases the ventilatory response of the respiratory centers to carbon dioxide, causing respiratory alkalosis. Progesterone causes depression of central nervous system causing drowsiness; therefore, bedtime administration of progesterone preparations may even help some patients to sleep.

Long-term administration of more potent progesterones, such as norgestrel, may increase glucose intolerance. Lipoprotein lipase activity and deposition of fat are stimulated by progesterone. Due to androgenic activity, the 19-norprogestins may have more pronounced effects on plasma lipids.

Placental progesterone is synthesized from cholesterol from the mother. Progesterone serum levels increase from approximately 25 ng/mL during the midluteal phase to 150 ng/mL at the end of pregnancy. Inhibition of prostaglandin synthesis causes uterine quiescence during pregnancy. Progesterone may have a potent immunomodulatory effect in blocking immune rejection of the developing fetus. [7]

See the list below:

To detect ovulation in the evaluation of function of corpus luteum

To monitor patients having ovulation during induction with human chorionic gonadotrophin (hCG), human menopausal gonadotrophins, follicle-stimulating hormone (FSH)/ luteinizing hormone-releasing hormone, or clomiphene [2]

To evaluate patients at risk for early abortion [2]

Therapeutic uses of progesterone are as follows:M

Contraception

Hormone-replacement therapy

Diagnostic aid for secondary amenorrhea

To decrease endometrial hyperplasia and carcinoma caused by unopposed estrogen

For emergency contraception after known or suspected unprotected intercourse, a levonorgestrel (progesterone preparation) is used. [6]

Progestational agents, gestagens, or progestins are substances that mimic the action of progesterone. They are used with synthetic estrogens as oral contraceptive agents. [8]

Bone-remodeling rates increase and favor bone resorption over bone formation when estrogen levels decline. Results of over 50 randomized, placebo-controlled trials demonstrated that hormone replacement therapy improve bone mineral density. [9] Treatment with estrogen plus progesterone prevents vertebral fractures in postmenopausal women not known to have osteoporosis. [5] The Women’s Health Initiative is the first study to show that antiresorptives decrease the incidence of hip fracture. This preventive effect was lost rapidly upon stopping of hormone replacement therapy. [10]

Women from the National Osteoporosis Risk Assessment (NORA) trial who had stopped estrogen therapy within the 5 years before the study showed a significantly higher hip fracture risk than those who never received estrogen therapy (odds ratio 1.69; 95% CI 1.08 to 2.66). [7]

Gardner DG SD. Appendix: Normal Hormone Reference Ranges. Gardner DG SD, editor. Greenspan’s Basic & Clinical Endocrinology. 9th ed. New York: McGraw-Hill; 2011.

Williamson MA, Snyder LM, Wallach JB. Wallach’s interpretation of diagnostic tests. 9th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health; 2011.

Gomella LG HS. Laboratory Diagnosis: Chemistry, Immunology, Serology. Gomella LG HS, editor. Clinician’s Pocket Reference: The Scut Monkey. 11 ed. New York: McGraw-Hill; 2007.

Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women’s Health Initiative randomized controlled trial. JAMA. 2002. 288(3):321-33. Epub 2002/07/19.

Anderson GL, Limacher M, Assaf AR, et al. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women’s Health Initiative randomized controlled trial. JAMA. 2004. 291(14):1701-12. Epub 2004/04/15.

Levin ER HS. Estrogens and Progestins. Brunton LL CB, Knollmann BC, editor. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill; 2011.

Schorge JO SJ, Pietz J, Halvorson LM, Hoffman BL, Bradshaw KD, Cunningham FG. The Mature Woman. Schorge JO SJ, Pietz J, Halvorson LM, Hoffman BL, Bradshaw KD, Cunningham FG, editor. Williams Gynecology. New York: McGraw-Hill; 2008.

Barrett KE BS, Boitano S, Brooks HL. Reproductive Development & Function of the Female Reproductive System. Barrett KE BS, Boitano S, Brooks HL, editor. Ganong’s Review of Medical Physiology. 24th ed. New York: McGraw-Hill; 2012.

Treatment of menopause-associated vasomotor symptoms: position statement of The North American Menopause Society. Menopause. 2004. 11(1):11-33. Epub 2004/01/13.

Barrett-Connor E, Grady D, Sashegyi A, et al. Raloxifene and cardiovascular events in osteoporotic postmenopausal women: four-year results from the MORE (Multiple Outcomes of Raloxifene Evaluation) randomized trial. JAMA. 2002. 287(7):847-57. Epub 2002/02/20.

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP Professor of Medicine, St Louis University School of Medicine

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP is a member of the following medical societies: American College of Physicians, American Medical Informatics Association, Royal College of Physicians and Surgeons of Glasgow, Healthcare Information and Management Systems Society, Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

Progesterone 

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