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PubMed1994

Trabecular bone in long-term depot-medroxyprogesterone acetate users.

A cross-sectional study was designed to determine trabecular bone density in 75 long-term depot-medroxyprogesterone acetate (DMPA) users (> 3 yr) matched with non-DMPA users by age, body mass index (18-25), limitation of age (< 45 yr), and body weight (< 60 kg). The long-term DMPA cases were divided into 3 groups according to duration of injectable contraceptive use. Neither cases nor controls had a smoking or chronic alcohol consumption history. Cases and controls were matched by age. Trabecular bone of the femoral neck were assessed by X-ray and interpreted by a single-blinded radiologist. Trabecular bone patterns were graded according to Singh's Index. Blood collection for determination of estradiol, prolactin, calcium, phosphorus, and medroxyprogesterone acetate were performed in cases and controls. Venous blood was taken at twelfth week of injection of DMPA and within 5 days after menstrual bleeding cessation in the controls. Mean trabecular bone in the cases was 5.5 +/- 0.6 (range 4-6). It was not statistically different from that in the controls (mean 5.5 +/- 0.6, range 2-6). No statistically significant difference of serum, calcium, phosphorus, prolactin, and estradiol was seen in the cases when compared to controls at mid follicular phase of normal menstrual cycle. Serum MPA of individual case at twelfth week of injection was 4.1 +/- 1.1 nmol/l. In conclusion, trabecular bone density in long-term DMPA users were not statistically different from normal menstruating women who have not received injectable DMPA.

Adolescent↗
PubMed1995

Continuous combined piperazine oestrone sulphate and medroxyprogesterone acetate hormone replacement therapy--a study of bleeding pattern, endometrial response, serum lipid and bone density changes.

This pilot study was conducted to establish the optimum oral dosage of medroxyprogesterone acetate (Provera) given daily in combination with a fixed dose of piperazine oestrone sulphate (Ogen), as hormone replacement therapy. A group of 32 nonhysterectomized, symptomatic menopausal women were randomly allocated to receive piperazine oestrone sulphate 1.25 mg daily and medroxyprogesterone acetate 2.5 mg, 5 mg or 10 mg daily for a 2-year period. This was an open study and the patients were reviewed at 3-monthly intervals for 2 years. Vaginal bleeding was reported by 58% of patients after the first 3 months of treatment. There was a gradual decline in the reported incidence of bleeding over the following 6 months particularly by women in the 5 mg and 10 mg Provera group. Only 10% of patients were still recording slight bleeding in the 10 mg group at 12 months. By 24 months all the women in the 5 mg and 10 mg Provera groups had ceased bleeding. There were 2 patients in the 2.5 mg Provera group with persistent proliferative endometrium at 24 months. All the remaining patients had atrophic endometrium. There was no significant difference in serum lipid changes between the 3 groups, but there was an overall reduction in total cholesterol, triglycerides and low density lipoprotein cholesterol in all women. There was no significant difference in bone mineral density changes between the groups over the 2-year period. Endometrial protection with increased incidence of amenorrhoea, without significant adverse effects, was seen with the use of 5 mg and 10 mg of provera.

Administration, Oral↗
PubMed1997

High-dose medroxyprogesterone acetate for the treatment of dysfunctional uterine bleeding in 24 adolescents.

The objective of the study was to evaluate the effectiveness of high-dose oral medroxyprogesterone acetate therapy in the management of excessive dysfunctional uterine bleeding in adolescents. The study group consisted of 24 adolescents who were hospitalized with the diagnosis of excessive uterine bleeding and anaemia. Oral medroxyprogesterone acetate tablets were administered at a total dose of 60-120 mg during the first day of admission and 20 mg per day for the following 10 days. The blood loss was reduced to acceptable levels in all patients, and actually stopped in 6 (25%) within the first 24 hours of the treatment; bleeding ceased in 29.2%, 20.8% and 25% on the second, third and fourth days respectively. Significant correlation was identified between the initial haemoglobin concentration and the time required for cessation of bleeding (r2 = 0.5, p = 0.001). Rapid saturation of the endometrium with progestogens seems to be an highly effective mode of treatment for excessive dysfunctional uterine bleeding in adolescents.

Adolescent↗
PubMed2004

Effects of conjugated equine estrogen and medroxyprogesterone acetate on lipoprotein(a) and other lipoproteins in japanese postmenopausal women with and without dyslipidemia.

BACKGROUND/AIM: The cardiovascular effects of postmenopausal hormone replacement are controversially discussed. We investigated the effects of 12 months of treatment with conjugated equine estrogen and medroxyprogesterone acetate on lipoprotein(a) [Lp(a)] and other lipoproteins in Japanese postmenopausal women (PMW) with and without dyslipidemia. METHODS: Forty-three normolipidemic and 17 dyslipidemic PMW [total cholesterol (TC) >/=220 mg/dl or triglyceride (TG) >/=150 mg/dl] received conjugated equine estrogen (0.625 mg) plus medroxyprogesterone acetate (2.5 mg) daily for 12 months, and the results were compared with those of 26 normolipidemic and 14 dyslipidemic subjects declining this treatment as controls. The fasting serum levels of Lp(a), TC, TG, high-density lipoprotein cholesterol, low- density lipoprotein cholesterol, apolipoprotein (Apo) AI, Apo AII, Apo B, Apo CII, and Apo E were measured in each subject at baseline and 12 months after this treatment initiation. RESULTS: The treatment decreased Lp(a) similarly in normolipidemic and dyslipidemic PMW and decreased TC, low-density lipoprotein cholesterol, Apo CII, and Apo E and increased high-density lipoprotein cholesterol, Apo AI, and Apo AII in both groups. The therapy also significantly increased TG in normolipidemic but not dyslipidemic subjects. In controls, the levels of Lp(a) and other lipoproteins were unaltered. CONCLUSIONS: In PMW with or without dyslipidemia, improvement in Lp(a) and other lipoproteins may represent cardiovascular benefits of hormone replacement therapy. However, an elevation of the TG levels seen with the therapy warrants caution, especially in PMW without dyslipidemia.

Asian People↗
PubMed1997

Effects of conjugated estrogens with or without medroxyprogesterone acetate on mammary carcinogenesis, uterine adenomyosis and femur in mice.

Although combined hormone replacement therapy using estrogens and progestins reduces the risk of endometrial cancer in postmenopausal women, it has been unclear whether the combined therapy is associated with an alteration of the risk of mammary cancer. Virgin mice of the SHN strain, which has a high potential for the development of mammary cancer and uterine adenomyosis, were given diets containing conjugated estrogens with or without medroxyprogesterone acetate for 230 days. The combined administration of conjugated estrogens and medroxyprogesterone acetate completely suppressed the development of uterine adenomyosis with a decrease in uterine thymidylate synthetase activity, significantly enhanced the bone mineral density in the femur and slightly shortened the latent period of mammary carcinogenesis.

Adenoma↗
PubMedDate not supplied

Pulmonary lymphangioleiomyomatosis: a case report in postmenopausal woman treated with pleurodesis and progesterone (medroxyprogesterone acetate).

The main problem in the treatment of pulmonary lymphangioleiomyomatosis, which frequently occurs in the reproductive age, is the control of chylothorax and disease progression. We herein report a case of a 62-year-old woman who underwent surgery for recurrent chylothorax. Histologic examination of lung and lymph node biopsies demonstrated lymphangioleiomyomatosis. Thirty-six months after tetracycline pleurodesis and high-dose medroxyprogesterone acetate therapy, the disease was stable and cyclothorax effectively controlled. It would therefore appear that hormonal treatment with medroxyprogesterone acetate may be beneficial in postmenopausal women.

Antineoplastic Agents, Hormonal↗
PubMed2002

Combined treatment with acetazolamide and medroxyprogesterone in chronic obstructive pulmonary disease patients.

Medroxyprogesterone acetate (MPA) and acetazolamide (ACET) are two ventilatory stimulants which are used in hypoxic and hypercapnic patients with chronic obstructive pulmonary disease (COPD). In a double-blind randomised study, the effects of a 2-week treatment with MPA (30 mg b.i.d.) or ACET (250 mg b.i.d.), followed by a 2-week treatment with a combination of both drugs (MPA/ACET), on daytime and nocturnal ventilatory and blood gas parameters in 17 stable hypercapnic COPD patients were investigated. ACET, MPA and MPA/ACET treatment decreased mean daytime carbon dioxide tension in arterial blood by 0.4, 0.7 and 1.2 kPa, respectively. Minute ventilation was improved only with combined therapy, from 9.3 to 11.2 L x min(-1). With MPA/ACET therapy, the hypercapnic and hypoxic ventilatory responses significantly increased, from 3.7 to 5.8 L x min(-1) x kPa(-1) and from -0.13 to -0.40 L x min(-1) x %(-1), respectively. The mouth exclusion pressure response to hypoxia increased during combination therapy, from -0.01 to -0.03 kPa %(-1). Nocturnal end-tidal carbon dioxide tension decreased with MPA and MPA/ACET treatment, by 0.9 and 1.4 kPa, respectively. MPA/ACET significantly increased mean nocturnal arterial oxygen saturation values, from 85.5 to 90.2%. The authors conclude that short-term combined treatment with medroxyprogesterone acetate and acetazolamide has a more favourable effect on day and night-time blood gas values and chemical drive than single drug treatment.

Acetazolamide↗
PubMed2002

Effect of medroxyprogesterone on arterial blood gases, leptin and neuropeptide Y in postmenopausal females.

Natural progesterone, a potent respiratory stimulant, stimulates leptin production in premenopausal females. Leptin and its counterpart neuropeptide Y (NPY) have recently been linked with respiration. The effect of medroxyprogesterone acetate (MPA) on arterial blood gases, serum leptin and NPY was evaluated in this study. Fourteen postmenopausal females with respiratory impairment, due mostly to chronic obstructive pulmonary disease, were recruited for a randomised, double-blind, placebo-controlled crossover trial. Arterial blood gases, serum leptin and NPY concentrations were measured at baseline and after 14 days of treatment with placebo and MPA, separated by a 6-week washout period. Thirteen patients completed the trial. The mean+/-SD carbon dioxide tension in arterial blood (Pa,CO2) was 5.4+/-0.6 kPa at baseline, and decreased by 0.8+/-0.3 kPa during treatment with MPA. The oxygen tension in arterial blood (Pa,O2) and pH did not change. At baseline, the mean base excess was 0.6+/-1.9 mmol x L(-1) and the mean bicarbonate (HCO3-) concentration was 25.1+/-1.6 mmol x L(-1). With MPA, base excess decreased by 2.2+/-1.2 mmol x L(-1) and HCO3- by 1.9+/-1.0 mmol x L(-1) from baseline. The mean concentrations of serum leptin (19.8+/-9.9 microg x L(-1) at baseline, 19.7+/-9.8 microg x L(-1) with MPA) or NPY (94.0+/-18.3 pmol x L(-1) at baseline, 85.1+/-41.2 pmol x L(-1) with MPA) did not change. However, the reduction in Pa,CO2 correlated with the reduction of serum leptin concentration. Medroxyprogesterone acetate effectively decreased the carbon dioxide tension in postmenopausal females with chronic respiratory impairment. The results suggest that a decrease in the carbon dioxide tension of > or = 0.9 kPa is necessary for a reduction in serum leptin concentration.

Aged↗
PubMed2005

Medroxyprogesterone improves nocturnal breathing in postmenopausal women with chronic obstructive pulmonary disease.

BACKGROUND: Progestins as respiratory stimulants in chronic obstructive pulmonary disease (COPD) have been investigated in males and during wakefulness. However, sleep and gender may influence therapeutic responses. We investigated the effects of a 2-week medroxyprogesterone acetate (MPA) therapy on sleep and nocturnal breathing in postmenopausal women. METHODS: A single-blind placebo-controlled trial was performed in 15 postmenopausal women with moderate to severe COPD. A 12-week trial included 2-week treatment periods with placebo and MPA (60 mg/d/14 days). All patients underwent a polysomnography with monitoring of SaO2 and transcutaneous PCO2 (tcCO2) at baseline, with placebo, with medroxyprogesterone acetate (MPA 60 mg/d/14 days), and three and six weeks after cessation of MPA. RESULTS: Thirteen patients completed the trial. At baseline, the average +/- SD of SaO2 mean was 90.6 +/- 3.2 % and the median of SaO2 nadir 84.8 % (interquartile range, IQR 6.1). MPA improved them by 1.7 +/- 1.6 %-units (95 % confidence interval (CI) 0.56, 2.8) and by 3.9 %-units (IQR 4.9; 95% CI 0.24, 10.2), respectively. The average of tcCO2 median was 6.0 +/- 0.9 kPa and decreased with MPA by 0.9 +/- 0.5 kPa (95% CI -1.3, -0.54). MPA improved SaO2 nadir and tcCO2 median also during REM sleep. Three weeks after cessation of MPA, the SaO2 mean remained 1.4 +/- 1.8 %-units higher than at baseline, the difference being not significant (95% CI -0.03, 2.8). SaO2 nadir was 2.7 %-units (IQR 4.9; 95% CI 0.06, 18.7) higher than at baseline. Increases in SaO2 mean and SaO2 nadir during sleep with MPA were inversely associated with baseline SaO2 mean (r = -0.70, p = 0.032) and baseline SaO2 nadir (r = -0.77, p = 0.008), respectively. Treatment response in SaO2 mean, SaO2 nadir and tcCO2 levels did not associate with pack-years smoked, age, BMI, spirometric results or sleep variables. CONCLUSION: MPA-induced respiratory improvement in postmenopausal women seems to be consistent and prolonged. The improvement was greater in patients with lower baseline SaO2 values. Long-term studies in females are warranted.

Aged↗
PubMed1993

Androgen receptor-mediated stimulation of 17 beta-hydroxysteroid dehydrogenase activity by dihydrotestosterone and medroxyprogesterone acetate in ZR-75-1 human breast cancer cells.

The estrogen-sensitive human breast cancer cell line ZR-75-1 was used to study the regulation of 17 beta-hydroxysteroid dehydrogenase (17 beta HSD), the enzyme responsible for the interconversion of estrone (E1) and estradiol (E2). We, thus, investigated the effects of a 6-day exposure to various steroids or growth factors on the reductive (E1-->E2) and oxidative (E2-->E1) 17 beta HSD activities in ZR-75-1 cells as measured during a subsequent 16-h incubation with [3H]E1 or [3H]E2. The reductive 17 beta HSD activity was approximately 3-fold higher than the corresponding oxidative (E2-->E1) activity in control cells, thus favoring the predominance of E2 within the cell. Exposure to dihydrotestosterone (DHT) increased by 1.4-fold the reductive 17 beta HSD activity, with the stimulatory effect exerted at an EC50 value of 0.09 nM DHT, while the oxidative pathway was increased by 4.15-fold at an EC50 value of 0.17 nM. Incubation with medroxyprogesterone acetate, on the other hand, enhanced reductive 17 beta HSD activity by 1.87-fold, while the same treatment increased oxidative 17 beta HSD activity by 2.85-fold; the effects were exerted at EC50 values of 0.4 and 5 nM, respectively. The stimulatory effect of both steroids on 17 beta HSD activity was almost completely reversed by simultaneous exposure to the pure antiandrogen hydroxyflutamide (3 microM), thus supporting an action exerted through the androgen receptor. On the other hand, the synthetic estrogen ethynyl estradiol (EE2) inhibited the reductive and oxidative 17 beta HSD activities by 40% and 33%, respectively, whereas dexamethasone (300 nM) increased by 2.5- and 1.9-fold the reductive and oxidative 17 beta HSD activities, respectively. The present data showing that DHT and the androgenic compound medroxyprogesterone acetate favor the degradation of E2 into E1 suggest that the potent antiproliferative activity of these two compounds in E2-stimulated ZR-75-1 human breast cancer cells could be at least partially exerted through changes in 17 beta HSD activity.

17-Hydroxysteroid Dehydrogenases↗
PubMed1997

Effects of estradiol and medroxyprogesterone-acetate treatment on erythrocyte antioxidant enzyme activities and malondialdehyde plasma levels in amenorrhoic women.

Plasma levels of 17 beta-estradiol (E2) and malondialdehyde and erythrocyte antioxidant enzyme [superoxide dismutase, catalase, and glutathione-peroxidase (GSH-Px)] activities were evaluated in 20 healthy eumenorrhoic women (EW) on day 7 of the menstrual cycle and in 48 secondary hypothalamic amenorrhea patients (AP) (time 0). The AP were randomly divided into four subgroups of 12 subjects and treated with transdermal E2 for 30 days (subgroup A), oral medroxyprogesterone-acetate for 30 days (subgroup B), and transdermal E2 plus medroxyprogesterone-acetate for 30 days (subgroup C). The fourth subgroup acted as control. E2 and malondialdehyde plasma levels and superoxide dismutase, catalase, and GSH-Px activities were evaluated in subgroups A, B, and C on day 30 of therapy and in the control subgroup. GSH-Px activity was significantly higher in EW than in AP at time 0. A statistically significant increase in E2 plasma levels and GSH-Px activity was observed in subgroups A and C on day 30 of treatment, and there was a significant positive correlation between E2 plasma levels and GSH-Px activity in both subgroups. After a month of treatment, erythrocyte GSH-Px activity in subgroups A and C was not significantly different from that observed in EW. After a month of treatment, no significant variation was found in subgroup B nor in the control group. These results strongly suggest that when plasma E2 is restored to physiological levels in AP, it stimulates erythrocyte GSH-Px activity. Progesterone therapy did not induce significant modifications.

Adult↗
PubMed1999

Hormone replacement therapy with estrogen or estrogen plus medroxyprogesterone acetate is associated with increased epithelial proliferation in the normal postmenopausal breast.

The relative effects of postmenopausal hormone replacement therapy (HRT) with estrogen alone vs. estrogen+progestin on breast cell proliferation and on breast cancer risk are controversial. A cross-sectional observational study was carried out to examine the proliferative effects of HRT with estrogen or estrogen plus the progestin, medroxyprogesterone acetate, in breast tissue of postmenopausal women. Benign breast biopsies from 86 postmenopausal women were analyzed with antiproliferating cell nuclear antigen (anti-PCNA) and Ki67 antibodies to measure relative levels of cell proliferation. Epithelial density and estrogen and progesterone receptor status were also determined. The women were categorized either as users of: 1) estrogen (E) alone; 2) estrogen+medroxyprogesterone acetate (E+P); or 3) no HRT. Compared with no HRT, the breast epithelium of women who had received either E+P or E alone had significantly higher PCNA proliferation indices, and treatment with E+P had a significantly higher index (PCNA and Ki67) than treatment with E alone. Breast epithelial density was significantly greater in postmenopausal women treated with E and E+P, compared with no HRT. Thus, the present study shows that postmenopausal HRT with E+P was associated with greater breast epithelial cell proliferation and breast epithelial cell density than E alone or no HRT. Furthermore, with E+P, breast proliferation was localized to the terminal duct-lobular unit of the breast, which is the site of development of most breast cancers. Further studies are needed to assess the possible association between the mitogenic activity of progestins and breast cancer risk.

Adult↗
PubMed1999

Distinguishing androgen receptor agonists and antagonists: distinct mechanisms of activation by medroxyprogesterone acetate and dihydrotestosterone.

Natural and pharmacological androgen receptor (AR) ligands were tested for their ability to induce the AR NH2-terminal and carboxyl-terminal (N/C) interaction in a two-hybrid protein assay to determine whether N/C complex formation distinguishes in vivo AR agonists from antagonists. High-affinity agonists such as dihydrotestosterone, mibolerone, testosterone, and methyltrienolone at concentrations between 0.1 and 1 nM induce the N/C interaction more than 40-fold. The lower affinity anabolic steroids, oxandrolone and fluoxymesterone, require concentrations of 10-100 nM for up to 23-fold induction of the N/C interaction. However no N/C interaction was detected in the presence of the antagonists, hydroxyflutamide, cyproterone acetate, or RU56187, at concentrations up to 1 microM, or with 1 microM estradiol, progesterone, or medroxyprogesterone acetate; each of these steroids at 1-500 nM inhibited the dihydrotestosterone-induced N/C interaction, with medroxyprogesterone acetate being the most effective. In transient and stable cotransfection assays using the mouse mammary tumor virus reporter vector, all ligands displayed concentration-dependent AR agonist activity that paralleled induction of the N/C interaction, with antagonists and weaker agonists failing to induce the N/C interaction. AR dimerization and DNA binding in mobility shift assays and AR stabilization reflected, but were not dependent on, the N/C interaction. The results indicate that the N/C interaction facilitates agonist potency at low physiological ligand concentrations as detected in transcription, dimerization/DNA binding, and stabilization assays. However the N/C interaction is not required for agonist activity at sufficiently high ligand concentrations, nor does its inhibition imply antagonist activity.

Androgen Antagonists↗
PubMed1997

Premenopausal ovariectomy-related bone loss: a randomized, double-blind, one-year trial of conjugated estrogen or medroxyprogesterone acetate.

The purpose of this study was to contrast the effects of conventional estrogen treatment with medroxyprogesterone on cancellous and cortical bone change in the first year following premenopausal ovariectomy. This 1-year double-blind randomized therapy trial was stratified by osteoporosis family history and performed in an academic medical center and community hospitals. Premenopausal women 45 +/- 5 years old, postovariectomy for benign diseases were provided 600 mg/day of calcium and randomized to daily therapy with conjugated equine estrogen (CEE, 0.6 mg) or medroxyprogesterone (MPA, 10 mg). The primary outcome variable was spinal quantitative computed tomography (QCT) bone density change over 1 year with additional outcomes of dual-energy X-ray absorptiometry (DXA) of proximal femur (FN), whole body (WB), and spine segment (WBS) and N-telopeptide, bone-specific alkaline phosphatase, and other bone marker, hormonal, and weight changes. Results in the 33 women completing the study, whose initial bone densities were normal (QCT 133 mg/cm3, femoral neck 0.94 g/cm2, whole body DXA 1.13 g/cm2), showed annual QCT loss during CEE therapy of -11.5 mg/cm3 (p < 0.0007) and MPA bone loss of -19.7 mg/cm3 (p < 0.0001). Losses were marginally greater on MPA than CEE (p = 0.04). Extremely high postovariectomy (5 days) and pretreatment resorption markers (> 3 SD above premenopausal normal levels) were significantly related to bone loss. Across the year, resorption decreased during CEE but increased on MPA treatment. Significant DXA bone losses were prevented by CEE treatment (-1.4% FN, -.4% WB, and -1.5% WBS, all NS). However, DXA bone loss was not prevented by MPA treatment (-5% FN, -2.8% WB, and -6.1% WBS, all p < 0.03). Average weight gain was significant (+ 3.2 +/- 4.0 kg) and greater on CEE than MPA (+ 4.7 vs. + 2.0 kg, p = 0.049). In conclusion, CEE therapy did not prevent significant 8% cancellous spinal bone loss in the first year following premenopausal ovariectomy, despite supplementation with 600 mg/day of calcium, good control of vasomotor symptoms, and nearly 5 kg of gain in weight. Significant DXA bone loss, however, was prevented by CEE, but not by MPA therapy. These unexpected results were statistically related to high bone resorption following ovariectomy, which CEE suppressed but MPA did not. Bone formation markers increased during MPA therapy but were unchanged during CEE therapy.

Absorptiometry, Photon↗
PubMed2000

Medroxyprogesterone acetate inhibits human pancreatic carcinoma cell growth by inducing apoptosis in association with Bcl-2 phosphorylation.

BACKGROUND: A previous study found that medroxyprogesterone acetate (MPA) delayed the in vivo growth of three (AsPC-1, Capan-2, and MiaPaCa-2) of nine human pancreatic carcinoma cell lines transplanted into nude mice (Cancer 1995; 75:1263-72). The current study was undertaken to evaluate the basis for this inhibitor. METHODS: The estrogen receptor (ER) and progesterone receptor (PgR) status in nine human pancreatic carcinoma cell lines, AsPC-1, BxPC-3, Capan-1, Capan-2, Hs-700T, Hs-766T, MiaPaCa-2, PANC-1, and SUIT-2, was assessed using an enzyme immunoassay (EIA). The authors tested the growth inhibitory activity of MPA and the morphologic changes in these nine pancreatic carcinoma cell lines. Cell cycle progression and DNA fragmentation also were evaluated in these cell lines. Immunoblot analysis was used to determine bcl-2 expression and phosphorylation. RESULTS: In the EIA assay, ER was detected in three cell lines (BxPC-3, Capan-2, and MiaPaCa-2), and PgR was also detected in three (AsPC-1, Capan-2, and MiaPaCa-2). Medroxyprogesterone acetate inhibited the growth of three cell lines (AsPC-1, Capan-2, and MiaPaCa-2) with IC50 values ranging from 2.3 x 10(7) to 6.1 x 10(-7) M. In these three responsive cell lines, MPA caused cell detachment and decreased cell density. The nuclei of the MPA-treated cells were condensed and often fragmented. Cell cycle analysis of these three cell lines showed that MPA induced the appearance of a sub-G1 peak, which is characteristic of early apoptotic cells. DNA degradation assay after MPA treatment showed a typical DNA ladder pattern consistent with apoptosis. Immunoblot analysis of MPA-treated cells that overexpressed bcl-2 revealed a pattern consistent with bcl-2 phosphorylation. CONCLUSIONS: Clinically attainable concentrations of MPA can inhibit the growth of some human pancreatic carcinoma cells in vitro by inducing apoptosis, probably through their PgR, in association with the phosphorylation of bcl-2. This agent may be useful for treating patients with pancreatic carcinoma.

Animals↗
PubMed2000

[Use captopril and estradiol-medroxyprogesterone in premenopausal hypertensive patients].

INTRODUCTION: The premenopause period is that which precedes the actual menopause, when a decrease of the ovarian hormones is present, leading to cardiovascular diseases as arterial hypertension, acute myocardial infarction and cerebrovascular diseases. OBJECTIVE: We evaluated the antihypertensive response of the estradiol-medroxyprogesterone, to reduce arterial pressure in the premenopausal patient. MATERIAL AND METHODS: In a clinical trial from March 1997 to September 1998, 106 patients with systemic hypertension, symptoms hypoestrogenism and estradiol levels less than 30 pg/mL were evaluated. They were randomized at a trial in two groups with pursuit of 6 months. Group A: 53 with captopril, Group B: 53 with estradiol-medroxyprogesterone. The arterial pressure, cholesterol, triglycerides and symptoms hypoestrogenism were analyzed before and after the treatment. The statistical analysis was performed with Student T. RESULTS: A decrease of arterial pressure was observed with estradiol, the same as with captopril with a p < 0.05. Decrease of cholesterol and triglycerides were more significant in the estradiol group with a p < 0.05. A bigger attenuation of symptoms of the hypoestrogenism existed in the estradiol group. CONCLUSIONS: The antihypertensive response with estradiol was the same as with captopril in the premenopausal patient with systemic hypertension.

Antihypertensive Agents↗
PubMed2001

Comparison of the resorbable barrier interceed (TC7) and preoperative use of medroxyprogesterone acetate in postoperative adhesion prevention.

PURPOSE: The purpose of this study was to compare the effectiveness of barrier agent Interceed (TC7) (Johnson & Johnson Medical, Inc) and preoperative use of commonly used progesterone, medroxyprogesterone acetate. METHODS: Forty-five Spraque-Dawley white rats of reproductive age (225-250 g) were employed as a model for postsurgical adhesion formation. Group 1 consisted of control rats, Group 2 consisted only of rats with Interceed applied to the denuded areas, Group 3 consisted of rats where preoperative MPA was used. Fifteen rats were exposed to daily IM injections of 15 mg medroxyprogesterone acetate (MPA) two weeks before the surgery. RESULTS: The total adhesion score of the MPA group was significantly less than the control and Interceed group respectively (chi2=10.15) (p<0.001), (chi2=4.67) (p<0.03). There was no significant difference between the Interceed and the control group (p>0.05). CONCLUSION: Preoperative long-term MPA treatment significantly decreases primary adhesion formation. It seems that there are some other mechanisms responsible for this effect rather than anti-inflammation and/or immunosuppression. It may be that the hypoestrogenic milieu depends on the use of progesterone.

Abdomen↗
PubMedDate not supplied

Vaginal cytologic evaluation as a practical link between hormone blood levels and tumor hormone dependency in exclusive medroxyprogesterone treatment of recurrent or metastatic endometrial adenocarcinoma.

In one hundred patients treated by means of one gram medroxyprogesterone a week for disseminated or recurrent endometrial adenocarcinoma, vaginal cytohormonal evaluation seemed to be an important predictive factor of hormone dependency and tumoral responsiveness to progestational therapy. Almost all 51 patients, representing the responsive group, revealed an evident drop of the Karyopyknotic Index and a complete shift to the left of the Maturation Index. Both cytohormonal and tumoral response to medroxyprogesterone seemed directly related to estrogen-progestogen interaction on a cellular level. The striking LH response in the responsive group has previously not been integrated in this mechanism of action.

Adenocarcinoma↗