WordNet

a steroid hormone (trade name Lipo-Lutin) produced in the ovary; prepares and maintains the uterus for pregnancy (同)Lipo-Lutin
preceding and favoring gestation; of or relating to physiological changes associated with ovulation and formation of the corpus luteum
of or relating to progesterone (or to a drug with effects like those of progesterone)
a progestin compound (trade name Provera) used to treat menstrual disorders (同)Provera

PrepTutorEJDIC

黄体ホルモン
public relations

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/01/15 14:38:19」(JST)

wiki en

Progesterone also known as P4 (pregn-4-ene-3,20-dione) is a C-21 steroid hormone involved in the female menstrual cycle, pregnancy (supports gestation) and embryogenesis of humans and other species.^[1] Progesterone belongs to a class of hormones called progestogens, and is the major naturally occurring human progestogen.

1 Chemistry
2 Sources
- 2.1 Animal
- 2.2 Plants
3 Synthesis
- 3.1 Biosynthesis
- 3.2 Laboratory
4 Levels
5 Effects
- 5.1 Effects of Progesterone on Nicotine and Cocaine Addiction
- 5.2 Reproductive system
- 5.3 Nervous system
- 5.4 Other effects
6 Medical applications
- 6.1 Bioavailability
- 6.2 Prevention of preterm birth
- 6.3 Other specific uses
7 Role in aging
8 Role in brain damage
- 8.1 Proposed mechanism
- 8.2 Combination treatments
- 8.3 Clinical trials
9 See also
10 References
11 Additional images
12 External links

Chemistry[edit]

Progesterone was independently discovered by four research groups.^[2]^[3]^[4]^[5]

Willard Myron Allen co-discovered progesterone with his anatomy professor George Washington Corner at the University of Rochester Medical School in 1933. Allen first determined its melting point, molecular weight, and partial molecular structure. He also gave it the name Progesterone derived from Progestational Steroidal ketone.^[6]

Like other steroids, progesterone consists of four interconnected cyclic hydrocarbons. Progesterone contains ketone and oxygenated functional groups, as well as two methyl branches. Like all steroid hormones, it is hydrophobic.

Sources[edit]

Animal[edit]

Progesterone is produced in the ovaries (by the corpus luteum), the adrenal glands (near the kidney), and, during pregnancy, in the placenta. Progesterone is also stored in adipose (fat) tissue.

In humans, increasing amounts of progesterone are produced during pregnancy:

At first, the source is the corpus luteum that has been "rescued" by the presence of human chorionic gonadotropins (hCG) from the conceptus.

However, after the 8th week, production of progesterone shifts to the placenta. The placenta utilizes maternal cholesterol as the initial substrate, and most of the produced progesterone enters the maternal circulation, but some is picked up by the fetal circulation and used as substrate for fetal corticosteroids. At term the placenta produces about 250 mg progesterone per day.

An additional source of progesterone is milk products. After consumption of milk products the level of bioavailable progesterone goes up.^[7]

Plants[edit]

In at least one plant, Juglans regia, progesterone has been detected.^[8] In addition, progesterone-like steroids are found in Dioscorea mexicana. Dioscorea mexicana is a plant that is part of the yam family native to Mexico.^[9] It contains a steroid called diosgenin that is taken from the plant and is converted into progesterone.^[10] Diosgenin and progesterone are found in other Dioscorea species as well.

Another plant that contains substances readily convertible to progesterone is Dioscorea pseudojaponica native to Taiwan. Research has shown that the Taiwanese yam contains saponins — steroids that can be converted to diosgenin and thence to progesterone.^[11]

Many other Dioscorea species of the yam family contain steroidal substances from which progesterone can be produced. Among the more notable of these are Dioscorea villosa and Dioscorea polygonoides. One study showed that the Dioscorea villosa contains 3.5% diosgenin.^[12] Dioscorea polygonoides has been found to contain 2.64% diosgenin as shown by gas chromatography-mass spectrometry.^[13] Many of the Dioscorea species that originate from the yam family grow in countries that have tropical and subtropical climates.^[14]

Synthesis[edit]

Biosynthesis[edit]

Top: Conversion of cholesterol (1) into pregnenolone (3) to progesterone (6).

Bottom: Progesterone is important for aldosterone (mineralocorticoid) synthesis, as 17-hydroxyprogesterone is for cortisol (glucocorticoid), and androstenedione for sex steroids.

In mammals, progesterone (6), like all other steroid hormones, is synthesized from pregnenolone (3), which in turn is derived from cholesterol (1) (see the upper half of the figure to the right).

Cholesterol (1) undergoes double oxidation to produce 20,22-dihydroxycholesterol (2). This vicinal diol is then further oxidized with loss of the side chain starting at position C-22 to produce pregnenolone (3). This reaction is catalyzed by cytochrome P450scc. The conversion of pregnenolone to progesterone takes place in two steps. First, the 3-hydroxyl group is oxidized to a keto group (4) and second, the double bond is moved to C-4, from C-5 through a keto/enol tautomerization reaction.^[15] This reaction is catalyzed by 3beta-hydroxysteroid dehydrogenase/delta(5)-delta(4)isomerase.

Progesterone in turn (see lower half of figure to the right) is the precursor of the mineralocorticoid aldosterone, and after conversion to 17-hydroxyprogesterone (another natural progestogen) of cortisol and androstenedione. Androstenedione can be converted to testosterone, estrone and estradiol.

Pregnenolone and progesterone can also be synthesized by yeast.^[16]

Laboratory[edit]

The Marker semisynthesis of progesterone from diosgenin.^[17]

An economical semisynthesis of progesterone from the plant steroid diosgenin isolated from yams was developed by Russell Marker in 1940 for the Parke-Davis pharmaceutical company (see figure to the right).^[17] This synthesis is known as the Marker degradation. Additional semisyntheses of progesterone have also been reported starting from a variety of steroids. For the example, cortisone can be simultaneously deoxygenated at the C-17 and C-21 position by treatment with iodotrimethylsilane in chloroform to produce 11-keto-progesterone (ketogestin), which in turn can be reduced at position-11 to yield progesterone.^[18]

The Johnson total synthesis of progesterone.^[19]

A total synthesis of progesterone was reported in 1971 by W.S. Johnson (see figure to the right).^[19] The synthesis begins with reacting the phosphonium salt 7 with phenyl lithium to produce the phosphonium ylide 8. The ylide 8 is reacted with an aldehyde to produce the alkene 9. The ketal protecting groups of 9 are hydrolyzed to produce the diketone 10, which in turn is cyclized to form the cyclopentenone 11. The ketone of 11 is reacted with methyl lithium to yield the tertiary alcohol 12, which in turn is treated with acid to produce the tertiary cation 13. The key step of the synthesis is the π-cation cyclization of 13 in which the B-, C-, and D-rings of the steroid are simultaneously formed to produce 14. This step resembles the cationic cyclization reaction used in the biosynthesis of steroids and hence is referred to as biomimetic. In the next step the enol orthoester is hydrolyzed to produce the ketone 15. The cyclopentene A-ring is then opened by oxidizing with ozone to produce 16. Finally, the diketone 17 undergoes an intramolecular aldol condensation by treating with aqueous potassium hydroxide to produce progesterone.^[19]

Levels[edit]

In women, progesterone levels are relatively low during the preovulatory phase of the menstrual cycle, rise after ovulation, and are elevated during the luteal phase, as shown in diagram below. Progesterone levels tend to be < 2 ng/ml prior to ovulation, and > 5 ng/ml after ovulation. If pregnancy occurs, human chorionic gonadotropin is released maintaining the corpus luteum allowing it to maintain levels of progesterone. At around 12 weeks the placenta begins to produce progesterone in place of the corpus luteum, this process is named the luteal-placental shift. After the luteal-placental shift progesterone levels start to rise further and may reach 100-200 ng/ml at term. Whether a decrease in progesterone levels is critical for the initiation of labor has been argued and may be species-specific. After delivery of the placenta and during lactation, progesterone levels are very low.

Progesterone levels are relatively low in children and postmenopausal women.^[20] Adult males have levels similar to those in women during the follicular phase of the menstrual cycle.

Person type	Reference range for blood test
Person type	Lower limit	Upper limit	Unit
Female - menstrual cycle	(see diagram below)
Female - postmenopausal	<0.2^[21]	1^[21]	ng/mL
Female - postmenopausal	<0,6^[22]	3^[22]	nmol/L
Female on oral contraceptives	0.34^[21]	0.92^[21]	ng/mL
Female on oral contraceptives	1.1^[22]	2.9^[22]	nmol/L
Males ≥16 years	0.27^[21]	0.9^[21]	ng/mL
Males ≥16 years	0.86^[22]	2.9^[22]	nmol/L
Female or male 1–9 years	0.1^[21]	4.1^[21] or 4.5^[21]	ng/mL
Female or male 1–9 years	0.3^[22]	13^[22]	nmol/L

Progesterone levels during the menstrual cycle.^[23]
- The ranges denoted By biological stage may be used in closely monitored menstrual cycles in regard to other markers of its biological progression, with the time scale being compressed or stretched to how much faster or slower, respectively, the cycle progresses compared to an average cycle.
- The ranges denoted Inter-cycle variability are more appropriate to use in non-monitored cycles with only the beginning of menstruation known, but where the woman accurately knows her average cycle lengths and time of ovulation, and that they are somewhat averagely regular, with the time scale being compressed or stretched to how much a woman's average cycle length is shorter or longer, respectively, than the average of the population.

- The ranges denoted Inter-woman variability are more appropriate to use when the average cycle lengths and time of ovulation are unknown, but only the beginning of menstruation is given.

Effects[edit]

Micrograph showing changes to the endometrium due to progesterone (decidualization) H&E stain.

Progesterone exerts its primary action through the intracellular progesterone receptor although a distinct, membrane bound progesterone receptor has also been postulated.^[24]^[25] In addition, progesterone is a highly potent antagonist of the mineralocorticoid receptor (MR, the receptor for aldosterone and other mineralocorticosteroids). It prevents MR activation by binding to this receptor with an affinity exceeding even those of aldosterone and other corticosteroids such as cortisol and corticosterone.^[26]

Progesterone has a number of physiological effects that are amplified in the presence of estrogen. Estrogen through estrogen receptors upregulates the expression of progesterone receptors.^[27] Also, elevated levels of progesterone potently reduce the sodium-retaining activity of aldosterone, resulting in natriuresis and a reduction in extracellular fluid volume. Progesterone withdrawal, on the other hand, is associated with a temporary increase in sodium retention (reduced natriuresis, with an increase in extracellular fluid volume) due to the compensatory increase in aldosterone production, which combats the blockade of the mineralocorticoid receptor by the previously elevated level of progesterone.^[28]

Effects of Progesterone on Nicotine and Cocaine Addiction[edit]

Progesterone inhibits the enzyme monoamine oxidase (MAO) which is responsible for breaking down serotonin, the “feel good” neurotransmitter. In addition, progesterone enhances the serotonin receptor function in the brain, so too much or too little progesterone can cause significant problems on brain chemistry. This explains why people resort to substances that enhance serotonin activity such as nicotine, alcohol, and marijuana when their progesterone levels fall below optimal levels.^[29]

To examine the effects of progesterone on nicotine addiction specifically, one study researched the reinforcing effects of smoking in both men and women addicted to nicotine. Participants were either treated orally with a progesterone treatment, or treated with a placebo. When treated with progesterone, participants exhibited enhanced suppression of smoking urges, reported higher ratings of “bad effects” from IV nicotine, and reported lower ratings of “drug liking”. These results suggest that progesterone not only alters the subjective effects of nicotine, but reduces the urge to smoke cigarettes.^[30]

Further studies demonstrated sex differences such that changes in hormone levels may induce women to respond differently than men to nicotine. When women undergo cyclic changes or different hormonal transition phases (menopause, pregnancy, adolescence), there are changes in their progesterone levels.^[31] Therefore, females have an increased biological vulnerability to nicotine’s reinforcing effects compared to men and progesterone may be used to counter this enhanced vulnerability. This information helps us to understand how the female hormones profoundly impact brain functioning, and, thus behavior.^[29]

Furthermore, interestingly, past research suggests possible effects of progesterone on cocaine addiction. Similar to nicotine, cocaine also increases the release of dopamine in the brain. The neurotransmitter is involved in the reward center and is one of the main neurotransmitters involved with substance abuse and reliance. In a study of cocaine users, it was reported that progesterone reduced craving and the feeling of being stimulated by cocaine. Thus, progesterone was suggested as an agent that decreases cocaine craving by reducing the dopaminergic properties of the drug.^[32]

Reproductive system[edit]

Progesterone has key effects via non-genomic signalling on human sperm as they migrate through the female tract before fertilization occurs, though the receptor(s) as yet remain unidentified.^[33] Detailed characterisation of the events occurring in sperm in response to progesterone has elucidated certain events including intracellular calcium transients and maintained changes,^[34] slow calcium oscillations,^[35] now thought to possibly regulate motility.^[36] Interestingly progesterone has also been shown to demonstrate effects on octopus spermatozoa.^[37]

Progesterone modulates the activity of CatSper (cation channels of sperm) voltage-gated Ca²⁺ channels. Since eggs release progesterone, sperm may use progesterone as a homing signal to swim toward eggs (chemotaxis). Hence substances that block the progesterone binding site on CatSper channels could potentially be used in male contraception.^[38]^[39]

Progesterone is sometimes called the "hormone of pregnancy",^[40] and it has many roles relating to the development of the fetus:

Progesterone converts the endometrium to its secretory stage to prepare the uterus for implantation. At the same time progesterone affects the vaginal epithelium and cervical mucus, making it thick and impenetrable to sperm. If pregnancy does not occur, progesterone levels will decrease, leading, in the human, to menstruation. Normal menstrual bleeding is progesterone-withdrawal bleeding. If ovulation does not occur and the corpus luteum does not develop, levels of progesterone may be low, leading to anovulatory dysfunctional uterine bleeding.
During implantation and gestation, progesterone appears to decrease the maternal immune response to allow for the acceptance of the pregnancy.
Progesterone decreases contractility of the uterine smooth muscle.^[40]
In addition progesterone inhibits lactation during pregnancy. The fall in progesterone levels following delivery is one of the triggers for milk production.
A drop in progesterone levels is possibly one step that facilitates the onset of labor.

The fetus metabolizes placental progesterone in the production of adrenal steroids.

Nervous system[edit]

Progesterone, like pregnenolone and dehydroepiandrosterone, belongs to the group of neurosteroids. It can be synthesized within the central nervous system and also serves as a precursor to another major neurosteroid, allopregnanolone.

Neurosteroids affect synaptic functioning, are neuroprotective, and affect myelination.^[41] They are investigated for their potential to improve memory and cognitive ability. Progesterone affects regulation of apoptotic genes.

Its effect as a neurosteroid works predominantly through the GSK-3 beta pathway, as an inhibitor. (Other GSK-3 beta inhibitors include bipolar mood stabilizers, lithium and valproic acid.)

Other effects[edit]

It raises epidermal growth factor-1 levels, a factor often used to induce proliferation, and used to sustain cultures, of stem cells.
It increases core temperature (thermogenic function) during ovulation.^[42]
It reduces spasm and relaxes smooth muscle. Bronchi are widened and mucus regulated. (Progesterone receptors are widely present in submucosal tissue.)
It acts as an antiinflammatory agent and regulates the immune response.
It reduces gall-bladder activity.^[43]
It normalizes blood clotting and vascular tone, zinc and copper levels, cell oxygen levels, and use of fat stores for energy.
It may affect gum health, increasing risk of gingivitis (gum inflammation) and tooth decay.^[44]
It appears to prevent endometrial cancer (involving the uterine lining) by regulating the effects of estrogen.
Progesterone plays an important role in the signaling of insulin release and pancreatic function, and may affect the susceptibility to diabetes or gestational diabetes.^[45]^[46]
It is related with apoptosis theory <not just Abstract> and increase monocytes

Medical applications[edit]

Prometrium 100 mg Oral Capsule

The use of progesterone and its analogues have many medical applications, both to address acute situations and to address the long-term decline of natural progesterone levels. Because of the poor bioavailability of progesterone when taken orally, many synthetic progestins have been designed with improved oral bioavailability and have been used long before progesterone formulations became available.^[47] Progesterone was approved by the United States Food and Drug Administration as vaginal gel on July 31, 1997,^[48] an oral capsule on May 14, 1998^[49] in an injection form on April 25, 2001^[50] and as a vaginal insert on June 21, 2007.^[51] In Italy and Spain, Progesterone is sold under the trademark Progeffik.

Bioavailability[edit]

The route of administration impacts the effect of the drug. Given orally, progesterone has a wide person-to-person variability in absorption and bioavailability while synthetic progestins are rapidly absorbed with a longer half-life than progesterone and maintain stable levels in the blood.^[52]

Progesterone does not dissolve in water and is poorly absorbed when taken orally unless micronized in oil. Products are often sold as capsules containing micronised progesterone in oil. Progesterone can also be administered through vaginal or rectal suppositories or pessaries, transdermally through a gel or cream,^[53] or via injection (though the latter has a short half-life requiring daily administration).

Transdermal "natural progesterone" products made with Progesterone USP do not require a prescription. Some of these products also contain "wild yam extract" derived from Dioscorea villosa, but there is no evidence that the human body can convert its active ingredient (diosgenin, the plant steroid that is chemically converted to produce progesterone industrially^[17]) into progesterone.^[54]^[55]

Prevention of preterm birth[edit]

Vaginally dosed progesterone is being investigated as potentially beneficial in preventing preterm birth in women at risk for preterm birth. The initial study by Fonseca suggested that vaginal progesterone could prevent preterm birth in women with a history of preterm birth.^[56] According to a recent study, women with a short cervix that received hormonal treatment with a progesterone gel had their risk of prematurely giving birth reduced. The hormone treatment was administered vaginally every day during the second half of a pregnancy.^[57] A subsequent and larger study showed that vaginal progesterone was no better than placebo in preventing recurrent preterm birth in women with a history of a previous preterm birth,^[58] but a planned secondary analysis of the data in this trial showed that women with a short cervix at baseline in the trial had benefit in two ways: a reduction in births less than 32 weeks and a reduction in both the frequency and the time their babies were in intensive care.^[59] In another trial, vaginal progesterone was shown to be better than placebo in reducing preterm birth prior to 34 weeks in women with an extremely short cervix at baseline.^[60] An editorial by Roberto Romero discusses the role of sonographic cervical length in identifying patients who may benefit from progesterone treatment.^[61] A meta-analysis published in 2011 found that vaginal progesterone cut the risk of premature births by 42 percent in women with short cervixes.^[62] The meta-analysis, which pooled published results of five large clinical trials, also found that the treatment cut the rate of breathing problems and reduced the need for placing a baby on a ventilator.^[63]

Other specific uses[edit]

Progesterone is used for luteal support in Assisted Reproductive Technology (ART) cycles such as In-vitro Fertilization (IVF).
Progesterone is used to control persistent anovulatory bleeding. It is also used to prepare uterine lining in infertility therapy and to support early pregnancy. Patients with recurrent pregnancy loss due to inadequate progesterone production may receive progesterone.
Progesterone is also used in nonpregnant women with a delayed menstruation of one or more weeks, in order to allow the thickened endometrial lining to slough off. This process is termed a progesterone withdrawal bleed. The progesterone is taken orally for a short time (usually one week), after which the progesterone is discontinued and bleeding should occur.^{[citation needed]}
Progesterone is being investigated as potentially beneficial in treating multiple sclerosis, since the characteristic deterioration of nerve myelin insulation halts during pregnancy, when progesterone levels are raised; deterioration commences again when the levels drop.
Progesterone also has a role in skin elasticity and bone strength, in respiration, in nerve tissue and in female sexuality, and the presence of progesterone receptors in certain muscle and fat tissue may hint at a role in sexually dimorphic proportions of those.^[64]^{[copyright violation?]}
Progesterone receptor antagonists, or selective progesterone receptor modulators (SPRM)s, such as RU-486 (Mifepristone), can be used to prevent conception or induce medical abortions (Note that methods of hormonal contraception do not contain progesterone but a progestin).
Progesterone may affect male behavior.^[65]
Progesterone is starting to be used in the treatment of the skin condition hidradenitis suppurativa.^{[citation needed]}
Progesterone is sometimes used as a component of hormone replacement therapy (male-to-female) for the treatment of gender dysphoria. This is an off-label use.^[66]

Role in aging[edit]

Since most progesterone in males is created during testicular production of testosterone, and most in females by the ovaries, the shutting down (whether by natural or chemical means), or removal, of those inevitably causes a considerable reduction in progesterone levels. Previous concentration upon the role of progestogens (progesterone and molecules with similar effects) in female reproduction, when progesterone was simply considered a "female hormone", obscured the significance of progesterone elsewhere in both sexes.

The tendency for progesterone to have a regulatory effect, the presence of progesterone receptors in many types of body tissue, and the pattern of deterioration (or tumor formation) in many of those increasing in later years when progesterone levels have dropped, is prompting widespread research into the potential value of maintaining progesterone levels in both males and females.

Role in brain damage[edit]

Studies as far back as 1987 show that female sex hormones have an effect on the recovery of traumatic brain injury.^[67] In these studies, it was first observed that pseudopregnant female rats had reduced edema after traumatic brain injury. Recent clinical trials have shown that among patients that have suffered moderate traumatic brain injury, those that have been treated with progesterone are more likely to have a better outcome than those who have not.^[68]

Previous studies have shown that progesterone supports the normal development of neurons in the brain, and that the hormone has a protective effect on damaged brain tissue. It has been observed in animal models that females have reduced susceptibility to traumatic brain injury and this protective effect has been hypothesized to be caused by increased circulating levels of estrogen and progesterone in females.^[69] A number of additional animal studies have confirmed that progesterone has neuroprotective effects when administered shortly after traumatic brain injury.^[70] Encouraging results have also been reported in human clinical trials.^[71]^[72]

Proposed mechanism[edit]

The mechanism of progesterone protective effects may be the reduction of inflammation that follows brain trauma.^[73]

Damage incurred by traumatic brain injury is believed to be caused in part by mass depolarization leading to excitotoxicity. One way in which progesterone helps to alleviate some of this excitotoxicity is by blocking the voltage-dependent calcium channels that trigger neurotransmitter release.^[74] It does so by manipulating the signaling pathways of transcription factors involved in this release. Another method for reducing the excitotoxicity is by up-regulating the inhibitory neurotransmitter receptor, GABAA.^[75]

Progesterone has also been shown to prevent apoptosis in neurons, a common consequence of brain injury.^[67] It does so by inhibiting enzymes involved in the apoptosis pathway specifically concerning the mitochondria, such as activated caspase 3 and cytochrome c.

Not only does progesterone help prevent further damage, it has also been shown to aid in neuroregeneration. One of the serious effects of traumatic brain injury includes edema. Animal studies show that progesterone treatment leads to a decrease in edema levels by increasing the concentration of macrophages and microglia sent to the injured tissue.^[74]^[76] This was observed in the form of reduced leakage from the blood brain barrier in secondary recovery in progesterone treated rats. In addition, progesterone was observed to have antioxidant properties, reducing the concentration of oxygen free radicals faster than without.^[75] There is also evidence that the addition of progesterone can also help remyelinate damaged axons due to trauma, restoring some lost neural signal conduction.^[75] Another way progesterone aids in regeneration includes increasing the circulation of endothelial progenitor cells in the brain.^[77] This helps new vasculature to grow around scar tissue which helps repair the area of insult.

Combination treatments[edit]

Vitamin D and progesterone separately have neuroprotective effects after traumatic brain injury, but when combined their effects are synergistic.^[78] When used at their optimal respective concentrations, the two combined have been shown to reduce cell death more than when alone.

One study looks at a combination of progesterone with estrogen. Both progesterone and estrogen are known to have antioxidant-like qualities and are shown to reduce edema without injuring the blood-brain barrier. In this study, when the two hormones are administered alone it does reduce edema, but the combination of the two increases the water content, thereby increasing edema.^[79]

Clinical trials[edit]

The clinical trials for progesterone as a treatment for traumatic brain injury have only recently begun. ProTECT, a phase II trial conducted in Atlanta at Grady Memorial Hospital in 2007, the first to show that progesterone reduces edema in humans. Since then, trials have moved on to phase III. The National Institute of Health began conducting a nationwide phase III trial in 2011 led by Emory University.^[68] A global phase III initiative called SyNAPSe®, initiated in June 2010, is run by a U.S.-based private pharmaceutical company, BHR Pharma, and is being conducted in the United States, Argentina, Europe, Israel and Asia.^[80]^[81] Approximately 1,200 patients with severe (Glasgow Coma Scale scores of 3-8), closed-head TBI will be enrolled in the study at nearly 150 medical centers.

References[edit]

^ "Metabocard for Hydroxyprogesterone". Human Metabolome Database. Retrieved 31 July 2013.
^ Allen WM (1935). "The isolation of crystalline progestin". Science 82 (2118): 89–93. doi:10.1126/science.082.2118.89. PMID 17747122.
^ Butenandt A, Westphal U (1934). "Zur Isolierung und Charakterisierung des Corpusluteum-Hormons". Berichte Deu0tsche chemische Gesellschaft 67 (8): 1440–1442. doi:10.1002/cber.19340670831.
^ Hartmann M, Wettstein A (1934). "Ein krystallisiertes Hormon aus Corpus luteum". Helvetica Chimica Acta 17: 878–882. doi:10.1002/hlca.193401701111.
^ Slotta KH, Ruschig H, Fels E (1934). "Reindarstellung der Hormone aus dem Corpusluteum". Berichte Deutsche chemische Gesellschaft 67 (7): 1270–1273. doi:10.1002/cber.19340670729.
^ Allen WM (1970). "Progesterone: how did the name originate?". South. Med. J. 63 (10): 1151–5. doi:10.1097/00007611-197010000-00012. PMID 4922128.
^ Goodson III WH, Handagama P, Moore II DH, Dairkee S (2007-12-13). "Milk products are a source of dietary progesterone". 30th Annual San Antonio Breast Cancer Symposium. pp. abstract # 2028. Retrieved 2008-03-12.
^ Pauli GF, Friesen JB, Gödecke T, Farnsworth NR, Glodny B (January 2010). "Occurrence of Progesterone and Related Animal Steroids in Two Higher Plants". J Nat Prod 73 (3): 338–45. doi:10.1021/np9007415. PMID 20108949. Cite uses deprecated parameters (help)
^ Applezweig N (May 1969). "Steroids". Chem Week 104: 57–72. PMID 12255132. Cite uses deprecated parameters (help)
^ Noguchi E, Fujiwara Y, Matsushita S, Ikeda T, Ono M, Nohara T (September 2006). "Metabolism of tomato steroidal glycosides in humans". Chem. Pharm. Bull. 54 (9): 1312–4. doi:10.1248/cpb.54.1312. PMID 16946542. Cite uses deprecated parameters (help)
^ Yang DJ, Lu TJ, Hwang LS (October 2003). "Isolation and identification of steroidal saponins in Taiwanese yam cultivar (Dioscorea pseudojaponica Yamamoto)". J. Agric. Food Chem. 51 (22): 6438–44. doi:10.1021/jf030390j. PMID 14558759. Cite uses deprecated parameters (help)
^ Hooker E (2004). "Final report of the amended safety assessment of Dioscorea Villosa (Wild Yam) root extract". Int. J. Toxicol. 23 Suppl 2: 49–54. doi:10.1080/10915810490499055. PMID 15513824.
^ Niño J, Jiménez DA, Mosquera OM, Correa YM (2007). "Diosgenin quantification by HPLC in a Dioscorea polygonoides tuber collection from colombian flora". Journal of the Brazilian Chemical Society 18 (5): 1073–1076. doi:10.1590/S0103-50532007000500030.
^ Myoda T, Nagai T, Nagashima T (2005). "Properties of starches in yam (Dioscorea spp.) tuber". Current Topics in Food Science and Technology. pp. 105–114. ISBN 81-308-0003-9
^ Dewick, Paul M. (2002). Medicinal natural products: a biosynthetic approach. New York: Wiley. p. 244. ISBN 0-471-49641-3.
^ Duport C, Spagnoli R, Degryse E, Pompon D (February 1998). "Self-sufficient biosynthesis of pregnenolone and progesterone in engineered yeast". Nat. Biotechnol. 16 (2): 186–9. doi:10.1038/nbt0298-186. PMID 9487528. Cite uses deprecated parameters (help)
^ ^a ^b ^c Marker RE, Krueger J (1940). "Sterols. CXII. Sapogenins. XLI. The Preparation of Trillin and its Conversion to Progesterone". J. Am. Chem. Soc. 62 (12): 3349–3350. doi:10.1021/ja01869a023.
^ Numazawa M, Nagaoka M, Kunitama Y (September 1986). "Regiospecific deoxygenation of the dihydroxyacetone moiety at C-17 of corticoid steroids with iodotrimethylsilane". Chem. Pharm. Bull. 34 (9): 3722–6. doi:10.1248/cpb.34.3722. PMID 3815593. Cite uses deprecated parameters (help)
^ ^a ^b ^c Johnson WS, Gravestock MB, McCarry BE (August 1971). "Acetylenic bond participation in biogenetic-like olefinic cyclizations. II. Synthesis of dl-progesterone". J. Am. Chem. Soc. 93 (17): 4332–4. doi:10.1021/ja00746a062. PMID 5131151. Cite uses deprecated parameters (help)
^ NIH Clinical Center (2004-08-16). "Progesterone Historical Reference Ranges". United States National Institutes of Health. Retrieved 2008-03-12.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ Progesterone Reference Ranges, Performed at the Clinical Center at the National Institutes of Health, Bethesda MD, 03Feb09
^ ^a ^b ^c ^d ^e ^f ^g ^h Converted from mass values using molar mass of 314.46 g/mol
^ Reference ranges for estradiol, progesterone, luteinizing hormone and follicle-stimulating hormone during the menstrual cycle. Wikiversity, peer reviewed 2013.
^ Luconi M, Bonaccorsi L, Maggi M, Pecchioli P, Krausz C, Forti G, Baldi E (1998). "Identification and characterization of functional nongenomic progesterone receptors on human sperm membrane". J. Clin. Endocrinol. Metab. 83 (3): 877–85. doi:10.1210/jc.83.3.877. PMID 9506743.
^ Jang S, Yi LS (2005). "Identification of a 71 kDa protein as a putative non-genomic membrane progesterone receptor in boar spermatozoa". J. Endocrinol. 184 (2): 417–25. doi:10.1677/joe.1.05607. PMID 15684349.
^ Rupprecht R, Reul JM, van Steensel B, Spengler D, Söder M, Berning B, Holsboer F, Damm K (1993). "Pharmacological and functional characterization of human mineralocorticoid and glucocorticoid receptor ligands". Eur J Pharmacol 247 (2): 145–54. doi:10.1016/0922-4106(93)90072-H. PMID 8282004.
^ Kastner P, Krust A, Turcotte B, Stropp U, Tora L, Gronemeyer H, Chambon P (1990). "Two distinct estrogen-regulated promoters generate transcripts encoding the two functionally different human progesterone receptor forms A and B". EMBO J. 9 (5): 1603–14. PMC 551856. PMID 2328727.
^ Landau RL, Bergenstal DM, Lugibihl K, Kascht ME. (1955). "The metabolic effects of progesterone in man". J Clin Endocrinol Metab 15 (10): 1194–215. doi:10.1210/jcem-15-10-1194. PMID 13263410.
^ ^a ^b 1=Exp Clin Psychopharmacol. 2010 December; 18(6): 451–461
^ 2=Hum Psychopharmacol. 2009 Oct;24(7):559-64. doi: 10.1002/hup.1055.
^ 3=Arch Gen Psychiatry. 2012;69(4):418427.doi:10.1001/archgenpsychiatry.2011.1465.
^ 4=Neuropsychopharmacology. 2011 Oct;36(11):2187-99. doi: 10.1038/npp.2011.130. Epub 2011 Jul 27
^ Correia JN, Conner SJ, Kirkman-Brown JC (May 2007). "Non-genomic steroid actions in human spermatozoa. "Persistent tickling from a laden environment"". Semin. Reprod. Med. 25 (3): 208–19. doi:10.1055/s-2007-973433. PMID 17447210. Cite uses deprecated parameters (help)
^ Kirkman-Brown JC, Bray C, Stewart PM, Barratt CL, Publicover SJ (June 2000). "Biphasic elevation of [Ca(2+)](i) in individual human spermatozoa exposed to progesterone". Developmental Biology 222 (2): 326–35. doi:10.1006/dbio.2000.9729. ISSN 0012-1606. PMID 10837122. Cite uses deprecated parameters (help)
^ Kirkman-Brown JC, Barratt CL, Publicover SJ (March 2004). "Slow calcium oscillations in human spermatozoa". The Biochemical Journal 378 (Pt 3): 827–32. doi:10.1042/BJ20031368. PMC 1223996. PMID 14606954. Cite uses deprecated parameters (help)
^ Harper CV, Barratt CL, Publicover SJ (October 2004). "Stimulation of human spermatozoa with progesterone gradients to simulate approach to the oocyte. Induction of [Ca(2+)](i) oscillations and cyclical transitions in flagellar beating". The Journal of Biological Chemistry 279 (44): 46315–25. doi:10.1074/jbc.M401194200. PMID 15322137. Cite uses deprecated parameters (help)
^ Tosti E, Di Cosmo A, Cuomo A, Di Cristo C, Gragnaniello G (May 2001). "Progesterone induces activation in Octopus vulgaris spermatozoa". Mol. Reprod. Dev. 59 (1): 97–105. doi:10.1002/mrd.1011. PMID 11335951. Cite uses deprecated parameters (help)
^ Strünker T, Goodwin N, Brenker C, Kashikar ND, Weyand I, Seifert R, Kaupp UB (March 2011). "The CatSper channel mediates progesterone-induced Ca2+ influx in human sperm". Nature 471 (7338): 382–6. doi:10.1038/nature09769. PMID 21412338. Lay summary – Nature News. Cite uses deprecated parameters (help)
^ Lishko PV, Botchkina IL, Kirichok Y (March 2011). "Progesterone activates the principal Ca2+ channel of human sperm". Nature 471 (7338): 387–91. doi:10.1038/nature09767. PMID 21412339. Cite uses deprecated parameters (help)
^ ^a ^b Bowen R (2000-08-06). "Placental Hormones". Retrieved 2008-03-12.
^ Schumacher M, Guennoun R, Robert F, et al. (2004). "Local synthesis and dual actions of progesterone in the nervous system: neuroprotection and myelination". Growth Horm. IGF Res. 14 Suppl A: S18–33. doi:10.1016/j.ghir.2004.03.007. PMID 15135772.
^ Physiology at MCG 5/5ch9/s5ch9_13
^ Hould FS, Fried GM, Fazekas AG, Tremblay S, Mersereau WA (1988). "Progesterone receptors regulate gallbladder motility". J. Surg. Res. 45 (6): 505–12. doi:10.1016/0022-4804(88)90137-0. PMID 3184927.
^ "Hormones and Oral Health". WebMD.
^ Picard F, Wanatabe M, Schoonjans K, Lydon J, O'Malley BW, Auwerx J (2002). "Progesterone receptor knockout mice have an improved glucose homeostasis secondary to beta -cell proliferation". Proceedings of the National Academy of Sciences 99 (24): 15644–15648. doi:10.1073/pnas.202612199. PMC 137770. PMID 12438645. edit
^ Brănişteanu DD, Mathieu C (March 2003). "Progesterone in gestational diabetes mellitus: guilty or not guilty?". Trends Endocrinol. Metab. 14 (2): 54–6. doi:10.1016/S1043-2760(03)00003-1. PMID 12591170. Cite uses deprecated parameters (help) edit
^ Schindler AE, Campagnoli C, Druckmann R, Huber J, Pasqualini JR, Schweppe KW, Thijssen JH (2008). "Classification and pharmacology of progestins". Maturitas 61 (1–2): 171–80. doi:10.1016/j.maturitas.2003.09.014. PMID 19434889.
^ "Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations: 020701". Food and Drug Administration. 2010-07-02. Retrieved 2010-07-07.
^ "Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations: 019781". Food and Drug Administration. 2010-07-02. Retrieved 2010-07-07.
^ "Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations: 075906". Food and Drug Administration. 2010-07-02. Retrieved 2010-07-07.
^ "Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations: 022057". Food and Drug Administration. 2010-07-02. Retrieved 2010-07-07.
^ Schindler AE, Campagnoli C, Druckmann R, Huber J, Pasqualini JR, Schweppe KW, Thijssen JH (2003). "Classification and pharmacology of progestins". Maturitas. 46 Suppl 1: S7–S16. PMID 14670641. edit
^ Lark, Susan (1999). Making the Estrogen Decision. McGraw-Hill Professional. p. 22. ISBN 0-87983-696-2, 9780879836962 Check |isbn= value (help).
^ Zava DT, Dollbaum CM, Blen M (1998). "Estrogen and progestin bioactivity of foods, herbs, and spices". Proc. Soc. Exp. Biol. Med. 217 (3): 369–78. PMID 9492350.
^ Komesaroff PA, Black CV, Cable V, Sudhir K (2001). "Effects of wild yam extract on menopausal symptoms, lipids and sex hormones in healthy menopausal women". Climacteric 4 (2): 144–50. doi:10.1080/713605087. PMID 11428178.
^ da Fonseca EB, Bittar RE, Carvalho MH, Zugaib M (2003). "Prophylactic administration of progesterone by vaginal suppository to reduce the incidence of spontaneous preterm birth in women at increased risk: a randomized placebo-controlled double-blind study". Am. J. Obstet. Gynecol. 188 (2): 419–24. doi:10.1067/mob.2003.41. PMID 12592250.
^ Harris, Gardiner (2011-05-02). "Hormone Is Said to Cut Risk of Premature Birth". New York Times. Retrieved 5 May 2011.
^ O'Brien JM, Adair CD, Lewis DF, Hall DR, Defranco EA, Fusey S, Soma-Pillay P, Porter K, How H, Schackis R, Eller D, Trivedi Y, Vanburen G, Khandelwal M, Trofatter K, Vidyadhari D, Vijayaraghavan J, Weeks J, Dattel B, Newton E, Chazotte C, Valenzuela G, Calda P, Bsharat M, Creasy GW (2007). "Progesterone vaginal gel for the reduction of recurrent preterm birth: primary results from a randomized, double-blind, placebo-controlled trial". Ultrasound Obstet Gynecol 30 (5): 687–96. doi:10.1002/uog.5158. PMID 17899572.
^ DeFranco EA, O'Brien JM, Adair CD, Lewis DF, Hall DR, Fusey S, Soma-Pillay P, Porter K, How H, Schakis R, Eller D, Trivedi Y, Vanburen G, Khandelwal M, Trofatter K, Vidyadhari D, Vijayaraghavan J, Weeks J, Dattel B, Newton E, Chazotte C, Valenzuela G, Calda P, Bsharat M, Creasy GW (2007). "Vaginal progesterone is associated with a decrease in risk for early preterm birth and improved neonatal outcome in women with a short cervix: a secondary analysis from a randomized, double-blind, placebo-controlled trial". Ultrasound Obstet Gynecol 30 (5): 697–705. doi:10.1002/uog.5159. PMID 17899571.
^ Fonseca EB, Celik E, Parra M, Singh M, Nicolaides KH (2007). "Progesterone and the risk of preterm birth among women with a short cervix". N. Engl. J. Med. 357 (5): 462–9. doi:10.1056/NEJMoa067815. PMID 17671254.
^ Romero R (2007). "Prevention of spontaneous preterm birth: the role of sonographic cervical length in identifying patients who may benefit from progesterone treatment". Ultrasound Obstet Gynecol 30 (5): 675–86. doi:10.1002/uog.5174. PMID 17899585.
^ Hassan SS, Romero R, Vidyadhari D, Fusey S, Baxter JK, Khandelwal M, Vijayaraghavan J, Trivedi Y, Soma-Pillay P, Sambarey P, Dayal A, Potapov V, O'Brien J, Astakhov V, Yuzko O, Kinzler W, Dattel B, Sehdev H, Mazheika L, Manchulenko D, Gervasi MT, Sullivan L, Conde-Agudelo A, Phillips JA, Creasy GW (July 2011). "Vaginal progesterone reduces the rate of preterm birth in women with a sonographic short cervix: a multicenter, randomized, double-blind, placebo-controlled trial". Ultrasound Obstet Gynecol 38 (1): 18–31. doi:10.1002/uog.9017. PMID 21472815. Lay summary – WebMD. Cite uses deprecated parameters (help)
^ "Progesterone helps cut risk of pre-term birth". Women's health. msnbc.com. 2011-12-14. Retrieved 2011-12-14.
^ Sriram, D (2007). Medicinal Chemistry. New Delhi: Dorling Kindersley India Pvt. Ltd. p. 432. ISBN 81-317-0031-3. |accessdate= requires |url= (help)
^ Schneider JS, Stone MK, Wynne-Edwards KE, Horton TH, Lydon J, O'Malley B, Levine JE (2003). "Progesterone receptors mediate male aggression toward infants". Proc. Natl. Acad. Sci. U.S.A. 100 (5): 2951–6. doi:10.1073/pnas.0130100100. PMC 151447. PMID 12601162.
^ "Standards of Care for the Health of Transsexual, Transgender, and Gender-Nonconforming People, Version 7," International Journal of Transgenderism 13: 165-232.
^ ^a ^b Espinoza TR, Wright DW (2011). "The role of progesterone in traumatic brain injury". J Head Trauma Rehabil 26 (6): 497–9. doi:10.1097/HTR.0b013e31823088fa. PMID 22088981.
^ ^a ^b Stein DG (September 2011). "Progesterone in the treatment of acute traumatic brain injury: a clinical perspective and update". Neuroscience 191: 101–6. doi:10.1016/j.neuroscience.2011.04.013. PMID 21497181. Cite uses deprecated parameters (help)
^ Roof RL, Hall ED (May 2000). "Gender differences in acute CNS trauma and stroke: neuroprotective effects of estrogen and progesterone". J. Neurotrauma 17 (5): 367–88. doi:10.1089/neu.2000.17.367. PMID 10833057. Cite uses deprecated parameters (help)
^ Gibson CL, Gray LJ, Bath PM, Murphy SP (February 2008). "Progesterone for the treatment of experimental brain injury; a systematic review". Brain 131 (Pt 2): 318–28. doi:10.1093/brain/awm183. PMID 17715141. Cite uses deprecated parameters (help)
^ Wright DW, Kellermann AL, Hertzberg VS, Clark PL, Frankel M, Goldstein FC, Salomone JP, Dent LL, Harris OA, Ander DS, Lowery DW, Patel MM, Denson DD, Gordon AB, Wald MM, Gupta S, Hoffman SW, Stein DG (April 2007). "ProTECT: a randomized clinical trial of progesterone for acute traumatic brain injury". Ann Emerg Med 49 (4): 391–402, 402.e1–2. doi:10.1016/j.annemergmed.2006.07.932. PMID 17011666. Cite uses deprecated parameters (help)
^ Xiao G, Wei J, Yan W, Wang W, Lu Z (April 2008). "Improved outcomes from the administration of progesterone for patients with acute severe traumatic brain injury: a randomized controlled trial". Crit Care 12 (2): R61. doi:10.1186/cc6887. PMC 2447617. PMID 18447940. Cite uses deprecated parameters (help)
^ Pan DS, Liu WG, Yang XF, Cao F (October 2007). "Inhibitory effect of progesterone on inflammatory factors after experimental traumatic brain injury". Biomed. Environ. Sci. 20 (5): 432–8. PMID 18188998. Cite uses deprecated parameters (help)
^ ^a ^b Luoma JI, Stern CM, Mermelstein PG (August 2012). "Progesterone inhibition of neuronal calcium signaling underlies aspects of progesterone-mediated neuroprotection". J. Steroid Biochem. Mol. Biol. 131 (1-2): 30–6. doi:10.1016/j.jsbmb.2011.11.002. PMC 3303940. PMID 22101209. Cite uses deprecated parameters (help)
^ ^a ^b ^c Stein DG (March 2008). "Progesterone exerts neuroprotective effects after brain injury". Brain Res Rev 57 (2): 386–97. doi:10.1016/j.brainresrev.2007.06.012. PMC 2699575. PMID 17826842. Cite uses deprecated parameters (help)
^ Herson PS, Koerner IP, Hurn PD (May 2009). "Sex, sex steroids, and brain injury". Semin. Reprod. Med. 27 (3): 229–39. doi:10.1055/s-0029-1216276. PMC 2675922. PMID 19401954. Cite uses deprecated parameters (help)
^ Li Z, Wang B, Kan Z, Zhang B, Yang Z, Chen J, Wang D, Wei H, Zhang JN, Jiang R (January 2012). "Progesterone increases circulating endothelial progenitor cells and induces neural regeneration after traumatic brain injury in aged rats". J. Neurotrauma 29 (2): 343–53. doi:10.1089/neu.2011.1807. PMID 21534727. Cite uses deprecated parameters (help)
^ Cekic M, Sayeed I, Stein DG (July 2009). "Combination treatment with progesterone and vitamin D hormone may be more effective than monotherapy for nervous system injury and disease". Front Neuroendocrinol 30 (2): 158–72. doi:10.1016/j.yfrne.2009.04.002. PMC 3025702. PMID 19394357. Cite uses deprecated parameters (help)
^ Khaksari M, Soltani Z, Shahrokhi N, Moshtaghi G, Asadikaram G (January 2011). "The role of estrogen and progesterone, administered alone and in combination, in modulating cytokine concentration following traumatic brain injury". Can. J. Physiol. Pharmacol. 89 (1): 31–40. doi:10.1139/y10-103. PMID 21186375. Cite uses deprecated parameters (help)
^ "Efficacy and Safety Study of Intravenous Progesterone in Patients With Severe Traumatic Brain Injury (SyNAPSe)". ClinicalTrials.gov. U.S. National Institutes of Health. Retrieved 2012-07-14.
^ "SyNAPse: The Global phase 3 study of progesterone in severe traumatic brain injury". BHR Pharma, LLC.

Additional images[edit]

Steroidogenesis, showing progesterone among the progestogens in yellow area.

Pregnenolone

Deoxycorticosterone

External links[edit]

Progesterone at the US National Library of Medicine Medical Subject Headings (MeSH)
Kimball JW (2007-05-27). "Progesterone". Kimball's Biology Pages. Retrieved 2008-06-18.
"Progesterone Resource Center". PMS, Menopause, and Progesterone Resource Center. Oasis Advanced Wellness, Inc. Retrieved 2008-06-18.
General discussion document on Progesterone, its uses and applications

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 閉経期のホルモン療法で用いる製剤 preparations for menopausal hormone therapy
2. 避妊の概要 overview of contraception
3. 自然早産のリスクを低下させるためのプロゲステロン補充 progesterone supplementation to reduce the risk of spontaneous preterm birth
4. プロゲステロン受容体モジュレーター（PRM）の薬理学および作用機序 pharmacology and mechanism of action of progesterone receptor modulators prms
5. 緊急避妊剤 emergency contraception

English Journal

The anti-progestin RU-486 inhibits viability of MCF-7 breast cancer cells by suppressing WNT1.

Benad P, Rauner M, Rachner TD, Hofbauer LC.SourceDivision of Endocrinology, Diabetes, and Metabolic Bone Diseases, Department of Medicine III, Dresden Technical University Medical Center, Germany.
Cancer letters.Cancer Lett.2011 Dec 15;312(1):101-8. Epub 2011 Aug 11.
The Wnt signaling pathway is activated in over 50% of women with breast cancer and contributes to tumor progression. Here, we investigated the effects of RU-486 on Wnt signaling in breast cancer cell lines. RU-486 reduced viability of the progesterone receptor-positive MCF-7 and T-47D cells, but had
PMID 21899945

Effects of neuroactive steroids on cochlear hair cell death induced by gentamicin.

Nakamagoe M, Tabuchi K, Nishimura B, Hara A.SourceDepartment of Otolaryngology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan.
Steroids.Steroids.2011 Dec 11;76(13):1443-50. Epub 2011 Aug 12.
As neuroactive steroids, sex steroid hormones have non-reproductive effects. We previously reported that 17β-estradiol (βE2) had protective effects against gentamicin (GM) ototoxicity in the cochlea. In the present study, we examined whether the protective action of βE2 on GM ototoxicity is media
PMID 21856322

Japanese Journal

<Case Reports>A case of apocrine ad enocarcinoma in the right axilla

Yoshida Masuki,Kawara Shigeru,Kawada Akira
Acta Medica Kinki University 36(1), 29-31, 2011-6
… Immunohistochemically, the tumor cells were negative for both estrogen and progesterone receptors and positive for CEA and GCDFP-15. …
NAID 120003291654

Conventional IVF でのlong protocol におけるhCG 投与日の血中progesterone 値と妊娠成績について

中野貴史,北澤正文,林田綾子,星野恵子,渡辺博,深澤一雄,稲葉憲之
Dokkyo journal of medical sciences 38(1), 71-78, 2011-03-25
… protocol(L)下でのconventional IVF(cIVF)において,hCG 切り替え日の血中progesterone(P)値とcIVF における種々の因子及び妊娠成績との関係について検討した.不妊外来を受診した患者で,L 下でcIVF を施行された486 例,706 周期を対象とした.hCG 切り替え日の血中P 値と血中estradiol(E2)値,総hMG 投与量,採卵数,正常受精(2PN)発生数,2PN 発生率,良好胚(G1)胚数,G1 胚発生率,子宮内膜厚(EM),leaf pattern の有無,妊娠率等との関係について検討した.P …
NAID 110008429830

Related Pictures

★リンクテーブル★

リンク元	「副腎皮質ホルモン」「プロゲステロン」「切迫早産」「PR」「progestational」
拡張検索	「medroxyprogesterone 17-acetate」「estrogen-progesterone challenge test」「17α-hydroxyprogesterone derivative」「20α-hydroxyprogesterone」「norprogesterone」

「副腎皮質ホルモン」

Progesterone
Systematic (IUPAC) name
	Pregn-4-ene-3,20-dione
Clinical data
Trade names	Crinone, Endometrin
AHFS/Drugs.com	monograph
MedlinePlus	a604017
Pregnancy cat.	B (USA)
Legal status	?
Routes	oral, implant, transdermal
Pharmacokinetic data
Bioavailability	prolonged absorption, half-life approx 25-50 hours
Protein binding	96%-99%
Metabolism	hepatic to pregnanediols and pregnanolones
Half-life	34.8-55.13 hours
Excretion	renal
Identifiers
CAS number	57-83-0
ATC code	G03DA04
PubChem	CID 5994
IUPHAR ligand	2377
DrugBank	DB00396
ChemSpider	5773
UNII	4G7DS2Q64Y
KEGG	D00066
ChEBI	CHEBI:17026
ChEMBL	CHEMBL103
Synonyms	4-pregnene-3,20-dione
Chemical data
Formula	C21H30O2
Mol. mass	314.46
	SMILES O=C4\C=C2/[C@]([C@H]1CC[C@@]3([C@@H](C(=O)C)CC[C@H]3[C@@H]1CC2)C)(C)CC4;
	InChI InChI=1S/C21H30O2/c1-13(22)17-6-7-18-16-5-4-14-12-15(23)8-10-20(14,2)19(16)9-11-21(17,18)3/h12,16-19H,4-11H2,1-3H3/t16-,17+,18-,19-,20-,21+/m0/s1 ; Key:RJKFOVLPORLFTN-LEKSSAKUSA-N ;
Physical data
Melt. point	126 °C (259 °F)
Spec. rot	[α]D
(what is this?) (verify)

　　[★]

英: adrenocortical hormone
同: 副腎皮質ステロイド adrenocorticoids
関: 副腎皮質刺激ホルモン放出ホルモン、副腎皮質刺激ホルモン; ステロイド
関: 副腎、副腎皮質、ステロイド、コルチコステロイド、ステロイドホルモン、コルチコイド。副腎皮質ホルモン剤

図：SP.891(組織),892(構造式)
副腎皮質の球状層、索状層、網状層で合成される

種類(主要なもののみ)

電解質コルチコイド

球状層から分泌される。アルドステロン

糖質コルチコイド

索状層から分泌される。コルチゾール

副腎アンドロジェン

網状層から分泌される。アンドロステンジオン

コレステロール cholesterol
↓CYP11A1
プレグネノロン pregnenolone	－－→ CYP17 17α-hydroxylase	17α-ヒドロキシプレグネノロン 17α-hydroxypregnenolone	－－→ CYP17 17α-hydroxylase	デヒドロエピアンドロステロン dehydroepiandrosterone DHEA
↓3β-HSD 3β-hydroxysteroid dehydrogenase		↓3β-HSD		↓3β-HSD
プロゲステロン progesterone	－－→ CYP17 17α-hydroxylase	17α-ヒドロキシプロゲステロン 17α-hydroxyprogesterone	－－→ CYP17 17α-hydroxylase	アンドロステンジオン androstenedione Δ⁴androstene-3,17-dion
↓CYP21 21-hydroxylase		↓CYP21 21-hydroxylase
デオキシコルチコステロン deoxycorticosterone		11-デオキシコルチゾール 11-deoxycortisol
↓CYP11B2　11β-hydroxylase		↓CYP11B1　11β-hydroxylase
コルチコステロン corticosterone		コルチゾール cortisol
↓CYP11B2 18-hydroxylase
18-ヒドロキシコルチコステロン 18-hydroxycorticosterone
↓CYP11B2 18-hydroxydehydrogenase
アルドステロン aldosterone

球状増 zona glomerulosa		索状層 zona fasciculata		網状層 zona reticularis

臨床関連

21-hydroxylaseが正常に機能しないことにより生じる (L.320)

薬理学

副腎皮質ホルモン製剤

副腎皮質から分泌されるホルモン (SP.895)

名称		血漿濃度 (ng/ml)	1日分泌量 (mg/day)
糖質コルチコイド	コルチゾール	40～180	15～20
糖質コルチコイド	コルチコステロン	2～6	2～5
鉱質コルチコイド	アルドステロン	0.05～0.20	0.05～0.15
鉱質コルチコイド	11-DOC	0.05～0.30	0.10～0.20
副腎アンドロジェン	DHEA	2～8	7～15
	DHEA-S	1～4
	アンドロステンジオン	1～2	2～3

「プロゲステロン」

　　[★]

英: progesterone (Z), P4
同: 黄体ホルモン corpus luteum hormone、プロジェステロン
商: プロゲホルモンルテウムプロゲストン, Crinone, Prochieve, Progestasert
関: エストロゲン、月経周期、ホルモン

分類

卵巣ホルモン

性状

ステロイド

産生組織

G10M.37

月経黄体
妊娠黄体(妊娠0-10週)
胎盤(妊娠10週以降)

標的組織

生理作用

	エストロゲン	プロゲステロン
子宮内膜	増殖期：増殖分泌期：プロゲステロンと協調して分泌期維持	分泌期：分泌期誘導
卵巣	卵胞の成長顆粒細胞に作用してエストロゲン受容体発現↑ →エストロゲンの正のフィードバック →エストロゲンの大量分泌
子宮筋	オキシトシンに対する感受性↓ 肥大増殖	オキシトシンに対する感受性↑
中枢神経への作用	視床下部、下垂体　少量→負のフィードバック　多量→正のフィードバック	視床下部体温中枢　刺激
その他	・子宮頚管粘液　量：↑、牽引性：↑、羊歯葉状結晶：↑ ・膣スメアの変化　成熟した表層細胞の出現　　角化、核濃縮、好酸性	・乳腺　腺房発育

子宮内膜：プロスタグランジンの合成を制御(増殖期には低値、月経期には高値)　→　月経前症候群・月経困難症との関連
妊娠中には下垂体前葉に作用してLHの分泌を抑制し、排卵を抑制する。(G10M.37)
乳腺組織のPRL受容体を減少させ、乳汁分泌を抑制する。(G10M.37)

作用機序

分泌調節

性周期・月経・妊娠との関連

非妊時

卵胞期：低値
排卵期～黄体期：高値
黄体期後期：漸減

妊娠時

妊娠時には0-10週にかけてなだらかに上昇してから下降するが、以降漸増する。(NGY.47)
妊娠時には10週までなだらかに増加し、以降増加。(G10M.37)

LAB.724

		エストロゲン			プロゲステロン
		エストロン	エストラジオール	エストリオール
		(pg/ml)	(pg/ml)	(pg/ml)	(ng/ml)
女性	卵胞期	10～60	10～150	0～20	0.5～1.5
	排卵期	25～100	50～380	5～40	1.5～6.8
	黄体期	25～80	30～300	5～40	5.0～28.0
	更年期	20～80	10～50	0～20	0.3～0.4
男性		30～60	10～60	0～15	0.2～0.4

「切迫早産」

　　[★]

英: threatened premature delivery
関: 早産、trimester

概念

早産(妊娠22-37週)に至る状態
原因は不明だが細菌感染症状によることが多い

症状

不規則で弱い子宮収縮。細菌感染症による発熱

診断

1. 症状から
2. tocolysis index
3. 頚管の状態と子宮収縮から

治療

安静
薬物療法：

β受容体刺激薬(リトドリン ritodrine,イソクスプリン isoxsuprine)　：子宮収縮の抑制
Mg剤、
progesterone　胎児肺成熟促進

絨毛膜羊膜炎の所見があるときは抗生物質の投与
頚管縫縮術：絨毛膜羊膜炎があるときはその治療後

参考

1. 切迫早産 - 日産婦誌５９巻１１号

http://www.jsog.or.jp/PDF/59/5911-664.pdf

「PR」

　　[★]

「progestational」

　　[★]

adj.

プロゲステロンの

関: progesterone

「medroxyprogesterone 17-acetate」

　　[★] メドロキシプロゲステロン。酢酸メドロキシプロゲステロン

「estrogen-progesterone challenge test」

　　[★] エストロゲン・プロゲステロン負荷試験

「17α-hydroxyprogesterone derivative」

　　[★] 17α-ヒドロキシプロゲステロン誘導体

「20α-hydroxyprogesterone」

　　[★] 20α-ヒドロキシプロゲステロン

「norprogesterone」

　　[★]

ノルプロゲステロン

[1] "Metabocard for Hydroxyprogesterone". Human Metabolome Database. Retrieved 31 July 2013.

[pmid17747122-2] Allen WM (1935). "The isolation of crystalline progestin". Science 82 (2118): 89–93. doi:10.1126/science.082.2118.89. PMID 17747122.

[Butenandt_1934-3] Butenandt A, Westphal U (1934). "Zur Isolierung und Charakterisierung des Corpusluteum-Hormons". Berichte Deu0tsche chemische Gesellschaft 67 (8): 1440–1442. doi:10.1002/cber.19340670831.

[Hartmann_1934-4] Hartmann M, Wettstein A (1934). "Ein krystallisiertes Hormon aus Corpus luteum". Helvetica Chimica Acta 17: 878–882. doi:10.1002/hlca.193401701111.

[Slotta_1934-5] Slotta KH, Ruschig H, Fels E (1934). "Reindarstellung der Hormone aus dem Corpusluteum". Berichte Deutsche chemische Gesellschaft 67 (7): 1270–1273. doi:10.1002/cber.19340670729.

[pmid4922128-6] Allen WM (1970). "Progesterone: how did the name originate?". South. Med. J. 63 (10): 1151–5. doi:10.1097/00007611-197010000-00012. PMID 4922128.

[titleResult_Content_View-7] Goodson III WH, Handagama P, Moore II DH, Dairkee S (2007-12-13). "Milk products are a source of dietary progesterone". 30th Annual San Antonio Breast Cancer Symposium. pp. abstract # 2028. Retrieved 2008-03-12.

[pmid20108949-8] Pauli GF, Friesen JB, Gödecke T, Farnsworth NR, Glodny B (January 2010). "Occurrence of Progesterone and Related Animal Steroids in Two Higher Plants". J Nat Prod 73 (3): 338–45. doi:10.1021/np9007415. PMID 20108949. Cite uses deprecated parameters (help)

[pmid12255132-9] Applezweig N (May 1969). "Steroids". Chem Week 104: 57–72. PMID 12255132. Cite uses deprecated parameters (help)

[pmid16946542-10] Noguchi E, Fujiwara Y, Matsushita S, Ikeda T, Ono M, Nohara T (September 2006). "Metabolism of tomato steroidal glycosides in humans". Chem. Pharm. Bull. 54 (9): 1312–4. doi:10.1248/cpb.54.1312. PMID 16946542. Cite uses deprecated parameters (help)

[pmid14558759-11] Yang DJ, Lu TJ, Hwang LS (October 2003). "Isolation and identification of steroidal saponins in Taiwanese yam cultivar (Dioscorea pseudojaponica Yamamoto)". J. Agric. Food Chem. 51 (22): 6438–44. doi:10.1021/jf030390j. PMID 14558759. Cite uses deprecated parameters (help)

[pmid15513824-12] Hooker E (2004). "Final report of the amended safety assessment of Dioscorea Villosa (Wild Yam) root extract". Int. J. Toxicol. 23 Suppl 2: 49–54. doi:10.1080/10915810490499055. PMID 15513824.

[13] Niño J, Jiménez DA, Mosquera OM, Correa YM (2007). "Diosgenin quantification by HPLC in a Dioscorea polygonoides tuber collection from colombian flora". Journal of the Brazilian Chemical Society 18 (5): 1073–1076. doi:10.1590/S0103-50532007000500030.

[14] Myoda T, Nagai T, Nagashima T (2005). "Properties of starches in yam (Dioscorea spp.) tuber". Current Topics in Food Science and Technology. pp. 105–114. ISBN 81-308-0003-9

[isbn0-471-49641-3-15] Dewick, Paul M. (2002). Medicinal natural products: a biosynthetic approach. New York: Wiley. p. 244. ISBN 0-471-49641-3.

[pmid9487528-16] Duport C, Spagnoli R, Degryse E, Pompon D (February 1998). "Self-sufficient biosynthesis of pregnenolone and progesterone in engineered yeast". Nat. Biotechnol. 16 (2): 186–9. doi:10.1038/nbt0298-186. PMID 9487528. Cite uses deprecated parameters (help)

[Marker_1940-17] Marker RE, Krueger J (1940). "Sterols. CXII. Sapogenins. XLI. The Preparation of Trillin and its Conversion to Progesterone". J. Am. Chem. Soc. 62 (12): 3349–3350. doi:10.1021/ja01869a023.

[pmid3815593-18] Numazawa M, Nagaoka M, Kunitama Y (September 1986). "Regiospecific deoxygenation of the dihydroxyacetone moiety at C-17 of corticoid steroids with iodotrimethylsilane". Chem. Pharm. Bull. 34 (9): 3722–6. doi:10.1248/cpb.34.3722. PMID 3815593. Cite uses deprecated parameters (help)

[pmid5131151-19] Johnson WS, Gravestock MB, McCarry BE (August 1971). "Acetylenic bond participation in biogenetic-like olefinic cyclizations. II. Synthesis of dl-progesterone". J. Am. Chem. Soc. 93 (17): 4332–4. doi:10.1021/ja00746a062. PMID 5131151. Cite uses deprecated parameters (help)

[titleHistorical_Reference_Ranges-20] NIH Clinical Center (2004-08-16). "Progesterone Historical Reference Ranges". United States National Institutes of Health. Retrieved 2008-03-12.

[nih2009-21] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ Progesterone Reference Ranges, Performed at the Clinical Center at the National Institutes of Health, Bethesda MD, 03Feb09

[mass-22] ^ ^a ^b ^c ^d ^e ^f ^g ^h Converted from mass values using molar mass of 314.46 g/mol

[23] Reference ranges for estradiol, progesterone, luteinizing hormone and follicle-stimulating hormone during the menstrual cycle. Wikiversity, peer reviewed 2013.

[pmid9506743-24] Luconi M, Bonaccorsi L, Maggi M, Pecchioli P, Krausz C, Forti G, Baldi E (1998). "Identification and characterization of functional nongenomic progesterone receptors on human sperm membrane". J. Clin. Endocrinol. Metab. 83 (3): 877–85. doi:10.1210/jc.83.3.877. PMID 9506743.

[pmid15684349-25] Jang S, Yi LS (2005). "Identification of a 71 kDa protein as a putative non-genomic membrane progesterone receptor in boar spermatozoa". J. Endocrinol. 184 (2): 417–25. doi:10.1677/joe.1.05607. PMID 15684349.

[pmid8282004-26] Rupprecht R, Reul JM, van Steensel B, Spengler D, Söder M, Berning B, Holsboer F, Damm K (1993). "Pharmacological and functional characterization of human mineralocorticoid and glucocorticoid receptor ligands". Eur J Pharmacol 247 (2): 145–54. doi:10.1016/0922-4106(93)90072-H. PMID 8282004.

[pmid2328727-27] Kastner P, Krust A, Turcotte B, Stropp U, Tora L, Gronemeyer H, Chambon P (1990). "Two distinct estrogen-regulated promoters generate transcripts encoding the two functionally different human progesterone receptor forms A and B". EMBO J. 9 (5): 1603–14. PMC 551856. PMID 2328727.

[pmid13263410-28] Landau RL, Bergenstal DM, Lugibihl K, Kascht ME. (1955). "The metabolic effects of progesterone in man". J Clin Endocrinol Metab 15 (10): 1194–215. doi:10.1210/jcem-15-10-1194. PMID 13263410.

[ReferenceA-29] 1=Exp Clin Psychopharmacol. 2010 December; 18(6): 451–461

[30] 2=Hum Psychopharmacol. 2009 Oct;24(7):559-64. doi: 10.1002/hup.1055.

[31] 3=Arch Gen Psychiatry. 2012;69(4):418427.doi:10.1001/archgenpsychiatry.2011.1465.

[32] 4=Neuropsychopharmacology. 2011 Oct;36(11):2187-99. doi: 10.1038/npp.2011.130. Epub 2011 Jul 27

[pmid17447210-33] Correia JN, Conner SJ, Kirkman-Brown JC (May 2007). "Non-genomic steroid actions in human spermatozoa. "Persistent tickling from a laden environment"". Semin. Reprod. Med. 25 (3): 208–19. doi:10.1055/s-2007-973433. PMID 17447210. Cite uses deprecated parameters (help)

[pmid10837122-34] Kirkman-Brown JC, Bray C, Stewart PM, Barratt CL, Publicover SJ (June 2000). "Biphasic elevation of [Ca(2+)](i) in individual human spermatozoa exposed to progesterone". Developmental Biology 222 (2): 326–35. doi:10.1006/dbio.2000.9729. ISSN 0012-1606. PMID 10837122. Cite uses deprecated parameters (help)

[pmid14606954-35] Kirkman-Brown JC, Barratt CL, Publicover SJ (March 2004). "Slow calcium oscillations in human spermatozoa". The Biochemical Journal 378 (Pt 3): 827–32. doi:10.1042/BJ20031368. PMC 1223996. PMID 14606954. Cite uses deprecated parameters (help)

[pmid15322137-36] Harper CV, Barratt CL, Publicover SJ (October 2004). "Stimulation of human spermatozoa with progesterone gradients to simulate approach to the oocyte. Induction of [Ca(2+)](i) oscillations and cyclical transitions in flagellar beating". The Journal of Biological Chemistry 279 (44): 46315–25. doi:10.1074/jbc.M401194200. PMID 15322137. Cite uses deprecated parameters (help)

[pmid11335951-37] Tosti E, Di Cosmo A, Cuomo A, Di Cristo C, Gragnaniello G (May 2001). "Progesterone induces activation in Octopus vulgaris spermatozoa". Mol. Reprod. Dev. 59 (1): 97–105. doi:10.1002/mrd.1011. PMID 11335951. Cite uses deprecated parameters (help)

[pmid21412338-38] Strünker T, Goodwin N, Brenker C, Kashikar ND, Weyand I, Seifert R, Kaupp UB (March 2011). "The CatSper channel mediates progesterone-induced Ca2+ influx in human sperm". Nature 471 (7338): 382–6. doi:10.1038/nature09769. PMID 21412338. Lay summary – Nature News. Cite uses deprecated parameters (help)

[pmid21412339-39] Lishko PV, Botchkina IL, Kirichok Y (March 2011). "Progesterone activates the principal Ca2+ channel of human sperm". Nature 471 (7338): 387–91. doi:10.1038/nature09767. PMID 21412339. Cite uses deprecated parameters (help)

[colostate-40] Bowen R (2000-08-06). "Placental Hormones". Retrieved 2008-03-12.

[pmid15135772-41] Schumacher M, Guennoun R, Robert F, et al. (2004). "Local synthesis and dual actions of progesterone in the nervous system: neuroprotection and myelination". Growth Horm. IGF Res. 14 Suppl A: S18–33. doi:10.1016/j.ghir.2004.03.007. PMID 15135772.

[GeorgiaPhysiology-42] Physiology at MCG 5/5ch9/s5ch9_13

[pmid3184927-43] Hould FS, Fried GM, Fazekas AG, Tremblay S, Mersereau WA (1988). "Progesterone receptors regulate gallbladder motility". J. Surg. Res. 45 (6): 505–12. doi:10.1016/0022-4804(88)90137-0. PMID 3184927.

[44] "Hormones and Oral Health". WebMD.

[45] Picard F, Wanatabe M, Schoonjans K, Lydon J, O'Malley BW, Auwerx J (2002). "Progesterone receptor knockout mice have an improved glucose homeostasis secondary to beta -cell proliferation". Proceedings of the National Academy of Sciences 99 (24): 15644–15648. doi:10.1073/pnas.202612199. PMC 137770. PMID 12438645. edit

[46] Brănişteanu DD, Mathieu C (March 2003). "Progesterone in gestational diabetes mellitus: guilty or not guilty?". Trends Endocrinol. Metab. 14 (2): 54–6. doi:10.1016/S1043-2760(03)00003-1. PMID 12591170. Cite uses deprecated parameters (help) edit

[pmid19434889-47] Schindler AE, Campagnoli C, Druckmann R, Huber J, Pasqualini JR, Schweppe KW, Thijssen JH (2008). "Classification and pharmacology of progestins". Maturitas 61 (1–2): 171–80. doi:10.1016/j.maturitas.2003.09.014. PMID 19434889.

[48] "Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations: 020701". Food and Drug Administration. 2010-07-02. Retrieved 2010-07-07.

[49] "Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations: 019781". Food and Drug Administration. 2010-07-02. Retrieved 2010-07-07.

[50] "Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations: 075906". Food and Drug Administration. 2010-07-02. Retrieved 2010-07-07.

[51] "Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations: 022057". Food and Drug Administration. 2010-07-02. Retrieved 2010-07-07.

[52] Schindler AE, Campagnoli C, Druckmann R, Huber J, Pasqualini JR, Schweppe KW, Thijssen JH (2003). "Classification and pharmacology of progestins". Maturitas. 46 Suppl 1: S7–S16. PMID 14670641. edit

[Lark1999-53] Lark, Susan (1999). Making the Estrogen Decision. McGraw-Hill Professional. p. 22. ISBN 0-87983-696-2, 9780879836962 Check |isbn= value (help).

[pmid9492350-54] Zava DT, Dollbaum CM, Blen M (1998). "Estrogen and progestin bioactivity of foods, herbs, and spices". Proc. Soc. Exp. Biol. Med. 217 (3): 369–78. PMID 9492350.

[pmid11428178-55] Komesaroff PA, Black CV, Cable V, Sudhir K (2001). "Effects of wild yam extract on menopausal symptoms, lipids and sex hormones in healthy menopausal women". Climacteric 4 (2): 144–50. doi:10.1080/713605087. PMID 11428178.

[pmid12592250-56] Fonseca EB, Bittar RE, Carvalho MH, Zugaib M (2003). "Prophylactic administration of progesterone by vaginal suppository to reduce the incidence of spontaneous preterm birth in women at increased risk: a randomized placebo-controlled double-blind study". Am. J. Obstet. Gynecol. 188 (2): 419–24. doi:10.1067/mob.2003.41. PMID 12592250.

[57] Harris, Gardiner (2011-05-02). "Hormone Is Said to Cut Risk of Premature Birth". New York Times. Retrieved 5 May 2011.

[pmid17899572-58] O'Brien JM, Adair CD, Lewis DF, Hall DR, Defranco EA, Fusey S, Soma-Pillay P, Porter K, How H, Schackis R, Eller D, Trivedi Y, Vanburen G, Khandelwal M, Trofatter K, Vidyadhari D, Vijayaraghavan J, Weeks J, Dattel B, Newton E, Chazotte C, Valenzuela G, Calda P, Bsharat M, Creasy GW (2007). "Progesterone vaginal gel for the reduction of recurrent preterm birth: primary results from a randomized, double-blind, placebo-controlled trial". Ultrasound Obstet Gynecol 30 (5): 687–96. doi:10.1002/uog.5158. PMID 17899572.

[pmid17899571-59] DeFranco EA, O'Brien JM, Adair CD, Lewis DF, Hall DR, Fusey S, Soma-Pillay P, Porter K, How H, Schakis R, Eller D, Trivedi Y, Vanburen G, Khandelwal M, Trofatter K, Vidyadhari D, Vijayaraghavan J, Weeks J, Dattel B, Newton E, Chazotte C, Valenzuela G, Calda P, Bsharat M, Creasy GW (2007). "Vaginal progesterone is associated with a decrease in risk for early preterm birth and improved neonatal outcome in women with a short cervix: a secondary analysis from a randomized, double-blind, placebo-controlled trial". Ultrasound Obstet Gynecol 30 (5): 697–705. doi:10.1002/uog.5159. PMID 17899571.

[pmid17671254-60] Fonseca EB, Celik E, Parra M, Singh M, Nicolaides KH (2007). "Progesterone and the risk of preterm birth among women with a short cervix". N. Engl. J. Med. 357 (5): 462–9. doi:10.1056/NEJMoa067815. PMID 17671254.

[pmid17899585-61] Romero R (2007). "Prevention of spontaneous preterm birth: the role of sonographic cervical length in identifying patients who may benefit from progesterone treatment". Ultrasound Obstet Gynecol 30 (5): 675–86. doi:10.1002/uog.5174. PMID 17899585.

[pmid21472815-62] Hassan SS, Romero R, Vidyadhari D, Fusey S, Baxter JK, Khandelwal M, Vijayaraghavan J, Trivedi Y, Soma-Pillay P, Sambarey P, Dayal A, Potapov V, O'Brien J, Astakhov V, Yuzko O, Kinzler W, Dattel B, Sehdev H, Mazheika L, Manchulenko D, Gervasi MT, Sullivan L, Conde-Agudelo A, Phillips JA, Creasy GW (July 2011). "Vaginal progesterone reduces the rate of preterm birth in women with a sonographic short cervix: a multicenter, randomized, double-blind, placebo-controlled trial". Ultrasound Obstet Gynecol 38 (1): 18–31. doi:10.1002/uog.9017. PMID 21472815. Lay summary – WebMD. Cite uses deprecated parameters (help)

[urlProgesterone_helps_cut_risk_of_pre-term_birth_-_Health_-_Womens_health_-_msnbc.com-63] "Progesterone helps cut risk of pre-term birth". Women's health. msnbc.com. 2011-12-14. Retrieved 2011-12-14.

[medicinalchem-64] Sriram, D (2007). Medicinal Chemistry. New Delhi: Dorling Kindersley India Pvt. Ltd. p. 432. ISBN 81-317-0031-3. |accessdate= requires |url= (help)

[pmid12601162-65] Schneider JS, Stone MK, Wynne-Edwards KE, Horton TH, Lydon J, O'Malley B, Levine JE (2003). "Progesterone receptors mediate male aggression toward infants". Proc. Natl. Acad. Sci. U.S.A. 100 (5): 2951–6. doi:10.1073/pnas.0130100100. PMC 151447. PMID 12601162.

[66] "Standards of Care for the Health of Transsexual, Transgender, and Gender-Nonconforming People, Version 7," International Journal of Transgenderism 13: 165-232.

[pmid22088981-67] Espinoza TR, Wright DW (2011). "The role of progesterone in traumatic brain injury". J Head Trauma Rehabil 26 (6): 497–9. doi:10.1097/HTR.0b013e31823088fa. PMID 22088981.

[pmid21497181-68] Stein DG (September 2011). "Progesterone in the treatment of acute traumatic brain injury: a clinical perspective and update". Neuroscience 191: 101–6. doi:10.1016/j.neuroscience.2011.04.013. PMID 21497181. Cite uses deprecated parameters (help)

[pmid10833057-69] Roof RL, Hall ED (May 2000). "Gender differences in acute CNS trauma and stroke: neuroprotective effects of estrogen and progesterone". J. Neurotrauma 17 (5): 367–88. doi:10.1089/neu.2000.17.367. PMID 10833057. Cite uses deprecated parameters (help)

[pmid17715141-70] Gibson CL, Gray LJ, Bath PM, Murphy SP (February 2008). "Progesterone for the treatment of experimental brain injury; a systematic review". Brain 131 (Pt 2): 318–28. doi:10.1093/brain/awm183. PMID 17715141. Cite uses deprecated parameters (help)

[pmid17011666-71] Wright DW, Kellermann AL, Hertzberg VS, Clark PL, Frankel M, Goldstein FC, Salomone JP, Dent LL, Harris OA, Ander DS, Lowery DW, Patel MM, Denson DD, Gordon AB, Wald MM, Gupta S, Hoffman SW, Stein DG (April 2007). "ProTECT: a randomized clinical trial of progesterone for acute traumatic brain injury". Ann Emerg Med 49 (4): 391–402, 402.e1–2. doi:10.1016/j.annemergmed.2006.07.932. PMID 17011666. Cite uses deprecated parameters (help)

[pmid18447940-72] Xiao G, Wei J, Yan W, Wang W, Lu Z (April 2008). "Improved outcomes from the administration of progesterone for patients with acute severe traumatic brain injury: a randomized controlled trial". Crit Care 12 (2): R61. doi:10.1186/cc6887. PMC 2447617. PMID 18447940. Cite uses deprecated parameters (help)

[pmid18188998-73] Pan DS, Liu WG, Yang XF, Cao F (October 2007). "Inhibitory effect of progesterone on inflammatory factors after experimental traumatic brain injury". Biomed. Environ. Sci. 20 (5): 432–8. PMID 18188998. Cite uses deprecated parameters (help)

[pmid22101209-74] Luoma JI, Stern CM, Mermelstein PG (August 2012). "Progesterone inhibition of neuronal calcium signaling underlies aspects of progesterone-mediated neuroprotection". J. Steroid Biochem. Mol. Biol. 131 (1-2): 30–6. doi:10.1016/j.jsbmb.2011.11.002. PMC 3303940. PMID 22101209. Cite uses deprecated parameters (help)

[pmcid2699575-75] Stein DG (March 2008). "Progesterone exerts neuroprotective effects after brain injury". Brain Res Rev 57 (2): 386–97. doi:10.1016/j.brainresrev.2007.06.012. PMC 2699575. PMID 17826842. Cite uses deprecated parameters (help)

[pmid19401954-76] Herson PS, Koerner IP, Hurn PD (May 2009). "Sex, sex steroids, and brain injury". Semin. Reprod. Med. 27 (3): 229–39. doi:10.1055/s-0029-1216276. PMC 2675922. PMID 19401954. Cite uses deprecated parameters (help)

[pmid21534727-77] Li Z, Wang B, Kan Z, Zhang B, Yang Z, Chen J, Wang D, Wei H, Zhang JN, Jiang R (January 2012). "Progesterone increases circulating endothelial progenitor cells and induces neural regeneration after traumatic brain injury in aged rats". J. Neurotrauma 29 (2): 343–53. doi:10.1089/neu.2011.1807. PMID 21534727. Cite uses deprecated parameters (help)

[pmid19394357-78] Cekic M, Sayeed I, Stein DG (July 2009). "Combination treatment with progesterone and vitamin D hormone may be more effective than monotherapy for nervous system injury and disease". Front Neuroendocrinol 30 (2): 158–72. doi:10.1016/j.yfrne.2009.04.002. PMC 3025702. PMID 19394357. Cite uses deprecated parameters (help)

[pmid21186375-79] Khaksari M, Soltani Z, Shahrokhi N, Moshtaghi G, Asadikaram G (January 2011). "The role of estrogen and progesterone, administered alone and in combination, in modulating cytokine concentration following traumatic brain injury". Can. J. Physiol. Pharmacol. 89 (1): 31–40. doi:10.1139/y10-103. PMID 21186375. Cite uses deprecated parameters (help)

[ClinicalTrials.gov__SyNAPSe-80] "Efficacy and Safety Study of Intravenous Progesterone in Patients With Severe Traumatic Brain Injury (SyNAPSe)". ClinicalTrials.gov. U.S. National Institutes of Health. Retrieved 2012-07-14.

[81] "SyNAPse: The Global phase 3 study of progesterone in severe traumatic brain injury". BHR Pharma, LLC.

匿名

検索

案内

progesterone