SEARCH · PubMed Health

Results for “Progestins”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources

PubMed1987

[Parenteral contraceptive drugs: depot progestins].

Depot progestins as injectables, implantables or vaginal rings are suitable for contraception in those female patients, in which risk factors (e.g. cardiovascular risk) exclude the use of estrogen-progestin mixtures. In this paper the mode of action, indications, contraindications, advantages and disadvantages of the various methods using depot-progestins are discussed. Injectables contain either medroxyprogesterone acetate or norethistronenantate; both steroids are released slowly within a limited time interval (2 to 4 months) out of a depot. The major effect is a change of the cervical mucus. Side-effects are disturbances of the menstrual cycle (e.g. breakthrough bleedings) as well as an amenorrhea after frequent use (up to 50% of all cases). The subdermal implantables (Norplant 2 or 5) release levonorgestrel out of a depot over a time period of at least 5 years. Steroid plasma levels are lower than in those patients using a progestin-only pill. Side-effects of implantables are disturbances of the menstrual cycle (e.g. breakthrough bleeding); in patients who desire to conceive a child or suffer from undesirable side-effects the implantables can be removed at every time. The progestin releasing vaginal rings are in a stage of controlled clinical trials. The advantages depend on ethe easy mode of administration (implantation or removal). Side-effects are also breakthrough bleedings.

Administration, Intravaginal↗

PubMed1984

Potential risks, benefits of progestins in birth control pills outlined.

Progestins in oral contraceptives (OCs) produce potential complications, as well as noncontraceptive benefits, according to Robert A. Hatcher, MD, MPH, professor of gynecology and obstetrics, Emory University Medical School. Hatcher told CTU that lowering the progestin content in an OC may decrease complications, but could also decrease the benefits experienced by women. "The extent to which that will happen remains to be seen," he said. Hatcher cited the following potential complications of progestins in OC: hypertension; decreased levels of high density lipoproteins; acne; oily skin; headaches between pill cycles; dilated leg veins; pelvic congestion syndrome; thrombosis of superficial leg veins; gallstones; Monilia vaginitis; cholestatic jaundice; and depression, fatigue, and decreased libido. Progestins, according to Hatcher, also produce these noncontraceptive benefits: protection against PID; decreased dysmenorrhea; decreased menstrual blood loss, decreased iron deficiency anemia; protection against endometrial cancer; protection against fibrocystic breast disease, and fibroadenomas of the breast; decreased bleeding from fibroids; decreased growth of fibroids. When ovulation is suppressed, Hatcher emphasized, additional benefits that may occur include the following: decreased risk of functional ovarian cysts; elimination of mittleschmerz pain; decreased rick of ovarian cancer; protection against endometriosis.

Behavior↗

PubMed2003

Combined hormonal versus nonhormonal versus progestin-only contraception in lactation.

BACKGROUND: Contraception for women who are breastfeeding is a public health issue of global importance. Each year over 100 million women make decisions about beginning or resuming contraception after childbirth. These decisions include both the choice of contraceptive method and the time at which its use begins, both of which continue to be debated by experts. Choices of contraception may be limited for lactating women due to concerns about hormonal effects on quality and quantity of milk, passage of hormones to the infant, and infant growth. Ideally, the contraceptive method chosen should not interfere with lactation. Additionally, because the return of menstruation and ovulation can be unpredictable in breastfeeding women, the timing of contraception initiation is important. OBJECTIVES: To determine the effect of combined oral contraceptives and progestin-only contraceptives on lactation. The a priori hypothesis is that combined oral contraception impairs lactation, making it less appropriate than progestin-only or nonhormonal contraception for breastfeeding women. SEARCH STRATEGY: We used PUBMED, POPLINE, EMBASE, LILACS, and Cochrane Controlled Trials Register computer searches, supplemented by review articles and contact with investigators. SELECTION CRITERIA: We sought all randomized controlled trials, reported in any language, that included any form of hormonal contraception compared with another form of hormonal contraception, nonhormonal contraception, or placebo during lactation. Hormonal contraception could include combined oral or injectable contraceptives, progestin-only oral or injectable contraceptives, hormonal implants, or hormonal intrauterine devices. Study participants included breastfeeding women of any age or parity who desired contraception. DATA COLLECTION AND ANALYSIS: We evaluated the methodological quality of each report and sought to identify duplicate reporting of data from multicenter trials. We abstracted data onto data collection forms. Principal outcome measures included quantity of milk; biochemical analysis of milk composition; initiation, maintenance and duration of lactation; infant growth; efficacy of contraceptive method while breastfeeding; and timing of contraception initiation and its effects on lactation. Because the trials did not have uniform interventions, often lacked quantifiable outcomes, and had poor methodological quality, we could not aggregate the data in a meta-analyses. MAIN RESULTS: Seven reports from five randomized controlled trials met our inclusion criteria. Most of the five trials did not specify their method used to generate a random sequence, method of allocation concealment, blinding of treatments, or use of an intention-to-treat analysis. Additionally, high loss to follow-up rates invalidated at least two studies. The findings from two reports comparing oral contraceptives to placebo during lactation were conflicting. Another trial found no inhibitory effects on lactation from progestin-only contraceptives. Finally, the WHO trial found no effect of progestin-only contraceptives on lactation but a decline in breast milk volume from combination contraceptives during lactation. High loss to follow-up rates, however, undermine the credibility of the WHO trial. No significant differences in infant growth or weight appeared in any of the included trials as a result of the use of hormonal contraception during lactation. REVIEWER'S CONCLUSIONS: Evidence from randomized controlled trials on the effect of hormonal contraceptives during lactation is limited and of poor quality; results should be interpreted with caution. The existing randomized controlled trials are insufficient to establish an effect of hormonal contraception, if any, on milk quality and quantity. Evidence is inadequate to make recommendations regarding hormonal contraceptive use for lactating women. At least one properly conducted randomized controlled trial of adequate size is urgently needed to address this question.

Contraceptives, Oral, Combined↗

PubMed1989

Regulation of epidermal growth factor receptor by progestins and glucocorticoids in human breast cancer cell lines.

Human breast cancer cells secrete a number of autocrine peptides which modulate their proliferation rates. The known effects of steroid hormones on breast cancer cell proliferation may be mediated in part by altering the production of these growth factors and/or their interactions with cellular receptor sites. Receptors for epidermal growth factor (EGF), which also bind the autocrine growth factor, alpha-transforming growth factor, are present on a number of breast cancer cell lines and it has previously been shown that T-47D and MCF-7 cells respond to progestins with an increase in the concentration of EGF receptors (EGF-R). In the present study we examined the effects of both progestins and glucocorticoids on EGF binding in 10 human breast cell lines. Five of these lines were progesterone receptor positive and all lines expressed the glucocorticoid receptor (GR). All cell lines were initially incubated for 24 hr with increasing concentrations of the synthetic progestin, medroxyprogesterone acetate (MPA), and the level of specifically bound EGF was determined. An increase in specific binding of EGF was confirmed in two PR-positive lines but, in addition, increases in EGF binding were observed in 4 PR-negative cell lines. In these last lines the synthetic glucocorticoid, dexamethasone, was a more potent inducer of EGF binding than MPA, a known glucocorticoid agonist, while the high-affinity PR ligand, ORG 2058, was without effect. Furthermore, MPA competed with dexamethasone for binding to GR in these cell lines, supporting the view that the induction of EGF binding by MPA in these cells was mediated via the GR. This conclusion was further supported by studies in which addition of the glucocorticoid and progestin antagonist, RU 486, inhibited the effect of ORG 2058 in two cell lines and completely abrogated the effect of dexamethasone in two other lines. Detailed binding studies revealed that the increase in EGF binding was accompanied by an increase in the concentration of EGF-R. This effect was observed when EGF binding was assayed at either 0 degree or 37 degrees C. Further studies demonstrated that the increases in EGF binding following ORG 2058 and dexamethasone treatment were accompanied by increases in EGF-R mRNA levels. Our data illustrate that the binding of EGF by some human breast cancer cells can be regulated by both progestins and glucocorticoids acting via their respective receptors and inducing increases in EGF-R mRNA levels.

Breast Neoplasms↗

PubMed1990

Progestin induction of 17 beta-hydroxysteroid dehydrogenase enzyme protein in the T-47D human breast-cancer cell line.

Steroid regulation of 17 beta-hydroxysteroid dehydrogenase (17-HSD) was studied in the T-47D human breast-cancer cell line, using a radioimmunoassay. In addition, 3 mRNA species (2.4, 1.4, and 0.9 kb) specific for the enzyme were shown to be present in these cells. All the synthetic progestins tested (ORG 2058, R5020, medroxyprogesterone acetate) significantly increased the immunoreactive enzyme protein concentration, while other types of steroids, such as testosterone, oestradiol and dexamethasone, were ineffective. The progestin-specific induction of 17-HSD was dose-related and was maximum in about 5 days. An antiprogestin, RU 486, when used in combination with synthetic progestins, blocked the progestin-induced increase of 17-HSD concentration very effectively. A good correlation was observed in the different experiments between the enzyme activity and the immunoreactive 17-HSD concentration. We conclude that progestins induce 17-HSD in T-47D cells and that the induction occurs via an increased accumulation of enzyme protein.

Breast Neoplasms↗

PubMed1993

Effects of the progestin antagonist RU 486 on T-47D breast cancer cell cycle kinetics and cell cycle regulatory genes.

Possible mechanisms by which the progestin antagonist RU 486 inhibits cell growth were investigated by comparing the effects of the antiprogestin with those of progestin and antiestrogen. Exposure of T-47D breast cancer cells to RU 486 caused a decline in the proportion of cells in S phase, indicative of a block to cell cycle progression in G1 phase. This was accompanied by a marked decrease in c-myc expression but no change in cyclin D1 expression. The cell kinetic data suggest that progestin antagonist inhibition of proliferation and progestin stimulation of proliferation are mediated by opposing effects on the same mechanism. Both estrogen antagonists and progestin antagonists appear to act at a similar part of G1 phase but there are clear differences in their effects on cyclin D1 expression, suggesting that the mechanisms by which these compounds inhibit proliferation are distinct.

Breast Neoplasms↗

PubMed1983

Binding of progestins to the glucocorticoid receptor. Correlation to their glucocorticoid-like effects on in vitro functions of human mononuclear leukocytes.

A number of physiological and synthetic progestins were tested for their ability to compete with [3H]dexamethasone for the binding to the glucocorticoid receptor of human mononuclear leukocytes and their ability to elicit glucocorticoid-like effects on the same cells. As compared to the reference compound dexamethasone (relative receptor binding affinity defined as 100%), two potent synthetic progestins with a pregnane-type structure, megestrol acetate and medroxyprogesterone acetate, were found to display a considerable binding affinity towards the receptor (46 and 42%, respectively). The relative binding affinity of the naturally occurring ligand, cortisol, to the receptor was clearly lower (25%). The effective binding of medroxyprogesterone acetate to the glucocorticoid receptor was confirmed by direct binding studies utilizing a tritiated derivative of this steroid. No evidence for the existence of a specific progesterone receptor in human mononuclear leukocytes was obtained as judged by the results of competition experiments where a progesterone receptor-specific ligand [3H]Org 2058 was used. Medroxyprogesterone acetate and megestrol acetate also induced glucocorticoid-like effects on the lymphocyte functions. These included inhibition of the proliferative responses to the T-cell mitogens concanavalin A and phytohaemagglutinin and an enhanced accumulation of immunoglobulin secreting cells in pokeweed mitogen-stimulated cultures. The progestin effect appears to be mediated through a radiosensitive (suppressor) subpopulation of T lymphocytes. In contrast, the synthetic progestins related structurally to 19-nortestosterone, norethisterone and d-norgestrel, were virtually devoid of binding affinity towards the glucocorticoid receptor nor did they measurably influence the in vitro lymphocyte functions. These studies demonstrate that certain progestins in common clinical use probably possess inherent glucocorticoid activity and suggest that side effects attributable to this character (e.g. suppression of the pituitary-adrenal axis) might be expected when these compounds are used in pharmacological doses.

DNA Replication↗

PubMed1979

In vitro inhibition of rat uterine contractility induced by 5 alpha and 5 beta progestins.

Ten natural progestins were evaluated for their capacity to inhibit the in vitro motility of rat's uterus. Progestins with their ring A reduced in the 5 beta position were significantly more potent than delta 4-3 keto and 5 alpha reduced progestins. These last progestins were ineffective to inhibit uterine motility excepting 3 alpha-hydroxy-5 alpha-pregnan-20-one which was slightly less effective than progesterone. The potency of the progestins to inhibit uterine motility was related to their capacity to induce membrane stabilization. The data indicates that 5 beta, but not 5 alpha reduction of progesterone, may be important for regulating myometrial activity.

20-alpha-Dihydroprogesterone↗

PubMed1983

Diethylpyrocarbonate, a histidine selective reagent, inhibits progestin binding to chick oviduct cytosol.

In this report we describe experiments showing that diethylpyrocarbonate, a histidine selective reagent, inhibits progestin binding to the chick oviduct progesterone receptor. Because this inhibition is reversed by hydroxylamine, we suggest that the chick oviduct progesterone receptor contains one or more histidine residues that regulate progestin binding. We also find that the progestin R5020 protects the progesterone receptor from diethylpyrocarbonate mediated inhibition of progestin binding. From this we infer that the progestin binding site contains a histidine residue(s) important for progesterone binding to its receptor in chick oviduct.

Animals↗

PubMed1988

Cyclosporine differentially affects estrogen and progestin synthesis by rat granulosa cells in vitro.

Potential side-effects of the immunosuppressive drug cyclosporine (also cyclosporin A, CsA) on ovarian endocrine function have been investigated using granulosa cells isolated from immature estrogen-primed rats and cultured in a chemically defined medium. The FSH-dependent differentiation of steroidogenic pathways for estrogen and progestin secretion was shown to be differentially affected by CsA in vitro, at drug concentrations that approximate immunosuppressive concentrations in blood of humans or animals. CsA at 0.1-1 microgram/ml synergistically enhanced FSH-stimulated aromatase activity as measured by the conversion of exogenous testosterone to 17 beta-estradiol, while production of the progestins (progesterone + 20 alpha-hydroxypregn-4-en-3-one + pregnenolone) was little affected at up to 0.1 microgram/ml CsA and reduced at higher concentrations. CsA alone did not stimulate basal steroid secretion. The action of CsA to augment FSH-stimulated induction of aromatase activity was seen both in the presence or absence of testosterone. The effects of CsA (1 microgram/ml), either stimulatory on aromatase activity or inhibitory on progestin secretion, were in general increased with greater times of cell exposure throughout the culture period, although the temporal effects on 17 beta-estradiol and the progestins were not identical following delayed addition or removal of CsA from the culture medium. Higher concentrations of CsA (3-10 micrograms/ml) were generally toxic to granulosa cells as indicated by marked decreases in 17 beta-estradiol and progestin secretion and in incorporation of [3H]leucine. These results suggest that therapeutic concentrations of CsA might directly influence ovarian function by differentially modulating the FSH-dependent steroidogenic pathways of granulosa cells.

Animals↗

PubMed1980

Characterization of a progestin-binding component in lactating rat mammary glands.

Experiments were carried out to identify progestin-binding receptors in the mammary gland where casein synthesis is known to be inhibited by this hormone. A progestin-binding component with high affinity, low capacity and a sedimentation coefficient of 8.8 S was isolated from the cytosol of lactating rat mammary glands. This component strongly bound [3H]R5020 (17,21-dimethyl-19-nor-4,9-pregnadiene-3,20-dione) with a dissociation constant of 3.9 . 10(-9) M under low-salt conditions and with that of 8.2 . 10(-10) M in the presence of 0.3 M KCl. Specificity studies showed a high degree of progestin specificity under high salt conditions. In the absence of KCl, binding of [3H]-R5020 was inhibited by unlabeled glucocorticoid in the same degree as unlabeled progestin, but the inhibition by glucocorticoid was greatly diminished by the presence of 0.3 M KCl. These observations suggest that the [3H]R5020-binding-component is the progestin receptor and that its function may be regulated by the concentration of glucocorticoid and salt.

Animals↗

PubMed1996

Cancer risk in women receiving estrogen-progestin replacement therapy.

OBJECTIVES AND METHODS: The epidemiological literature was reviewed in order to evaluate the relationship between hormone replacement therapy and risk of cancer in the breast and reproductive organs. RESULTS: For breast cancer, there is no evidence of an overall increase in the risk. According to several studies, but not all, the duration of intake seems to affect the risk. Many years of intake of both estradiol compounds and conjugated estrogens can be assumed to increase the risk of breast cancer 1.5-2-fold. The addition of progestins does not seem to alter (reduce) the duration-risk relationship. The magnitude of risk increase is likely to be small and may be explained partly by methodological problems, or by differences in study populations. The prognosis in patients with HRT-related breast cancer seems to be more favourable than for non-exposed breast cancer patients. Because of the importance of the issue, and inconsistencies in results, further research is urgent. Especially, there is an urgent need to define sub-groups of women who would be susceptible to an adverse influence of HRT. Regarding endometrial cancer, a duration-dependent strong risk relationship with long-term intake of estrogens only is established. The level of risk increase is about 10-fold after 10 or more years of intake, a risk relationship that seems to decrease after discontinuation of treatment. Added progestins for at least 10 days per cycle can reduce or eliminate the risk increase. Tumors occurring after estrogen replacement have favourable biological characteristics. Future research will be needed to define the long-term safety of various progestin regimens. Ovarian cancer risk does not seem to be affected by HRT. Available data are inconsistent and contradictory. Due to the pronounced protective effect of oral contraceptives, further research is needed to measure effects of estrogen-progestin combined regimens. Cervical cancer risk has not been shown to be affected by HRT. CONCLUSIONS: It is concluded that hormone replacement therapy, with estrogens alone or estrogens combined with progestins, may have important effects on the risk of cancer, particularly in the breast and endometrium. Therefore, when making a risk-benefit assessment of long-term HRT, possible risk relationships should be considered.

Breast Neoplasms↗

PubMed1996

Estrogens, progestins and lipid metabolism.

OBJECTIVES: To review some aspects in the recent literature related to the effects of postmenopausal estrogen and progestin use on major plasma lipoprotein risk factors for coronary heart disease (CHD). METHODS: Collection of relevant information from medical journals, and by the use of Medline and Current Contents. RESULTS: The beneficial effects of estrogen (LDL cholesterol reduction and HDL cholesterol elevation) are well established. The effects on HDL are modified to different degrees by progestins, depending on the androgenic properties of the latter: the 'sex steroid sensitive' HDL2 subfraction is decreased by nortestosterone derived progestins with androgenic activity. Recently developed methodology employing stable isotopes has helped to clarify underlying mechanisms. Progestins alone, as well as estrogen-progestin combinations have been shown to reduce the plasma levels of Lp(a), another lipoprotein risk factor for CHD. According to one study, estrogen administered alone had a similar effect. CONCLUSIONS: The effects of hormone replacement therapies on lipid metabolism have been partly established and investigations on the underlying mechanisms are being published. This information will be useful for developing new replacement regimens with more protection against CHD and less adverse effects.

Adult↗

PubMed1994

A comparison of the pregnancy-terminating potencies of three anti-progestins in guinea-pigs, and the effects of sulprostone.

The anti-progestins mifepristone, lilopristone (ZK 98734) and HRP 2000 were equipotent at terminating the pregnancy of guinea-pigs during mid-gestation, although mifepristone was more effective at low doses. Sulprostone administration on the day following anti-progestin treatment tended to increase the effectiveness of mifepristone and HRP 2000, without affecting the time interval between the start of the anti-progestin treatment and the day of abortion. It is concluded that, of the three afferent anti-progestins used, none is more potent than the other two at terminating pregnancy in the animal model used. The co-administration of a prostaglandin E2 (PGE2) analogue tends to increase the effectiveness of the anti-progestin.

Abortifacient Agents↗

PubMed1993

The relationship between affinity of progestins and antiprogestins for the progesterone receptor in breast cancer cells (ZR-PR-LT) and ability to down-regulate the receptor: evidence for heterospecific receptor modulation via the glucocorticoid receptor.

In a human breast cancer cell line (ZR-PR-LT) we have found a poor overall correlation between affinity of progestins and anti-progestins for the progesterone receptor (PGR), concentration required for receptor down-regulation and anti-proliferative potency. Medroxyprogesterone acetate (MPA) and the anti-progestin RU 38.486, which possess glucocorticoid and antiglucocorticoid activity, respectively, cause receptor down-regulation at lower concentrations than their Kdi for [3H] ORG 2058 binding sites. In addition dexamethasone markedly down-regulates PGR at concentrations which fail to interact with PGR suggesting that heterospecific modulation of PGR occurs via the glucocorticoid receptor. In contrast the progestin ORG2058 and the anti-progestin ZK 98.299 caused 50% PGR down-regulation at a concentration (EC50) 50-fold higher than their Kdi values. ZK 112.993 was 500-fold more potent at PGR down-regulation than ZK 98.299 but had only a 5-fold higher affinity for PGR. Anti-proliferative concentrations of progestins/anti-progestins showing were generally higher than either Kdi values or EC50 values.

Binding, Competitive↗

PubMed2004

In vitro and ex vivo evidence for modulation of P-glycoprotein activity by progestins.

The well known gender-related differences in drug action may partly be explained by changes in activity and expression of drug metabolising enzymes, but also by modulation of active drug transport systems (e.g. P-glycoprotein, Pgp) by sexual steroids, which is yet not well investigated. Because many women are using hormones (e.g. as oral contraceptives) we investigated the influence of different synthetic progestins on Pgp activity. Pgp inhibition of progesterone, medroxyprogesterone, chlormadinone, cyproterone, levonorgestrel, norethisterone, desogestrel, and norgestimate was measured in vitro in two Pgp over-expressing cell lines (L-MDR1, P388/dx cells) and the corresponding parental cell lines by means of calcein assay, and ex vivo in human peripheral blood mononuclear cells (PBMCs) by rhodamine123 efflux. For most progestins tested, concentrations needed to double baseline fluorescence (f2) in L-MDR1 cells were similar to that of the potent Pgp inhibitor quinidine, whereas levonorgestrel and norethisterone did not reach f2. The results in P388/dx cells essentially confirmed our findings in L-MDR1 cells. Additionally, Pgp inhibitory activity of all progestins tested was also shown ex vivo in PBMCs. The potent Pgp inhibition by several synthetic progestins in vitro and ex vivo suggests that such an interaction might be clinically relevant despite generally low plasma concentrations of progestins. The results may be of particular importance for Pgp substrates, such as protease inhibitors and chemotherapeutic agents, for which intracellular concentrations are critical.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2004

Absence of an effect of injectable and implantable progestin-only contraceptives on subsequent risk of breast cancer.

Animal data indicate that both estrogens and progestins could be carcinogenic and that progestins could serve as tumor promoters. Human studies have not confirmed an increased risk of breast cancer from long-term use of oral contraceptives, but have shown an increased risk from hormone replacement therapy including progestins. The present study analyzed the relationship between breast cancer and use of injectable and implantable progestin-only contraceptives. Analyses were performed on data collected in a population-based, multicenter, case-control study, the Women's Contraceptive and Reproductive Experiences Study of the National Institute of Child Health and Human Development. The study involved 4575 randomly sampled cases with invasive breast cancer diagnosed between 1994 and 1998, and 4682 controls, identified using random digit dialing. We assessed the association between exposure to injectable contraceptives and risk of breast cancer. The use of injectable contraceptives was not associated with an increased risk of breast cancer [odds ratio (OR) = 0.9, 95% confidence interval (CI): 0.7, 1.2]. Risk was not increased among current users, defined as women who used injectable contraceptives within 1 year of the reference date (OR = 0.7, 95% CI: 0.4, 1.3) or those who initiated use in the 5 years immediately preceding the reference date (OR = 0.9, 95% CI: 0.5, 1.4), or with use beginning before age 35 (OR = 0.9, 95% CI: 0.6, 1.3). Among users, risk increased with increasing duration of use (p = 0.03). However, short-term users (<6 months duration) were at decreased risk relative to never users (OR = 0.6, 95% CI: 0.4, 1.0). When the short-term users were then excluded from the duration-response analysis, the slope of the duration-response became slightly (and nonsignificantly) negative. Risk was not increased among women with 24 or more months of use relative to never users (OR = 1.4, 95% CI: 0.8, 2.5). No increased risk was seen from implantable contraceptives either, although the sample sizes were small. This study does not support an increased risk of breast cancer associated with the use of injectable or implantable progestin-only contraceptives in women aged 35 to 64.

Absorbable Implants↗

PubMed2003

Classification and pharmacology of progestins.

Besides the natural progestin, progesterone, there are different classes of progestins, such as retroprogesterone (i.e. dydrogesterone), progesterone derivatives (i.e. medrogestone) 17alpha-hydroxyprogesterone derivatives (i.e. chlormadinone acetate, cyproterone acetate, medroxyprogesterone acetate, megestrol acetate), 19-norprogesterone derivatives (i.e. nomegestrol, promegestone, trimegestone, nesterone), 19-nortestosterone derivatives norethisterone (NET), lynestrenol, levonorgestrel, desogestrel, gestodene, norgestimate, dienogest) and spironolactone derivatives (i.e. drospirenone). Some of the synthetic progestins are prodrugs, which need to be metabolized to become active compounds. Besides the progestogenic effect, which is in common for all progestins, there is a wide range of biological effects, which are different for the various progestins and have to be taken into account, when medical treatment is considered.

Female↗