Progesterone 

Updated: Jan 16, 2014
  • Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP; Chief Editor: Eric B Staros, MD  more...
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Reference Range

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.

Reference ranges – female

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

Reference ranges – male

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]
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Interpretation

Progesterone is decreased in the following: [2]

  • 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
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Collection and Panels

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]
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Background

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]

Indications

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]

Considerations

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]

Estrogen and progesterone replacement

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]

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