Disease relevance of MEDROGESTONE

• Medrogestone is a progestational agent that may reduce outflow obstruction secondary to benign prostatic hyperplasia [1].
• In the present study we explored the effect of Medrogestone (Prothil) on 17beta-hydroxysteroid dehydrogenase (17beta-HSD) activities of the hormone-dependent MCF-7 and T-47D human breast cancer cell lines [2].
• OBJECTIVES: To evaluate the effectiveness of transdermal oestrogen replacement therapy plus medrogestone (HRT) in postmenopausal bone loss prevention by means of US [3].

High impact information on MEDROGESTONE

• CONCLUSIONS: The administration of CEE with cyclical medrogestone supplementation to postmenopausal women induces a statistically significant reduction in the PI of cerebral arteries [4].
• Medrogestone: a prospective study in the pharmaceutical management of benign prostatic hyperplasia [1].
• Control of sulfatase and sulfotransferase activities by medrogestone in the hormone-dependent MCF-7 and T-47D human breast cancer cell lines [5].
• In addition, it was demonstrated that different progestins (medrogestone, nomegestrol acetate, TX-525) and org OD14 can stimulate the sulfotransferase activity for the formation of the biologically inactive E1S [6].
• Medrogestone significantly inhibits this transformation, at all the concentrations tested (5x10(-8) to 5x10(-5) mol/l), in both cell lines [5].

Chemical compound and disease context of MEDROGESTONE

• In the present study, we explored the effect of the progestin medrogestone on the sulfatase and sulfotransferase activities in the hormone-dependent MCF-7 and T-47D human breast cancer cell lines [5].
• It was demonstrated that in the hormone-dependent breast cancer cells, various progestins (nomegestrol acetate, tibolone, medrogestone, promegestone) are potent sulfatase inhibitory agents [7].

Biological context of MEDROGESTONE

• BACKGROUND: Two sequential hormone replacement regimens, containing either estradiol valerate plus medroxyprogesterone acetate (E2V/MPA) or conjugated estrogens plus medrogestone (CE/MED), were compared with respect to effects on climacteric symptoms, lipid metabolism, and hemostasis [8].
• Twenty-three cases of the climacteric syndrome were analysed in a double-blind study comparing the effect of conjugated equine oestrogen (Premarin) and medrogestone (Colpro) with clonidine (Dixarit) on various clinical parameters [9].
• Effects of conjugated equine oestrogens with and without the addition of cyclical medrogestone on hot flushes, liver function, blood pressure and endocrinological indices [10].

Anatomical context of MEDROGESTONE

• On the contrary, the same dose of medrogestone induced a consistent decrease of estrogen primed endometrium with only 4 cases of full secretory transformation [11].
• In the intact adult rat, medrogestone was found to be effective in causing the involution of the prostate and seminal vesicle [12].

Associations of MEDROGESTONE with other chemical compounds

• The effect of medrogestone on plasma lipids and lipoproteins in postmenopausal women using conjugated estrogens: an open randomized comparative study [13].
• Effects of medrogestone (6,17 alpha-dimethyl-4-,6-pregnadiene-3, 20-dione; Colprone) on the release of testosterone (T) and 5 alpha-dehydrotestosterone (5 alpha-DHT) in the reproductive organs of the male rat were tested in vitro [14].
• In estrogen receptor-positive and lymph-node-negative patients, treatment by a nonaromatizable progestin, such as medrogestone or medroxyprogesterone acetate (MPA), can be introduced to relieve the patient from her postmenopausal syndrome [15].

Gene context of MEDROGESTONE

• Medrogestone has a biphasic effect on sulfotransferase activity in both cell lines [5].
• This effect may be due to glucocorticoid receptor mediated actions of medrogestone on bone [16].
• More 5 alpha-DHT was released into the medium from the testes mince in the presence of hCG, while the addition of 10 or 50 micrometers of Colprone inhibited 5 alpha-DHT release as compared to hCG controls [14].
• Medrogestone had a synergistic effect on the lowering of FSH, LH and PRL [10].
• RFA Argus, the Air Training Ship, was identified as the potential Primary Casualty Reception Ship (PCRS) and at the end of September 1990 plans were drawn up to convert the forward hangar into a two-storey 100-bed hospital in collective protection (COLPRO) [17].

Analytical, diagnostic and therapeutic context of MEDROGESTONE

• After 24 h of the cell culture, Medrogestone significantly inhibits this transformation in a dose-dependent manner by 39% and 80% at 5 x 10(-8) M and 5 x 10(-5) M, respectively in T-47D cells; the effect is less intense in MCF-7 cells: 25% and 55% respectively [2].
• Twenty patients, aged 30-60 yr, who had undergone bilateral ovariectomy, were treated orally with 5 mg medrogestone (6,17-dimethylpregna-4,6-diene-3,20-dione) and 1.25 mg conjugated oestrogens per day, according to a constant dosage pattern during the cycle (22 + 6 days) [18].
• Determination of medrogestone in plasma by high-performance liquid chromatography [19].
• The limit of quantitative concentration for medrogestone in HPLC was 1 ng/ml [19].
• Argus arrived in the Gulf in mid-November as the PCRS with, all in COLPRO, a 10-bed intensive care unit (ICU), a 14-bed high dependency unit (HDU), a 76-bed low dependency unit (LDU) plus four operating tables in two theatres with full support services [17].

References