Disease relevance of Medroxyprogesterone acetate

• Based on these data we now manage hot flashes associated with LHRH analogues with 400 mg of MPA [1].
• Serum levels of cortisol (C), androstenedione (A), dehydroepiandrosterone (D), estrone (E1) and estradiol (E2) were chosen as parameters to compare the bioavailability of megestrol acetate (MA) and medroxyprogesterone acetate (MPA) in postmenopausal patients with advanced breast cancer [2].
• OBJECTIVE: To evaluate endocrine responses to short-term medroxyprogesterone acetate (MPA) administered as a respiratory stimulant in postmenopausal women with mild nocturnal hypoxemia [3].
• Therefore, we investigated whether in vivo exposure to 17beta-estradiol (E) and/or P or MPA modifies inflammation in the cerebral vasculature, a key process in the evolution of ischemic brain injury [4].
• OBJECTIVE: To determine the efficacy of medroxyprogesterone acetate (MPA), 50 mg/d for 3 months, in treating endometriosis, with a follow-up of 6 months [5].

Psychiatry related information on Medroxyprogesterone acetate

• RESULTS: MPA exposure 4 or 6 weeks after DMBA reduced the latency period for appearance of tumors in a dose-dependent manner and increased tumor incidence [6].
• CEE + MPA did not significantly influence positive affect, negative affect, or depressive symptoms [7].
• The time study of the effect of E showed that enhancement of AA required at least 10 h of incubation of E with MPA conditioned cells [8].
• Heart rate variability (HRV) was calculated in time and frequency domains during various sleep stages on and off MPA, and the results were correlated to respiratory variables [9].
• Forty men, ages 16 to 78 years, with sex-offending behavior, were treated with combined medroxyprogesterone acetate (MPA), group therapy, and individual psychotherapy [10].

High impact information on Medroxyprogesterone acetate

• Stimulation of L-plastin synthesis by E2 and MPA was also evident by examination of protein synthesis using high-resolution two-dimensional gel electrophoresis and Western blotting [11].
• There were no significant changes in MPA area under the concentration curve, peak or trough concentrations, or apparent clearance in the nelfinavir, efavirenz, or nevirapine groups compared to the control group [12].
• EXPERIMENTAL DESIGN: Medroxyprogesterone acetate (MPA) pellets were implanted 2, 4, or 6 weeks after DMBA exposure; RU-486 was given 3 days before MPA [6].
• RU-486 delayed the latency period and decreased tumor incidence in animals exposed to MPA at 4 weeks after DMBA treatment, indicating that the progesterone receptor may be partially responsible for transmission of proliferative signals [6].
• Treatment with trilostane, P(4), 21OH-6OP, or MPA plus 21OH-6OP reversed P(4) and MPA up-regulation of PGDH activity [13].

Chemical compound and disease context of Medroxyprogesterone acetate

• RU-486 also delayed the latency period but failed to reduce overall tumor incidence when animals were exposed to MPA at 6 weeks after DMBA treatment, indicating that other factors may also control MPA-induced acceleration [6].
• This study evaluated the effectiveness of parenteral medroxyprogesterone acetate (MPA) in reducing the frequency and severity of these hot flashes [1].
• Since one of the possible explanations for this effect was its progestagenic effects, we decided to investigate whether progesterone (Pg) alone could also induce mammary adenocarcinomas in our model and if MPA at doses lower than those used to establish the model was also carcinogenic [14].
• Oestrogen receptor (ER) and progesterone receptor (PR) content and the response in vitro to tamoxifen (T), medroxyprogesterone acetate (MPA) and to a combination of the two hormones were determined in 21 epithelial ovarian carcinomas [15].
• CONCLUSION: Treatment with LA depot plus conjugated equine Es and MPA for 2 years was a safe and effective therapy for women with endometriosis and pelvic pain in this small retrospective study [16].

Biological context of Medroxyprogesterone acetate

• To study RU 486 involvement in steroid withdrawal leading to menstruation, HESCs were decidualized during 10 days incubation with E2 + MPA, and parallel cultures were kept in E2 + MPA or withdrawn to either control or RU 486-containing medium [17].
• MPA stimulated cell growth and PRL production rate during days 5-20 of culture [18].
• This combination of CEE and MPA resulted in a 60% improvement (P less than 0.05) compared to the luteal phase of control months in both behavioral (14.1 +/- 3.9 vs. 4.2 +/- 0.8) and total (17.8 +/- 4.8 vs. 6.5 +/- 1.8) symptoms [19].
• However, it appears that MPA with significant glucocorticoid (GC) activity may decrease bone density [20].
• 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 [21].

Anatomical context of Medroxyprogesterone acetate

• PRL was one of the five major secretory proteins (23-25K, 32K, 42K, 78K, and 150K daltons, sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reducing condition) induced by MPA and RLX in endometrial stromal cells [18].
• To study the interaction of P(4) and F on the regulation of PGDH, we treated chorion and placental trophoblast cells in culture with combinations of F, dexamethasone, P(4), trilostane, and medroxyprogesterone acetate (MPA) [22].
• A representative analogue, 8, demonstrated similar oral potency to MPA in the uterine wet weight/mammary gland morphology assay in ovariectomized rats [23].
• Serum progesterone concentrations remained low, and corpora lutea regressed, although viable fetuses were maintained with MPA [24].
• MPA down-regulated PgR content and increased uterus weight (36%), but failed to modify ER and PgR nuclear retention [25].

Associations of Medroxyprogesterone acetate with other chemical compounds

• Progesterone was 20-40% less effective in stimulating PRL than MPA [18].
• Immunoblot analysis using a specific polyclonal antibody against stromelysin-1 revealed that the progestin medroxyprogesterone acetate (MPA) produced a time-dependent reduction in a band at 50,000 mol wt [26].
• E2, MPA, E2 plus MPA, and GnRH analog treatments resulted in an increase in total TGF beta 1 production, whereas GnRH agonist and GnRH-Ant2, but not GnRH-An1, inhibited active TGF beta 1 (P < 0.05) [27].
• In a primate model for long-term HRT, surgically, postmenopausal cynomolgus macaques were treated for 35 months with conjugated equine estrogens (CEE), medroxyprogesterone acetate (MPA), CEE + MPA and tamoxifen (n = 5 in all groups) [28].
• We examined the effects of two clinically used progestogens, progesterone and medroxyprogesterone acetate (MPA), on prostacyclin production by cultured human umbilical vein endothelial cells (HUVEC) and the possible role of progesterone receptors and both COX enzymes [29].

Gene context of Medroxyprogesterone acetate

• The expression of p27 in hyperplastic epithelia before the MPA treatment was negligible, whereas it was greatly increased after the treatment [30].
• Progesterone and MPA, both at 10 nmol/l, increased mRNA expression and protein content of both COX [29].
• RESULTS: With MPA, FSH decreased 42.7% (P <.001, 95% confidence interval [CI] -54.2, -31.6), LH 62.1% (P <.01; 95% CI -81. 0, -32.6), and SHBG 58.1% (P <.001; 95% CI -63.0, -43.9) [31].
• Tam + MPA association produced the same results as Tam alone for ER and PgR nuclear retention, but receptor content was not significantly different from that of controls [25].
• In stromal cells, MPA alone caused a slight increase (2-4-fold) of the production rate of IGFBP-1 whereas MPA plus RLX synergistically increased (>40-fold) the IGFBP-1 production [32].

Analytical, diagnostic and therapeutic context of Medroxyprogesterone acetate

• Postmenopausal women received daily doses of conjugated equine estrogen (CEE, 0.625 mg) plus medroxyprogesterone acetate (MPA, 2.5 mg) (standard-dose group, n = 18), CEE (0.3 mg) plus MPA (2.5 mg) (low-dose group, n = 18), or no treatment (control group, n = 15) for 3 months [33].
• After treatment with CE and medroxyprogesterone acetate (MPA), LH and PRL both increased (P less than 0.05 and P less than 0.01, respectively) [34].
• Quantitative real-time RT-PCR analysis showed a rapid and strong upregulation of hDlg5 mRNA in cells treated with synthetic progestin medroxyprogesterone acetate (MPA) in the presence of estrogen in MCF-7, T47D and ZR-75-1 cells [35].
• C(21) Progestin medroxyprogesterone acetate (MPA) is one of the most commonly prescribed progestins for hormone replacement therapy and in gynecologic practice [20].
• OBJECTIVES: To evaluate the effect of medroxyprogesterone acetate (MPA) therapy on pulmonary arterial pressure (PAP), exhaled nitric oxide (NO), electrocardiogram (ECG), and on arterial blood gases (ABG) [36].

References