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Medroxyprogesterone acetate (MPA) is a steroidal progestin, a synthetic variant of the steroid hormone progesterone.^[2]^[3] It is used as a contraceptive, in hormone replacement therapy and for the treatment of endometriosis as well as several other indications.

MPA is a more potent derivative of its parent compound medroxyprogesterone (MP). While medroxyprogesterone is sometimes used as a synonym for medroxyprogesterone acetate,^[3] what is almost always being referred to is MPA and not MP.^[4] It is on the World Health Organization's List of Essential Medicines, the most important medication needed in a basic health system.^[5]

1 Medical uses
2 Side effects
3 Interactions
4 Pharmacodynamics
- 4.1 Activity profile
  - 4.1.1 Steroid hormone receptor ligand
  - 4.1.2 Neurosteroidogenesis inhibitor
  - 4.1.3 Appetite stimulant
- 4.2 Comparison to medroxyprogesterone
5 Pharmacokinetics
6 Comparison with progesterone
7 History
8 See also
9 References

Medical uses

In females, the most common use of MPA is as an oral or depot-injected contraceptive and also as the progestin component of menopausal hormone replacement therapy to prevent endometrial hyperplasia and cancer. MPA is also used as a treatment for endometriosis, dysmenorrhea, and amenorrhea.^[6] MPA, along with other progestins were developed to allow the hormones to be taken orally, as progesterone (the hormone made by the human body) could not be taken orally before the process of micronization was developed.^[7]

In males, MPA has been used to control inappropriate sexual behavior to chemically castrate convicted sex offenders.^[8]

MPA is an extremely effective contraceptive when used with relatively high doses to prevent ovulation. It has also been used to treat benign prostatic hyperplasia, as a palliative appetite stimulant for cancer patients, and at high doses (800 mg per day) to treat hormone-dependent cancers of primarily the breast, but also other types.^[9]

Though not used as a treatment for epilepsy, MPA reduces the frequency of seizures and does not interact with anti-epileptic medications. MPA does not interfere with blood clotting and appears to improve blood parameters for women with sickle cell anemia. Similarly, MPA does not appear to affect liver metabolism, and may improve primary biliary cirrhosis and chronic active hepatitis. Women taking MPA may experience spotting shortly after starting the medication but is not usually serious enough to require medical intervention. With longer use amenorrhoea can occur as can irregular menstruation which is a major source of dissatisfaction, though both can result in improvements with iron deficiency and risk of pelvic inflammatory disease and often do not result in discontinuing the medication.^[9] MPA is also prescribed in combination with an estrogen to prevent endometrial hyperplasia in post-menopausal women who are undergoing hormone replacement therapy.^[10]

MPA has also been prescribed in hormone replacement therapy for male-to-female transgender individuals due to its progestogenic and antigonadotropic effects.

Side effects

In females, the most common adverse effects are acne, changes in menstrual flow, drowsiness, and can cause birth defects if taken by pregnant women. Other common side effects include breast tenderness, increased facial hair, decreased scalp hair, difficulty falling or remaining asleep, stomach pain, and weight loss or gain.^[6]

The Women's Health Initiative investigated the use of MPA and conjugated equine estrogens compared to placebo. The study was prematurely terminated when previously unexpected risks were discovered, specifically the finding that though the all-cause mortality was not affected by the hormone therapy, the benefits of the hormone replacement therapy (reduced risk of hip fracture, colorectal and endometrial cancer and all other causes of death) were offset by increased risk of coronary heart disease, breast cancer, strokes and pulmonary embolism.^[11] However, the study focused on MPA only and extrapolated the benefits versus risks to all synthetic progesterones—a conclusion that has been challenged by several researchers as unjustified and leading to unnecessary avoidance of HRT for many women as synthetic progesterones are not alike.^[12]

At high doses for the treatment of breast cancer, MPA can cause weight gain, worsen diabetes mellitus and edema (particularly of the face). Adverse effects peak at five weeks, and are reduced with lower doses. Less frequent effects may include thrombosis (though it is not clear if this is truly a risk, it cannot be ruled out), painful urination, anxiety, headache, nausea and vomiting. When used to treat benign prostatic hyperplasia, more frequent complaints include reduced libido, impotence, reduced ejaculate volume, and within three days, chemical castration. MPA may cause reduced bone density though this appears to be reversible to a normal level even after years of use. At extremely high doses (used to treat cancer, not for contraception) MPA may cause adrenal suppression and interfere with carbohydrate metabolism but does not cause diabetes.^[9]

Fetuses exposed to progesterones have demonstrated higher rates of genital abnormalities, low birth weight, and increased ectopic pregnancy particularly when MPA is used as an injected form of long-term birth control. When used as a form of injected birth control, MPA can reduce fertility for as long as 10 months, taking longer for overweight or obese women. When combined with conjugated equine estrogens (Premarin), MPA has been associated with an increased risk of breast cancer, dementia and thrombus in the eye. In combination with estrogens in general, MPA may increase the risk of cardiovascular disease, with a stronger association when used by post-menopausal women also taking CEE. MPA is not recommended for use prior to menarche or before or during recovery from surgery.^[3] It was because of these unexpected interactions that the Women's Health Initiative study was ended early due the extra risks of hormone replacement therapy,^[13] producing a dramatic decrease in both new and renewal prescriptions for hormone therapy.^[14]

MPA is known to produce symptoms of depression, anxiety, and irritability in some patients.^[15] In addition, unlike progesterone, lowered libido is a reported side effect of MPA in women.^[16]

Interactions

MPA increases the risk of breast cancer, dementia and thrombus when used in combination with conjugated equine estrogens to treat the symptoms of menopause.^[3] When used as a contraceptive, MPA does not generally interact with other drugs. When combined with aminoglutethimide to treat metastases from breast cancer, MPA is associated with an increase in depression.^[9] St John's wort may decrease its effectiveness as a contraceptive.^[3]

Pharmacodynamics

Activity profile

Steroid hormone receptor ligand

MPA acts as an agonist of the progesterone, androgen, and glucocorticoid receptors (PR, AR, and GR, respectively),^[1] activating these receptors with EC₅₀ values of approximately 0.01 nM, 1 nM, and 10 nM, respectively.^[17] It has very low and likely insignificant affinity for the estrogen and mineralocorticoid receptors (ER and MR, respectively).^[1] Although the EC₅₀ values of MPA at the PR and the AR and GR are separated by several orders of magnitude, because it is so potent, and because it is used at relatively high doses in humans, due to binding saturation, it is probable that the overall activation of each of the three receptors is fairly similar.^{[citation needed]} The intrinsic activities of MPA in activating the PR and the AR have been reported to be at least equivalent to those of progesterone and dihydrotestosterone (DHT), respectively, indicating that it is a full agonist of these receptors.^[18]^[19]

In addition to its direct effects on steroid receptors, MPA, at sufficient doses, inhibits the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axes, resulting in a marked suppression of gonadotropin, androgen, estrogen, adrenocorticotropic hormone (ACTH), and cortisol levels as well as concentrations of sex hormone-binding globulin (SHBG).^[20] There is evidence that the downregulatory effects of MPA on the HPG axis are mediated by activation of both PRs and ARs in the pituitary gland.^[21]^[22] Due to its effects on androgen levels, MPA has strong functional antiandrogen properties, and it is used in androgen-sensitive conditions such as precocious puberty in prepubescent boys and hypersexuality in men.^[23] In addition, since it affects estrogen levels similarly, unlike many other antiandrogens such as spironolactone and cyproterone acetate which have a high propensity for causing gynecomastia via indirect stimulation of estrogen, MPA is not thought to possess any estrogenic effects. Indeed, due to its inhibitory effects on estrogen levels, it has potent antiestrogenic effects, and has been used to treat precocious puberty in prepubescent girls. Accordingly, MPA should not be used in high doses without an estrogen in women due to the risk of osteoporosis and other symptoms associated with hypoestrogenism.^[24]

As mentioned above, MPA is a potent full agonist of the AR. Its activation of the AR has been shown to play an important and major role in its antigonadotropic effects and in its beneficial effects against breast cancer.^[21]^[25]^[26] However, although MPA does have the capacity to cause androgenic side effects such as acne and hirsutism in some patients (especially women),^[27]^[28] it seldom actually does so, and when it does, the effects tend to be only mild, regardless of the dosage used.^[21] In fact, likely due to its suppressive actions on androgen levels, it has been reported that MPA is generally highly effective in improving pre-existing symptoms of hirsutism in women with the condition.^[29]^[30] Moreover, MPA rarely causes any androgenic effects in children with precocious puberty, even at very high doses.^[31] The reason for the general lack of virilizing effects with MPA, despite it binding to and activating the AR with a high affinity and this action playing an important role in many of its physiological and therapeutic effects, is not entirely clear. However, MPA has been found to interact with the AR in a fundamentally different way than other agonists of the receptor such as dihydrotestosterone (DHT).^[18] The result of this difference appears to be that MPA binds to the AR with a similar affinity and intrinsic activity to that of DHT, but requires about 100-fold higher concentrations for a comparable induction of gene transcription, while at the same time not antagonizing the transcriptional activity of normal androgens like DHT at any concentration.^[18] Thus, this may explain the low propensity of MPA for producing androgenic side effects.

As an agonist of the GR, MPA has glucocorticoid properties, and as a result can cause symptoms of Cushing's syndrome,^[32] steroid diabetes, and adrenal insufficiency at sufficiently high doses.^[33]

Neurosteroidogenesis inhibitor

MPA is a known inhibitor of 3α-hydroxysteroid dehydrogenase.^[15]^[34] This enzyme is necessary for the synthesis of the endogenous neurosteroids allopregnanolone, THDOC, and 3α-androstanediol. These neurosteroids have antidepressant and anxiolytic effects, and the blockade of their production could be the cause of the symptoms of depression, anxiety, and irritability that are sometimes seen during treatment with MPA.^[15]^[35] Indeed, other drugs that are known to block the synthesis of these neurosteroids, such as 5α-reductase inhibitors like finasteride, have also been associated with symptoms of depression and anxiety.^[36]

Appetite stimulant

Although MPA and the related drug megestrol acetate (which is a close analogue) have been extensively used as appetite stimulants, the mechanism of action of their beneficial effects on appetite is not entirely clear. However, glucocorticoid, cytokine, and possibly anabolic-related mechanisms are all thought to possibly be involved, and a number of downstream changes have been implicated, including stimulation of the release of neuropeptide Y in the hypothalamus, modulation of calcium channels in the ventromedial hypothalamus, and inhibition of the secretion of proinflammatory cytokines including IL-1α, IL-1β, IL-6, and TNF-α, actions that have all been linked to an increased appetite.^[37]

Comparison to medroxyprogesterone

Medroxyprogesterone (MP), the parent drug of MPA, is a metabolite of MPA.^[38] While both MP and its acylated derivative MPA bind to the PR and both act as agonists, MPA has approximately 100 fold higher binding affinity and transactivation potency compared to MP.^[39] As such, MP is not used clinically, though it has seen some use in veterinary medicine.^[40]

Ligand	PR K_i (nM)	Coactivator recruitment EC₅₀ (nM)	Reporter cell line EC₅₀ (nM)
Progesterone	4.3 ± 1.0	0.9 ± 0.2	25 ± 11
Medroxyprogesterone acetate	1.2 ± 0.3	0.6 ± 0.08	0.15 ± 0.03
Medroxyprogesterone	241 ± 96	47 ± 14	32 ± 1

Pharmacokinetics

MPA is well-absorbed orally and through intramuscular injection, peaking at 2–4 hours for the former. The half life is 12 to 17 hours for an oral dose, and 40 to 50 days for an intramuscular injection. MPA binds to albumin in the blood, and is metabolized primarily through the liver via hydroxylation and conjugation.^[3] Intramuscular MPA is released slowly; a 150 mg dose is first detectable in the blood 30 minutes after injection, plateauing at 1.0 ng/mL for three months, followed by a gradual, tapering decline that lasts up to nine months in some women. The high levels of MPA in the blood inhibits luteinizing hormone and ovulation for several months, with an accompanying decrease in serum progesterone to below 0.4 ng/mL. Ovulation resumes when once blood levels of MPA fall below 0.1 ng/mL. Serum estradiol remains at approximately 50 pg/mL for approximately four months post-injection (with a range of 10-92 pg/mL after several years of use), rising once MPA levels fall below 0.5 ng/ml.^[41]

Hot flashes are rare while MPA is found at significant blood levels in the body, and the vaginal lining remains moist and creased. The endometrium undergoes atrophy, with small, straight glands and a stroma that is decidualized. Cervical mucus remains viscous. Because of its steady blood levels over the long term and multiple effects that prevent fertilisation, MPA is a very effective means of birth control.^[41]

Comparison with progesterone

Proponents of bioidentical hormone replacement therapy believe progesterone offers fewer side effects and improved quality of life compared to MPA.^[42] The evidence for this view has been questioned; MPA is better absorbed when taken orally, with a much longer half life leading to more stable blood levels^[43] though it may lead to greater breast tenderness and more sporadic vaginal bleeding.^[42] The two compounds do not differentiate in their ability to suppress endometrial hyperplasia,^[42] nor does either increase the risk of pulmonary embolism.^[44] The two compounds have not been adequately compared in direct tests to clear conclusions about safety and superiority.^[7]

History

MPA was independently discovered in 1956^[45] by Syntex^[46] and the Upjohn Company.^[47] It was introduced for clinical use in 1959.^[48]^[49]^[50]

References

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UpToDate Contents

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1. 避妊のための酢酸メドロキシプロゲステロンデポ剤 depot medroxyprogesterone acetate for contraception
2. 周産期心筋症：治療および予後 peripartum cardiomyopathy treatment and prognosis
3. 避妊している女性におけるホルモン剤内服中の出血のマネージメント management of unscheduled bleeding in women using contraception
4. 閉経期のホルモン療法で用いる製剤 preparations for menopausal hormone therapy
5. 月経抑制のためのホルモン避妊法 hormonal contraception for suppression of menstruation

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プロゲステロンおよび溶連菌製剤により肺転移巣の完全退縮をみた進行腎細胞癌の1例

長倉和彦,高尾雅也,松崎章二,家田和夫
日本泌尿器科學會雜誌 76(12), 1909-1913, 1985-12-20
medroxyprogesterone acetateとOK-432により肺転移巣の完全退縮をみた稀な腎細胞癌の一例を報告する.症例は59歳の男性で,血痰を主訴に来院,胸部X-P上,無数の小円形陰影を認め,諸検査の結果,左腎腫瘍と肺,副腎転移と診断した.ただちに左腎・副腎全摘術を行い,組織学的に淡明細胞を中心とする腎細胞癌と同側副腎転移と診断,また肺腫瘍に対しては気管支鏡的肺生検を行い,腎癌の転移 …
NAID 110006531487

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Provera Depo-provera | Buy Depo-provera PROVERA – Composição プロベラ10mg (Provera) の追加写真 PROVERA 5 MG tbl 24x 5mg DEPO-PROVERA (MEDROXYPROGESTERONE ACETATE)

★リンクテーブル★

リンク元	「メドロキシプロゲステロン」「DMPA」
拡張検索	「Depo-Provera」

「メドロキシプロゲステロン」

Medroxyprogesterone acetate
(INN, USAN, BAN, JAN)
Systematic (IUPAC) name
	17α-hydroxy-6α-methylpregn-4-ene-3,20-dione acetate
Clinical data
Trade names	Depo-Provera (injection), Provera (oral)
AHFS/Drugs.com	FDA Professional Drug Information
MedlinePlus	a604039
Pregnancy; category	US: X (Contraindicated); ;
Routes of; administration	Oral, IM
Legal status
Legal status	℞ (Prescription only);
Pharmacokinetic data
Bioavailability	99%
Protein binding	88% (to albumin)
Biological half-life	40-60 hours
Identifiers
CAS Number	71-58-9
ATC code	G03AC06 (WHO) G03DA02 (WHO), L02AB02 (WHO)
PubChem	CID 6279
IUPHAR/BPS	2879
DrugBank	DB00603
ChemSpider	6043
UNII	C2QI4IOI2G
KEGG	C08150
ChEBI	CHEBI:6716
ChEMBL	CHEMBL717
Synonyms	17α-hydroxy-6α-methylprogesterone acetate
Chemical data
Formula	C24H34O4
Molar mass	386.52 g/mol
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　　[★]

英: medroxyprogesterone
化: 酢酸メドロキシプロゲステロン medroxyprogesterone acetate MPA、medroxyprogesterone 17-acetate、メドロキシプロゲステロン酢酸エステル
商: ヒスロン、プロベラ、ヒスロンH、Provera, Depo-Provera, DMPA, Provera

合成プロゲストーゲン;抗悪性腫瘍薬

適応

子宮体癌、乳癌

黄体ホルモン療法は，類内膜腺癌G1あるいはプロゲステロン受容体陽性の進行・再発症例に用いられる（グレードB）。(参考1)

参考

1. 子宮体癌治療ガイドライン(2006年)

http://www.jsgo.gr.jp/guideline/taigan.html

「DMPA」

　　[★] メドロキシプロゲステロン。medroxyprogesterone acetate Provera, Depo-Provera

「Depo-Provera」

　　[★] 酢酸メドロキシプロゲステロン

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[33] Systemic Effects of Oral Glucocorticoids

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v t e Orexigenics (A15)

Exogenous	Amitriptyline Clonidine Cyproheptadine Dexamethasone Dronabinol/Tetrahydrocannabinol (Cannabis) Medroxyprogesterone acetate Megestrol acetate Mirtazapine Nabilone Nandrolone Olanzapine Omega-3 fatty acid Oxandrolone Pentoxifylline Prednisone Sugars Testosterone Thalidomide

Endogenous	ACTH/Corticotropin Adiponectin Agouti-related peptide Anandamide Cortisol/Hydrocortisone Cortisone Ghrelin Melanin-concentrating hormone Melatonin Neuropeptide Y Orexin/Hypocretin

v t e Steroid hormone metabolism modulators

20,22-Desmolase	Inhibitors: 22-ABC 3,3′-Dimethoxybenzidine 3-Methoxybenzidine Aminoglutethimide Canrenone Cyanoketone Danazol Etomidate Ketoconazole Mitotane Spironolactone Trilostane

17α-Hydroxylase, 17,20-Lyase	Inhibitors: 22-ABC 22-Oxime Δ⁴-Abiraterone Abiraterone Abiraterone acetate Amphenone Bifluranol Bifonazole Canrenone CFG-920 Clotrimazole Cyanoketone Cyproterone acetate Danazol Econazole Flutamide Galeterone Gestrinone Isoconazole Ketoconazole L-39 Levoketoconazole Liarozole LY-207,320 MDL-27,302 Miconazole Mifepristone Nilutamide Orteronel Pioglitazone Prochloraz Rosiglitazone Seviteronel Spironolactone Stanozolol SU-9055 SU-10603 TGF-β Tioconazole Troglitazone VN/87-1 YM116

3α-HSD	Inhibitors: Coumestrol Daidzein Genistein Indomethacin Medroxyprogesterone acetate Inducers: Fluoxetine Fluvoxamine Mirtazapine Paroxetine Sertraline Venlafaxine

3β-HSD	Inhibitors: 4-MA Δ⁴-Abiraterone Abiraterone Abiraterone acetate Azastene Cyanoketone Cyproterone acetate Danazol Epostane Genistein Gestrinone Medrogestone Metyrapone Norethisterone Oxymetholone Pioglitazone Rosiglitazone Trilostane Troglitazone

11β-HSD	Inhibitors: 11α-Hydroxyprogesterone 11β-Hydroxyprogesterone 18α-Glycyrrhizic acid ABT-384 Acetoxolone Carbenoxolone Enoxolone (glycyrrhetinic acid) Epigallocatechin gallate Glycyrrhizin (glycyrrhizic acid) Progesterone

21-Hydroxylase	Inhibitors: Aminoglutethimide Amphenone B Bifonazole Canrenone Clotrimazole Diazepam Econazole Genistein Isoconazole Ketoconazole Levoketoconazole Metyrapone Miconazole Midazolam Spironolactone Tioconazole

11β-Hydroxylase	Inhibitors: Δ⁴-Abiraterone Abiraterone Abiraterone acetate Aminoglutethimide Canrenone Etomidate Fadrozole FETO Ketoconazole Levoketoconazole Metomidate Metyrapol Metyrapone Mitotane Potassium canrenoate Spironolactone Trilostane

18-Hydroxylase	Inhibitors: 18-Ethynylprogesterone (18-ethinylprogesterone) 18-Vinylprogesterone Aminoglutethimide Canrenone FAD286 Fadrozole Ketoconazole LCI699 Metyrapone Mespirenone Potassium canrenoate Spironolactone

17β-HSD	Inhibitors: Danazol Simvastatin

5α-Reductase	Inhibitors: 22-Oxime Δ⁴-Abiraterone Abiraterone Abiraterone acetate Alfatradiol Azelaic acid β-Sitosterol Bexlosteride Chlormadinone acetate Cl-4AS-1 Dutasteride Epitestosterone Epristeride Fatty acids (α-linolenic acid, linoleic acid, γ-linolenic acid, monolinolein, oleic acid) Finasteride Ganoderic acid Izonsteride L-39 Lapisteride Oxendolone Saw palmetto TFM-4AS-1 Turosteride Vitamin B6 Zinc

Aromatase	Inhibitors: 4-AT 4-Cyclohexylaniline 4-Hydroxytestosterone 5α-DHNET Abyssinone II Aminoglutethimide Anastrozole Ascorbic acid (vitamin C) Atamestane ATD Bifonazole CGP-45,688 CGS-47,645 Chalconoids (e.g., isoliquiritigenin) Corynesidone A Clotrimazole DHT Difeconazole Econazole Ellagitannins Endosulfan Exemestane Fadrozole Fatty acids (e.g., conjugated linoleic acid, linoleic acid, linolenic acid, palmitic acid) Fenarimol Finrozole Flavonoids (e.g., 7-hydroxyflavone, 7-hydroxyflavanone, 7,8-DHF, acacetin, apigenin, baicalein, biochanin A, chrysin, EGCG, gossypetin, hesperetin, liquiritigenin, myricetin, naringenin, pinocembrin, rotenone, quercetin, sakuranetin, tectochrysin) Formestane Imazalil Isoconazole Ketoconazole Letrozole Liarozole Melatonin MEN-11066 Miconazole Minamestane Nimorazole NKS01 Norendoxifen ORG-33,201 Penconazole Phenytoin Prochloraz PGE2 (dinoprostone) Plomestane Prochloraz Propioconazole Pyridoglutethimide Quinolinoids (e.g., berberine, casimiroin, triptoquinone A, XHN22, XHN26, XHN27) Resorcylic acid lactones (e.g., zearalenone) Rogletimide Stilbenoids (e.g., resveratrol) Talarozole Terpenoids (e.g., dehydroabietic acid, (–)-dehydrololiolide, retinol (vitamin A), Δ⁹-THC, tretinoin) Testolactone Tioconazole Triadimefon Triadimenol Troglitazone Valproic acid Vorozole Xanthones (e.g., garcinone D, garcinone E, α-mangostin, γ-mangostin, monodictyochrome A, monodictyochrome B) YM-511 Zinc Inducers: Atrazine Flavonoids (e.g., genistein, quercetin)

27-Hydroxylase	Inhibitors: Anastrozole Bicalutamide Dexmedetomidine Fadrozole Posaconazole Ravuconazole

Others	Inhibitors: Inhibit estradiol degradation: Cimetidine Ranitidine

See also: Androgenics • Estrogenics • Glucocorticoidics • Mineralocorticoidics • Progestogenics

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Provera