Progesterone was first introduced for medical use in 1934 and the first progestin, ethisterone, was introduced for medical use in 1939.[6][7][8] More potent progestins, such as norethisterone, were developed and started to be used in birth control in the 1950s.[6] Around 60 progestins have been marketed for clinical use in humans or use in veterinary medicine.[9][10][11][12][13] These progestins can be grouped into different classes and generations.[1][14][15] Progestogens are available widely throughout the world and are used in all forms of hormonal birth control and in most menopausal hormone therapy regimens.[1][9][10][12][11]
Medical uses
Available forms
Progestogens marketed for clinical or veterinary use
Progestogens are used as a component of hormone therapy for transgender women and transgender men. They are used in transgender women in combination with estrogens to help suppress and block testosterone. Progestogens might also have other beneficial effects in transgender women, but these are controversial and unsupported at present. Examples of progestogens used in hormone therapy for transgender women include cyproterone acetate, medroxyprogesterone acetate, and progesterone. Progestogens, such as medroxyprogesterone and lynestrenol, are used in transgender men to help suppress menses. Progestogens have also been used to delay puberty in transgender boys and girls.
The progestogen challenge test or progestogen withdrawal test is used to diagnose amenorrhea. Due to the availability of assays to measure estrogen levels, it is now rarely used.
Certain progestins can be used at very high doses to increase appetite in conditions like cachexia, anorexia, and wasting syndromes. In general, they are used in combination with certain other steroid medications such as dexamethasone. Their effects take several weeks to become apparent, but are relatively long-lived when compared to those of corticosteroids. Furthermore, they are recognized as being the only medications to increase lean body mass. Megestrol acetate is the lead drug of this class for the management of cachexia, and medroxyprogesterone acetate is also used.[43][44] The mechanism of action of the appetite-related effects of these two medications is unknown and may not be related to their progestogenic activity. Very high doses of other progestogens, like cyproterone acetate, have minimal or no influence on appetite and weight.
The available evidence on the risk of mood changes and depression with progestogens in hormonal birth control is limited.[48][49] As of 2019, there is no consistent evidence for adverse effects on mood of hormonal birth control, including progestogen-only birth control and combined birth control, in the general population.[50][51] Most women taking combined birth control experience no influence or a beneficial effect on mood.[48][51][49] Adverse effects on mood appear to be infrequent, occurring only in a small percentage of women.[48][51][49] About 5 to 10% of women experience negative mood changes with combined birth control pills, and about 5% of women discontinue birth control pills due to such changes.[52][48] A study of about 4,000 women found that progestogen-only birth control with depotmedroxyprogesterone acetate had an incidence of depression of 1.5% and discontinuation due to depression of 0.5%.[51][53][54] Beneficial effects of hormonal birth control such as decreased menstrual pain and bleeding may positively influence mood.[48]
Mood with birth control pills may be better with monophasic and continuous formulations than with triphasic and cyclic formulations.[48][52] Limited and inconsistent evidence supports differences in mood with hormonal birth control using different doses of ethinylestradiol or different routes of administration, such as birth control pills versus contraceptive vaginal rings and contraceptive patches.[48][52] Combined birth control with less androgenic or antiandrogenic progestins like desogestrel, gestodene, and drospirenone may have a more favorable influence on mood than birth control with more androgenic progestins like levonorgestrel.[48][52] However, androgen supplementation with hormonal birth control has also been reported to improve mood.[48]
Hormonal birth control that suppresses ovulation is effective in the treatment of premenstrual dysphoric disorder (PMDD).[50][56] Combined birth control pills containing drospirenone are approved for the treatment of PMDD and may be particularly beneficial due to the antimineralocorticoid activity of drospirenone.[50][57][58] Studies on the influence of hormonal birth control on mood in women with existing mood disorders or polycystic ovary syndrome are limited and mixed.[50][48] Women with underlying mood disorders may be more likely to experience mood changes with hormonal birth control.[48][50][59] A 2016 systematic review found based on limited evidence from 6 studies that hormonal birth control, including combined birth control pills, depot medroxyprogesterone acetate, and levonorgestrel-containing intrauterine devices, was not associated with worse outcomes compared to non-use in women with depressive or bipolar disorders.[60] A 2008 Cochrane review found a greater likelihood of postpartum depression in women given norethisterone enanthate as a form of progestogen-only injectable birth control, and recommended caution on the use of progestogen-only birth control in the postpartum period.[61]
Estrogen therapy appears to have a beneficial influence on mood in depressed and euthymicperimenopausal women.[62][63][64] Conversely, research on combined estrogen and progestogen therapy for depressive symptoms in menopausal women is scarce and inconclusive.[62][63] Some researchers contend that progestogens have an adverse influence on mood and reduce the benefits of estrogens on mood,[65][66][2] whereas other researchers maintain that progestogens have no adverse influence on mood.[67][68] Progesterone differs from progestins in terms of effects in the brain and might have different effects on mood in comparison.[2][69][1] The available evidence, although limited, suggests no adverse influence of progesterone on mood when used in menopausal hormone therapy.[70]
Sexual function
In most women, sexual desire is unchanged or increased with combined birth control pills.[71] This is despite an increase in sex hormone-binding globulin (SHBG) levels and a decrease in total and free testosterone levels.[71][72] However, findings are conflicting, and more research is needed.[73]
Progestogens when used by themselves at typical clinical dosages, for instance in progestogen-only birth control, do not affect coagulation[81][82][83][84][75][77] and are not generally associated with a higher risk of venous thromboembolism (VTE).[85][86][87][88] An exception is medroxyprogesterone acetate as a progestogen-only injectable contraceptive, which has been associated with a 2- to 4-fold increase in risk of VTE relative to other progestogens and non-use.[89][90][91][92][93][94][88] The reasons for this are unknown, but the observations might be a statistical artifact of preferential prescription of depot medroxyprogesterone acetate to women at risk for VTE.[90] Alternatively, medroxyprogesterone acetate may be an exception among progestogens in terms of influence on VTE risk,[88][92][81][94] possibly due to its partialglucocorticoid activity.[1][6][81] In contrast to depot medroxyprogesterone acetate, no increase in VTE risk has been observed with moderately high doses of the related progestin chlormadinone acetate (10 mg/day for 18–20 days/cycle), though based on limited data.[94][95]
Very-high-dose progestogen therapy, including with medroxyprogesterone acetate, megestrol acetate, and cyproterone acetate, has been associated with activation of coagulation and a dose-dependent increased risk of VTE.[82][87][96][97][98][99] In studies with high-dose cyproterone acetate specifically, the increase in VTE risk has ranged from 3- to 5-fold.[96][98][99] The incidence of VTE in studies with very-high-dose progestogen therapy has been found to range from 2 to 8%.[82][100][101] However, the relevant patient populations, namely aged individuals with cancer, are already predisposed to VTE, and this greatly amplifies the risk.[82][87][102]
Estrogen plus progestogen therapy
In contrast to progestogen-only birth control, the addition of progestins to oralestrogen therapy, including in combined birth control pills and menopausal hormone therapy, is associated with a higher risk of VTE than with oral estrogen therapy alone.[103][104][105][106][107] The risk of VTE is increased by about 2-fold or less with such regimens in menopausal hormone therapy and by 2- to 4-fold with combined birth control pills containing ethinylestradiol, both relative to non-use.[103][76][106][107] In contrast to oral estrogen therapy, parenteral estradiol, such as with transdermalestradiol, is not associated with a higher risk of VTE.[103][92][106] This is likely due to its lack of first-pass effect in the liver.[1][89] Research is mixed on whether addition of progestins to transdermal estradiol is associated with a greater risk of VTE, with some studies finding no increase in risk and others finding higher risk.[103][92][106] Unlike the case of transdermal estradiol, VTE risk is not lower with ethinylestradiol-containing contraceptive vaginal rings and contraceptive patches compared to combined birth control pills with ethinylestradiol.[76][108][81] This is thought to be due to the resistance of ethinylestradiol to hepaticmetabolism.[1][109][89][81]
The type of progestogen in combined menopausal hormone therapy may also modulate VTE risk.[118][119] Oral estrogens plus dydrogesterone appears to have lower VTE risk relative to inclusion of other progestins.[120][121][106]Norpregnane derivatives such as nomegestrol acetate and promegestone have been associated with a significantly greater risk of VTE than pregnane derivatives such as medroxyprogesterone acetate and dydrogesterone and nortestosterone derivatives such as norethisterone and levonorgestrel.[118][119] However, these findings may just be statistical artifacts.[119] In contrast to progestins, the addition of oral progesterone to either oral or transdermal estrogen therapy is not associated with a higher risk of VTE.[92][122] However, oral progesterone achieves very low progesterone levels and has relatively weak progestogenic effects, which might be responsible for the absence of increase in VTE risk.[122] Parenteral progesterone, such as vaginal or injectable progesterone, which can achieve luteal-phase levels of progesterone and associated progestogenic effects, has not been characterized in terms of VTE risk.[122]
A 2012 meta-analysis estimated that the absolute risk of VTE is 2 per 10,000 women for non-use, 8 per 10,000 women for ethinylestradiol and levonorgestrel-containing birth control pills, and 10 to 15 per 10,000 women for birth control pills containing ethinylestradiol and a newer-generation progestin.[76] For comparison, the absolute risk of VTE is generally estimated as 1 to 5 per 10,000 woman-years for non-use, 5 to 20 per 10,000 woman-years for pregnancy, and 40 to 65 per 10,000 woman-years for the postpartum period.[76] Risk of VTE with estrogen and progestogen therapy is highest at the start of treatment, particularly during the first year, and decreases over time.[89][123] Older age, higher body weight, lower physical activity, and smoking are all associated with a higher risk of VTE with oral estrogen and progestogen therapy.[89][122][123][124] Women with thrombophilia have a dramatically higher risk of VTE with estrogen and progestogen therapy than women without thrombophilia.[76][108] Depending on the condition, risk of VTE can be increased as much as 50-fold in such women relative to non-use.[76][108]
Estrogens induce the production of sex hormone-binding globulin (SHBG) in the liver.[1][81] As such, SHBG levels indicate hepatic estrogenic exposure and may be a reliable surrogate marker for coagulation and VTE risk with estrogen therapy.[125][126][127] Combined birth control pills containing different progestins result in SHBG levels that are increased 1.5- to 2-fold with levonorgestrel, 2.5- to 4-fold with desogestrel and gestodene, 3.5- to 4-fold with drospirenone and dienogest, and 4- to 5-fold with cyproterone acetate.[125] SHBG levels differ depending on the progestin because androgenic progestins oppose the effect of ethinylestradiol on hepatic SHBG production as with its procoagulatory effects.[1][81]Contraceptive vaginal rings and contraceptive patches likewise have been found to increase SHBG levels by 2.5-fold and 3.5-fold, respectively.[125][81] Birth control pills containing high doses of ethinylestradiol (>50 μg) can increase SHBG levels by 5- to 10-fold, which is similar to the increase that occurs during pregnancy.[128] Conversely, increases in SHBG levels are much lower with estradiol, especially when it is used parenterally.[129][130][131][132][133]Estradiol-containing combined birth control pills, like estradiol valerate/dienogest and estradiol/nomegestrol acetate, and high-dose parenteral polyestradiol phosphate therapy have both been found to increase SHBG levels by about 1.5-fold.[81][134][132][131]
Hormone therapy with high-dose ethinylestradiol and cyproterone acetate in transgender women has been associated with a 20- to 45-fold higher risk of VTE relative to non-use.[102][123] The absolute incidence was about 6%.[102][123] Conversely, the risk of VTE in transgender women is much lower with oral or transdermal estradiol plus high-dose cyproterone acetate.[102][123] Ethinylestradiol is thought to have been primarily responsible for the VTE risk, but cyproterone acetate may have contributed as well.[102] Ethinylestradiol is no longer used in transgender hormone therapy,[135][136][137] and doses of cyproterone acetate have been reduced.[138][139]
"Unfortunately, there are few long-term clinical studies comparing different progestogens used in [hormone therapy] with respect to cardiovascular outcomes. However, some aspects of potential cardiovascular risk have been examined, namely effects on lipids, vascular function/blood pressure, inflammation, thrombosis, and carbohydrate metabolism. [...] Although progestins have differing effects on aspects of cardiovascular risk, in general, those more similar to progesterone have been associated with a lower impact than the more androgenic progestins on the beneficial effects of concomitant estrogen therapy. However, the limited number of long-term clinical studies makes it difficult to extrapolate the short-term effects on various markers of cardiovascular risk to long-term cardiovascular morbidity."[118]
Route of administration might also influence the cardiovascular health effects of progestogens, but more research is needed similarly.[150]
Breast cancer
Estrogen alone, progestogen alone, and combined estrogen and progestogen therapy are all associated with increased risks of breast cancer when used in menopausal hormone therapy for peri- and postmenopausal women relative to non-use.[151][152][153] These risks are higher for combined estrogen and progestogen therapy than with estrogen alone or progestogen alone.[151][153] In addition to breast cancer risk, estrogen alone and estrogen plus progestogen therapy are associated with higher breast cancer mortality.[154] With 20 years of use, breast cancer incidence is about 1.5-fold higher with estrogen alone and about 2.5-fold higher with estrogen plus progestogen therapy relative to non-use.[151] The increase in breast cancer risk with estrogen and progestogen therapy was shown to be causal with conjugated estrogens plus medroxyprogesterone acetate in the Women's Health Initiativerandomized controlled trials.[122][155]
The risk of breast cancer with estrogen and progestogen therapy in peri- and postmenopausal women is dependent on the duration of treatment, with more than 5 years of use being associated with significantly greater risk than less than five years of use.[151][152] In addition, continuous estrogen and progestogen therapy is associated with a higher risk of breast cancer than cyclic use.[151][152]
Progestogens mediate their contraceptive effects in women both by inhibiting ovulation (via their antigonadotropic effects) and by thickening cervical mucus, thereby preventing the possibility of fertilization of the ovum by sperm.[4][5] Progestogens have functional antiestrogenic effects in various tissues like the endometrium via activation of the PR, and this underlies their use in menopausal hormone therapy (to prevent unopposed estrogen-induced endometrial hyperplasia and endometrial cancer).[1] The PRs are induced in the breasts by estrogens, and for this reason, it is assumed that progestogens cannot mediate breast changes in the absence of estrogens.[167] The off-target activities of progestogens can contribute both to their beneficial effects and to their adverse effects.[1][2][58]
Progestogens have been found to maximally suppress circulating testosterone levels in men by up to 70 to 80% at sufficiently high doses.[219][220] This is notably less than that achieved by GnRH analogues, which can effectively abolish gonadal production of testosterone and suppress circulating testosterone levels by as much as 95%.[221] It is also less than that achieved by high-dose estrogen therapy, which can suppress testosterone levels into the castrate range similarly to GnRH analogues.[222]
The retroprogesteronederivativesdydrogesterone and trengestone are atypical progestogens and unlike all other clinically used progestogens do not have antigonadotropic effects nor inhibit ovulation even at very high doses.[1][223] In fact, trengestone may have progonadotropic effects, and is actually able to induce ovulation, with about a 50% success rate on average.[223] These progestins also show other atypical properties relative to other progestogens, such as a lack of a hyperthermic effect.[1][223]
The androgenic activity of androgenic progestins is mediated by two mechanisms: 1) direct binding to and activation of the androgen receptor; and 2) displacement of testosterone from sex hormone-binding globulin (SHBG), thereby increasing free (and thus bioactive) testosterone levels.[230] The androgenic activity of many androgenic progestins is offset by combination with ethinylestradiol, which robustly increases SHBG levels, and most oral contraceptives in fact markedly reduce free testosterone levels and can treat or improve acne and hirsutism.[230] An exception is progestin-only contraceptives, which do not also contain an estrogen.[230]
The relative androgenic activity of testosterone-derivative progestins and other progestins that have androgenic activity can be roughly ranked as follows:
The clinical androgenic and anabolic activity of the androgenic progestins listed above is still far lower than that of conventional androgens and anabolic steroids like testosterone and nandrolone esters. As such, they are only generally associated with such effects in women and often only at high doses. In men, due to their concomitant progestogenic activity and by extension antigonadotropic effects, these progestins can have potent functional antiandrogenic effects via suppression of testosterone production and levels.
Progestins with potent antimineralocorticoid activity like drospirenone may have properties more similar to those of natural progesterone, such as counteraction of cyclical estrogen-induced sodium and fluid retention, edema, and associated weight gain; lowered blood pressure; and possibly improved cardiovascular health.[261][262][263][264]
Due to the poor oral activity of progesterone and its short duration with intramuscular injection, progestins were developed in its place both for oral use and for parenteral administration.[280] Orally active progestins have high oral bioavailability in comparison to oral micronized progesterone.[1] Their bioavailability is generally in the range of 60 to 100%.[1] Their elimination half-lives are also much longer than that of progesterone, in the range of 8 to 80 hours.[1] Due mainly to their pharmacokinetic improvements, progestins have oral potency that is up to several orders of magnitude greater than that of oral micronized progesterone.[1] For example, the oral potency of medroxyprogesterone acetate is at least 30-fold that of oral micronized progesterone, while the oral potency of gestodene is at least 10,000-fold that of oral micronized progesterone.[1] Parenterally administered progestins, such as hydroxyprogesterone caproate in oil solution, norethisterone enanthate in oil solution, and medroxyprogesterone acetate in microcrystallineaqueous suspension, have durations in the range of weeks to months.[273][274][275][276][277]
^ abcdefghijAlso marketed under other brand names.
The recognition of progesterone's ability to suppress ovulation during pregnancy spawned a search for a similar hormone that could bypass the problems associated with administering progesterone (e.g. low bioavailability when administered orally and local irritation and pain when continually administered parenterally) and, at the same time, serve the purpose of controlling ovulation. The many synthetic hormones that resulted are known as progestins.
Progestins used in birth control are sometimes grouped, somewhat arbitrarily and inconsistently, into generations. One categorization of these generations is as follows:[14]
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^ abPattman R, Sankar KN, Elewad B, Handy P, Price DA, eds. (November 19, 2010). "Chapter 33. Contraception including contraception in HIV infection and infection reduction". Oxford Handbook of Genitourinary Medicine, HIV, and Sexual Health (2nd ed.). Oxford: Oxford University Press. p. 360. ISBN978-0-19-957166-6. Ovulation may be suppressed in 15–40% of cycles by POPs containing levonorgestrel, norethisterone, or etynodiol diacetate, but in 97–99% by those containing desogestrel.
^ abChristian Lauritzen, John W. W. Studd (22 June 2005). Current Management of the Menopause. CRC Press. p. 45. ISBN978-0-203-48612-2. Ethisterone, the first orally effective progestagen, was synthesized by Inhoffen and Hohlweg in 1938. Norethisterone, a progestogen still used worldwide, was synthesized by Djerassi in 1951. But this progestogen was not used immediately and in 1953 Colton discovered norethynodrel, used by Pincus in the first oral contraceptive. Numerous other progestogens were subsequently synthesized, e.g., lynestrenol and ethynodiol diacetate, which were, in fact, prhormones converted in vivo to norethisterone. All these progestogens were also able to induce androgenic effects when high doses were used. More potent progestogens were synthesized in the 1960s, e.g. norgestrel, norgestrienone. These progestogens were also more androgenic.
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^ abvon Schoultz B, Carlström K, Collste L, Eriksson A, Henriksson P, Pousette A, Stege R (1989). "Estrogen therapy and liver function--metabolic effects of oral and parenteral administration". Prostate. 14 (4): 389–95. doi:10.1002/pros.2990140410. PMID2664738. S2CID21510744.
^Ottosson UB, Carlström K, Johansson BG, von Schoultz B (1986). "Estrogen induction of liver proteins and high-density lipoprotein cholesterol: comparison between estradiol valerate and ethinyl estradiol". Gynecol. Obstet. Invest. 22 (4): 198–205. doi:10.1159/000298914. PMID3817605.
^Sitruk-Ware RL (October 2003). "Hormone therapy and the cardiovascular system: the critical role of progestins". Climacteric. 6 (Suppl 3): 21–28. PMID15018245.
^ abcdefYang Z, Hu Y, Zhang J, Xu L, Zeng R, Kang D (2017). "Estradiol therapy and breast cancer risk in perimenopausal and postmenopausal women: a systematic review and meta-analysis". Gynecol. Endocrinol. 33 (2): 87–92. doi:10.1080/09513590.2016.1248932. PMID27898258. S2CID205631264.
^Stanczyk FZ, Bhavnani BR (July 2014). "Use of medroxyprogesterone acetate for hormone therapy in postmenopausal women: is it safe?". J. Steroid Biochem. Mol. Biol. 142: 30–8. doi:10.1016/j.jsbmb.2013.11.011. PMID24291402. S2CID22731802.
^ abcFeingold KR, Anawalt B, Boyce A, Chrousos G, Dungan K, Grossman A, Hershman JM, Kaltsas G, Koch C, Kopp P, Korbonits M, McLachlan R, Morley JE, New M, Perreault L, Purnell J, Rebar R, Singer F, Trence DL, Vinik A, Wilson DP, Nota NM, den Heijer M, Gooren LJ (2000). "Evaluation and Treatment of Gender-Dysphoric/Gender Incongruent Adults". Endotext [Internet]. PMID31343858.
^Neumann F, Düsterberg B (1998). "Entwicklung auf dem Gebiet der Gestagene" [Development in the field of progestogens]. Reproduktionsmedizin. 14 (4): 257–264. doi:10.1007/s004440050042. ISSN1434-6931.
^Hammerstein J (1990). "Antiandrogens: Clinical Aspects". Hair and Hair Diseases. pp. 827–886. doi:10.1007/978-3-642-74612-3_35.
^Ufer J (1968). "Die therapeutische Anwendung der Gestagene beim Menschen" [Therapeutic Use of Progestagens in Humans]. Die Gestagene [Progestogens]. Springer-Verlag. pp. 1026–1124. doi:10.1007/978-3-642-99941-3_7. ISBN978-3-642-99941-3. Zur Transformation des Endometriums benotigten sie 200-400 mg [ethisterone] pro Cyclus und postulierten eine etwa sechsfach schwachere Wirkung gegenuber dem Progesteron i.m. appliziert.
^ abEndrikat J, Gerlinger C, Richard S, Rosenbaum P, Düsterberg B (December 2011). "Ovulation inhibition doses of progestins: a systematic review of the available literature and of marketed preparations worldwide". Contraception. 84 (6): 549–57. doi:10.1016/j.contraception.2011.04.009. PMID22078182. Table 1 Publications on ovulation inhibition doses of progestins: Progestin: Progesterone. Reference: Pincus (1956). Method: Urinary Pdiol. Daily dose (mg): 300.000. Total number of cycles in all subjects: 61. Total number of ovulation in all subjects: 30. % of ovulation in all subjects: 49.
^Milan Rastislav Henzl, John A. Edwards (10 November 1999). "Pharmacology of Progestins: 17α-Hydroxyprogesterone Derivatives and Progestins of the First and Second Generation". In Régine Sitruk-Ware, Daniel R. Mishell (eds.). Progestins and Antiprogestins in Clinical Practice. Taylor & Francis. pp. 101–132. ISBN978-0-8247-8291-7.
^Lobo RA, Stanczyk FZ (1994). "New knowledge in the physiology of hormonal contraceptives". American Journal of Obstetrics and Gynecology. 170 (5): 1499–1507. doi:10.1016/S0002-9378(12)91807-4. ISSN0002-9378.
^Ostergaard E (February 1965). "The oral progestational and anti-ovulatory properties of megestrol acetate and its therapeutic use in gynaecological disorders". J Obstet Gynaecol Br Emp. 72 (1): 45–48. doi:10.1111/j.1471-0528.1965.tb01372.x. PMID12332461. The anti-ovulatory properties of megestrol acetate 5 mg. plus Mestranol 0.1 mg. were demonstrated in thirty-five women by direct inspection of the ovaries. When given alone, megestrol acetate 5 mg. or Mestranol 0.1 mg. did not prevent ovulation in all cases.
^Schacter L, Rozencweig M, Canetta R, Kelley S, Nicaise C, Smaldone L (March 1989). "Megestrol acetate: clinical experience". Cancer Treat. Rev. 16 (1): 49–63. doi:10.1016/0305-7372(89)90004-2. PMID2471590. At 0.25 mg/day MA has no apparent effect on the histology of the endometrium and is not effective as a contraceptive (53). However, at doses of 0.35 and 0.5 mg/day the drug is an effective contraceptive (10). At the 0.5 mg/day dose MA does not inhibit ovulation but does reduce sperm motility in post-coital tests (68).
^Vessey M, Mears E, Andolšek L, Ogrinc-Oven M (1972). "Randomised double-blind trial of four oral progestagen-only contraceptives". The Lancet. 299 (7757): 915–922. doi:10.1016/S0140-6736(72)91492-4. ISSN0140-6736.
^Aufrère MB, Benson H (June 1976). "Progesterone: an overview and recent advances". J Pharm Sci. 65 (6): 783–800. doi:10.1002/jps.2600650602. PMID945344. Early studies on its use as an oral contraceptive showed that, at 300 mg/day (5th to 25th day of the menstrual cycle), progesterone was effective in preventing ovulation through four cycles (263). The related effect of larger doses of progesterone on gonadotropin excretion also has been investigated. Rothchild (264) found that continuous or intermittent intravenously administered progesterone (100-400 mg/day) for 10 days depressed the total amount of gonadotropin excreted into the urine. However, Paulsen et al. (265) found that oral progesterone at 1000 mg/day for 87 days did not have a significant effect on urinary gonadotropin excretion. The efficacy of progesterone as an oral contraceptive was never fully tested, because synthetic progestational agents, which were orally effective, were available.
^Pincus G (December 1958). "The hormonal control of ovulation and early development". Postgrad Med. 24 (6): 654–60. doi:10.1080/00325481.1958.11692305. PMID13614060. Table 1: Effects of oral progesterone on three indexes of ovulation: Medication: Progesterone. Number: 69. Mean cycle length: 25.5 ± 0.59. Per cent positive for ovulation by: Basal temperature: 27. Endometrial biopsy: 18. Vaginal smear: 6. [...] we settled on 300 mg. per day [oral progersterone] as a significantly effective [ovulation inhibition] dosage, and this was administered from the fifth day through the twenty-fourth day of the menstrual cycle. [...] We observed each of 33 volunteer subjects during a control, nontreatment cycle and for one to three successive cycles of medication immediately following the control cycle. As indexes of the occurrence of ovulation, daily basal temperatures and vaginal smears were taken, and at the nineteenth to twenty-second day of the cycle an endometrial biopsy. [...] Although we thus demonstrated the ovulation-inhibiting activity of progesterone in normally ovulating women, oral progesterone medication had two disadvantages: ( l) the large daily dosage ( 300 mg.) which presumably would have to be even larger if one sought 100 per cent inhibition1 [...]
^Pincus G (1956). "Some effects of progesterone and related compounds upon reproduction and early development in mammals". Acta Endocrinol Suppl (Copenh). 23 (Suppl 28): 18–36. doi:10.1530/acta.0.023S018. PMID13394044.
^Stone A, Kupperman HS (1955). "The Effects of Progesterone on Ovulation: A Preliminary Report". The Fifth International Conference on Planned Parenthood: Theme, Overpopulation and Family Planning: Report of the Proceedings, 24-29 October, 1955, Tokyo, Japan. International Planned Parenthood Federation. p. 185.
^S. Beier, B. Düsterberg, M. F. El Etreby, W. Elger, F. Neumann, Y. Nishino (1983). "Toxicology of Hormonal Fertility Regulating Agents". In Giuseppe Benagiano, Egon Diczfalusy (eds.). Endocrine Mechanisms in Fertility Regulation. Raven Press. pp. 261–346. ISBN978-0-89004-464-3.
^Henzl MR, Edwards JA (10 November 1999). "Pharmacology of Progestins: 17α-Hydroxyprogesterone Derivatives and Progestins of the First and Second Generation". In Sitruk-Ware R, Mishell DR (eds.). Progestins and Antiprogestins in Clinical Practice. Taylor & Francis. pp. 101–132. ISBN978-0-8247-8291-7.
^Becker H, Düsterberg B, Klosterhalfen H (1980). "[Bioavailability of cyproterone acetate after oral and intramuscular application in men (author's transl)]" [Bioavailability of Cyproterone Acetate after Oral and Intramuscular Application in Men]. Urologia Internationalis. 35 (6): 381–385. doi:10.1159/000280353. PMID6452729.
^Moltz L, Haase F, Schwartz U, Hammerstein J (May 1983). "[Treatment of virilized women with intramuscular administration of cyproterone acetate]" [Efficacy of Intra muscularly Applied Cyproterone Acetate in Hyperandrogenism]. Geburtshilfe und Frauenheilkunde. 43 (5): 281–287. doi:10.1055/s-2008-1036893. PMID6223851.
^Chu YH, Li Q, Zhao ZF (April 1986). "Pharmacokinetics of megestrol acetate in women receiving IM injection of estradiol-megestrol long-acting injectable contraceptive". The Chinese Journal of Clinical Pharmacology. The results showed that after injection the concentration of plasma MA increased rapidly. The meantime of peak plasma MA level was 3rd day, there was a linear relationship between log of plasma MA concentration and time (day) after administration in all subjects, elimination phase half-life t1/2β = 14.35 ± 9.1 days.
^Neumann F (1978). "The physiological action of progesterone and the pharmacological effects of progestogens--a short review". Postgraduate Medical Journal. 54 (Suppl 2): 11–24. PMID368741.
^Jacobi GH, Altwein JE, Kurth KH, Basting R, Hohenfellner R (1980). "Treatment of advanced prostatic cancer with parenteral cyproterone acetate: a phase III randomised trial". Br J Urol. 52 (3): 208–15. doi:10.1111/j.1464-410x.1980.tb02961.x. PMID7000222.
^Ferin J (January 1962). "Artificial induction of hypo-oestrogenic amenorrhea with methylestrenolone, or with lynestrenol". Acta Endocrinologica. 39 (1): 47–67. doi:10.1530/acta.0.0390047. PMID13892354.
^Saunders FJ, Drill VA (May 1956). "The myotrophic and androgenic effects of 17-ethyl-19-nortestosterone and related compounds". Endocrinology. 58 (5): 567–572. doi:10.1210/endo-58-5-567. PMID13317831.
^de Gooyer ME, Deckers GH, Schoonen WG, Verheul HA, Kloosterboer HJ (January 2003). "Receptor profiling and endocrine interactions of tibolone". Steroids. 68 (1): 21–30. doi:10.1016/S0039-128X(02)00112-5. PMID12475720. S2CID40426061. [Norethisterone] has similar and [norethynodrel] weaker androgenic effects compared to tibolone.
^Raynaud JP, Ojasoo T (1986). "The design and use of sex-steroid antagonists". J. Steroid Biochem. 25 (5B): 811–33. doi:10.1016/0022-4731(86)90313-4. PMID3543501. Similar androgenic potential is inherent to norethisterone and its prodrugs (norethisterone acetate, ethynodiol diacetate, lynestrenol, norethynodrel, quingestanol).
^Korn GW (March 1961). "The use of norethynodrel (enovid) in clinical practice". Canadian Medical Association Journal. 84 (11): 584–587. PMC1939348. PMID13753182. Pseudohermaphroditism should not be a problem in these patients as it appears that norethynodrel does not possess androgenic properties, but it is believed that Wilkins has now found one such case in a patient who has been on norethynodrel therapy.
^de Gooyer ME, Deckers GH, Schoonen WG, Verheul HA, Kloosterboer HJ (January 2003). "Receptor profiling and endocrine interactions of tibolone". Steroids. 68 (1): 21–30. doi:10.1016/s0039-128x(02)00112-5. PMID12475720. S2CID40426061.
^de Ruggieri P, Matscher R, Lupo C, Spazzoli G (1965). "Biological properties of 17α-vinyl-5(10)-estrene-17β-ol-3-one (norvinodrel) as a progestational and claudogenic compound". Steroids. 5 (1): 73–91. doi:10.1016/0039-128X(65)90133-9. ISSN0039-128X.
^Botella J, Paris J, Lahlou B (August 1987). "The cellular mechanism of the antiandrogenic action of nomegestrol acetate, a new 19-nor progestagen, on the rat prostate". Acta Endocrinologica. 115 (4): 544–550. doi:10.1530/acta.0.1150544. PMID3630545.
^ abPaulsen CA, Leach RB, Lanman J, Goldston N, Maddock WO, Heller CG (1962). "Inherent estrogenicity of norethindrone and norethynodrel: comparison with other synthetic progestins and progesterone". J. Clin. Endocrinol. Metab. 22 (10): 1033–9. doi:10.1210/jcem-22-10-1033. PMID13942007.
^Blanton MP, Xie Y, Dangott LJ, Cohen JB (February 1999). "The steroid promegestone is a noncompetitive antagonist of the Torpedo nicotinic acetylcholine receptor that interacts with the lipid-protein interface". Mol. Pharmacol. 55 (2): 269–78. doi:10.1124/mol.55.2.269. PMID9927618. S2CID491327.
^ abNeubauer H, Ma Q, Zhou J, Yu Q, Ruan X, Seeger H, Fehm T, Mueck AO (October 2013). "Possible role of PGRMC1 in breast cancer development". Climacteric. 16 (5): 509–13. doi:10.3109/13697137.2013.800038. PMID23758160. S2CID29808177.
^Ruan X, Neubauer H, Yang Y, Schneck H, Schultz S, Fehm T, Cahill MA, Seeger H, Mueck AO (October 2012). "Progestogens and membrane-initiated effects on the proliferation of human breast cancer cells". Climacteric. 15 (5): 467–72. doi:10.3109/13697137.2011.648232. PMID22335423. S2CID11302554.
^ abcFotherby K (August 1996). "Bioavailability of orally administered sex steroids used in oral contraception and hormone replacement therapy". Contraception. 54 (2): 59–69. doi:10.1016/0010-7824(96)00136-9. PMID8842581.
^Hargrove JT, Maxson WS, Wentz AC (October 1989). "Absorption of oral progesterone is influenced by vehicle and particle size". Am. J. Obstet. Gynecol. 161 (4): 948–51. doi:10.1016/0002-9378(89)90759-X. PMID2801843.
^Frick J (1973). "Control of spermatogenesis in men by combined administration of progestin and androgen". Contraception. 8 (3): 191–206. doi:10.1016/0010-7824(73)90030-9. ISSN0010-7824.
^Nieschlag E, Kumar N, Sitruk-Ware R (2013). "7α-methyl-19-nortestosterone (MENTR): the population council's contribution to research on male contraception and treatment of hypogonadism". Contraception. 87 (3): 288–95. doi:10.1016/j.contraception.2012.08.036. PMID23063338.
^Foegh M (1983). "Evaluation of steroids as contraceptives in men". Acta Endocrinol Suppl (Copenh). 260 (3_Supplb): 3–48. doi:10.1530/acta.0.104S009. PMID6415998. At the time our studies were initiated, 11 different gestagens have been tested in men. All the oral preparations were used in doses 5 to 12 fold that used in the female oral contraceptive. The only exception was levo-norgestrel which was used in a very low dose, namely 100 µg daily (Fotherby et al. 1972). However, no effect was obtained on sperm count and in vitro sperm penetration.
Stanczyk FZ (2007). "Structure –Function Relationships, Pharmacokinetics, and Potency of Orally and Parenterally Administered Progestogens". Treatment of the Postmenopausal Woman. pp. 779–798. doi:10.1016/B978-012369443-0/50067-3. ISBN978-0-12-369443-0.
Kuhl H (2011). "Pharmacology of progestogens"(PDF). Journal für Reproduktionsmedizin und Endokrinologie-Journal of Reproductive Medicine and Endocrinology. 8 (Special Issue 1): 157–176.
Lawrie TA, Helmerhorst FM, Maitra NK, Kulier R, Bloemenkamp K, Gülmezoglu AM (May 2011). "Types of progestogens in combined oral contraception: effectiveness and side-effects". Cochrane Database Syst Rev (5): CD004861. doi:10.1002/14651858.CD004861.pub2. PMID21563141.
Endrikat J, Gerlinger C, Richard S, Rosenbaum P, Düsterberg B (December 2011). "Ovulation inhibition doses of progestins: a systematic review of the available literature and of marketed preparations worldwide". Contraception. 84 (6): 549–57. doi:10.1016/j.contraception.2011.04.009. PMID22078182.
Moore NL, Hickey TE, Butler LM, Tilley WD (June 2012). "Multiple nuclear receptor signaling pathways mediate the actions of synthetic progestins in target cells". Mol. Cell. Endocrinol. 357 (1–2): 60–70. doi:10.1016/j.mce.2011.09.019. PMID21945474. S2CID20006148.
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