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Results for “MEDROXYPROGESTERONE”

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PubMed1996

The effectiveness of a mail reminder system for depot medroxyprogesterone injections.

To determine if a mail reminder system leads to an increase in the percentage of depot medroxyprogesterone acetate (Depo-Provera) injections administered on time, the charts of 184 women were reviewed. The reminder postcard included the due dates of both the next medroxyprogesterone injection and the next Papanicolaou test. Timeliness of injections improved with the reminder system from 64% administered on time to 76% (P < .02). Injections given late despite the reminders were late a mean of 8 days. Injections given late before the reminder system began were late a mean of 20 days (P < .05). If injections given during the injection's 14-day "grace" period are included, the on-time rate improved from 87% to 96% with the reminder system (P < .005). The reminder system was not effective in ensuring annual Papanicolaou testing. Vigilance is needed to ensure that women receiving medroxyprogesterone injections also receive timely Papanicolaou testing.

Adult↗

PubMed1980

Treatment of experimental herpetic interstitial keratitis with medroxyprogesterone.

A model of herpes simplex interstitial keratitis was developed in rabbits sensitized with live herpes simplex virus (HSV) type 2 and challenged intrastromally with live virus. This model was used to evaluate the effects of subconjunctival medroxyprogesterone acetate on the course of the disease and on collagenase levels in the treated corneas. Whether treated prophylactically or therapeutically, the medroxyprogesterone-treated groups had substantially less stromal infiltration and neovascularization than the controls. The clinical effects corresponded with a marked reduction in the polymorphonuclear leukocyte infiltrate histologically, and the suppression of latent and active collagenase activity in the treated corneas cultured in vitro. However, epithelial disease was exacerbated in prophylactically treated animals. Medroxyprogesterone appears to be useful in the treatment of herpetic interstitial keratitis as an anti-inflammatory agent as well as an inhibitor of collagenase production but, like the corticosteroids, it can exacerbate epithelial disease.

Animals↗

PubMed1981

Medroxyprogesterone on corneal ulceration. Its effects after alkali burns on rabbits.

The effect of medroxyprogesterone acetate treatment in preventing or retarding corneal ulceration after alkali burns was studied in rabbits in an attempt to correlate dose and response. The eyes were treated for 21 days with a 0.01% or 1% suspension administered topically four times a day or medroxyprogesterone acetate, 4 mg or 30 mg, given subconjunctivally on alternate days. None of these regimens was noticeably effective, although at times there was a trend toward retarding ulceration. Thus, it was not possible to confirm earlier reports of substantial efficacy of medroxyprogesterone. Corneal stroma with epithelial defects and/or ulcers persistently showed infiltration with neutrophils in the superficial stroma within the epithelial defect, implicating the tears as the source of the inflammatory cells.

Alkalies↗

PubMed2002

Use of medroxyprogesterone acetate in the treatment of Müllerian adenosarcoma: a case report.

BACKGROUND: Müllerianadenosarcoma is a rare pelvic malignancy that most commonly arises from the endometrium. These tumors are relatively insensitive to chemotherapy and radiation and are primarily treated by surgical resection. We report a case of müllerian adenosarcoma arising outside of the uterus from a background of endometriosis treated with a combination of surgical resection and medroxyprogesterone acetate. CASE: A 43-year-old woman with a history of endometriosis was diagnosed with advanced extrauterine müllerian adenosarcoma. After suboptimal tumor dubulking surgery she was treated with medroxyprogesterone acetate. Ten months postoperatively she remains without evidence of disease. CONCLUSION: Medroxyprogesterone acetate may be a useful drug in the treatment of advanced müllerian adenosarcoma.

Adenosarcoma↗

PubMed1994

Combined effects of estradiol, leuprorelin, tamoxifen and medroxyprogesterone acetate on cell growth and steroid hormone receptors in breast cancer cells.

Both tamoxifen and medroxyprogesterone acetate have a direct antitumor effect and are widely used in breast cancer therapy. Luteinizing-hormone-releasing hormone analogs inhibit the growth of breast cancer cells and could represent an alternative treatment for patients affected by breast cancer. Our study was carried out to investigate the effect of leuprorelin (TAP-144) alone or combined with tamoxifen or medroxyprogesterone acetate in human breast cancer cells. Ineffective when used in the absence of estrogens, TAP-144 inhibited the estrogen-stimulated growth of MCF-7, CG-5 and ZR-75-1 cells cultured in medium supplemented with charcoal-treated serum. The growth of estrogen-unresponsive MDA-MB-231 cells was not affected by TAP-144. The combination of TAP-144 with tamoxifen in CG-5 cells did not determine any enhancement of inhibition of cell growth, whereas in both CG-5 and MCF-7 cells, when 1 microM TAP-144 was associated with 0.1 microM medroxyprogesterone acetate, cell growth inhibition was increased, resulting in a subadditive effect. Progesterone receptor levels of CG-5 cells were significantly increased by TAP-144 in the presence of 17 beta-estradiol with respect to those present in control and 17 beta-estradiol-treated cells.

Breast Neoplasms↗

PubMed1991

Premenstrual tension: a placebo-controlled efficacy study with spironolactone and medroxyprogesterone acetate.

Forty-three healthy women with a characteristic history of premenstrual tension participated in a placebo controlled, crossover study. The effects of spironolactone (Aldactone) and medroxyprogesterone acetate (Gestapuran) on ten symptoms of premenstrual tension were evaluated. Placebo tablets as well as spironolactone and medroxyprogesterone acetate significantly improved a mood index score (which is a generally accepted method to measure premenstrual symptoms). Spironolactone and medroxyprogesterone acetate were however both significantly (P less than 0.05) better than placebo in relieving the symptoms.

Adult↗

PubMed1994

Premenopausal bone loss and depot medroxyprogesterone acetate administration.

A 39-year-old woman on depot medroxyprogesterone acetate for 17 years developed multiple fractures after falling from a stationary horse. Densitometry revealed significant osteopenia. Although the reported patient was a thin, Caucasian woman, she did not have any other significant risk factors for osteoporosis except for a possible state of partial estrogen deficiency induced by the use of depot medroxyprogesterone acetate. Studies have shown that the estradiol levels of premenopausal women who have received this hormonal contraceptive for more than 1 year never reach those seen in the mid-cycle or luteal phase of the normal menstrual cycle. The estradiol levels are comparable only with those found in the early follicular phase. Therefore, women who use depot medroxyprogesterone acetate are in a state of partial estrogen deficiency, which may be associated with increased bone loss.

Adult↗

PubMed1985

Effects of oestradiol, testosterone and medroxyprogesterone on subcellular fraction marker enzyme activities from rat liver and brain.

The following enzymes have been studied (subcellular fractions are shown between parentheses): NAG and beta-glucuronidase (lysosomes); SDH (mitochondrial); glucose-6-phosphatase (endoplasmic reticulum); 5'-nucleotidase and (Na+, K+)Mg2+ ATPase (plasma membranes). Alterations on their activities were observed after subcutaneous injection of sex hormones, compared with controls. NAG activity from liver was always significantly decreased in lysosomal and microsomal fractions after the hormonal treatment. In the same conditions, NAG from brain was always increased. beta-Glucuronidase behaves like NAG in brain; in liver it was not modified by testosterone and it was slightly increased in lysosomal fraction after oestradiol treatment. SDH activity was not modified in mitochondrial fractions from liver, but this activity was always significantly increased in brain. Glucose-6-phosphatase activity was always significantly decreased in microsomal fractions from liver. It was increased in brain after oestradiol and testosterone injection, but medroxyprogesterone treatment caused a decreased activity. 5'-Nucleotidase and (Na+, K+)Mg2+ ATPase from brain were significantly increased in microsomal fractions by oestradiol and testosterone. Medroxyprogesterone, however, caused an increase in ATPase, but did not affect 5'-nucleotidase. Both activities in liver were decreased by oestradiol and increased by testosterone, but medroxyprogesterone caused (Na+, K+)Mg2+ ATPase to rise and 5'-nucleotidase to fall.

5'-Nucleotidase↗

PubMed2005

Double-blinded randomized controlled trial of estrogen supplementation in adolescent girls who receive depot medroxyprogesterone acetate for contraception.

OBJECTIVE: The purpose of this clinical trial was to evaluate the effect of estrogen supplementation on bone mineral density in adolescent girls who received depot medroxyprogesterone acetate for contraception. STUDY DESIGN: One hundred twenty-three adolescents who began receiving depot medroxyprogesterone acetate injections every 12 weeks were assigned randomly to receive monthly injections of estradiol cypionate or placebo. The main outcome was bone mineral density that was measured by dual energy x-ray absorptiometry for 12 (n = 69) to 24 (n = 36) months. Participants, technicians, and physicians were blinded to estrogen treatment. RESULTS: Over the 24-month period, the percentage of change from baseline bone mineral density at the lumbar spine was 2.8% in the estradiol cypionate group versus -1.8% in the placebo group ( P <.001). At the femoral neck, the percentage of change from baseline bone mineral density was 4.7% in the estradiol cypionate group versus -5.1% in the placebo group ( P <.001). CONCLUSION: Our results suggest that estrogen supplementation is protective of bone in adolescent girls who receive depot medroxyprogesterone acetate injections.

Absorptiometry, Photon↗

PubMed2004

Effects of levonorgestrel, medroxyprogesterone acetate, norethindrone, and 17beta-estradiol on vascular endothelial growth factor isomers 121 and 165 in Ishikawa cells.

OBJECTIVE: To determine the effect of 17beta-E(2), levonorgestrel, medroxyprogesterone acetate, and norethindrone on the expression of vascular endothelial growth factor (VEGF) isoforms 121 and 165 in Ishikawa cells in vitro. DESIGN: Prospective basic research study. SETTING: Basic research laboratory. PATIENT(S): None. INTERVENTION(S): Ishikawa cells were cultured in vitro. After 24 hours' incubation in serum-free media, 1.0, 0.1, and 0.01 microM concentrations of E(2), levonorgestrel, medroxyprogesterone acetate, and norethindrone were added for a further 24 hours of incubation. MAIN OUTCOME MEASURE(S): Isolation and identification of VEGF isoforms 121 and 165 using semiquantitative polymerase chain reaction, gel electrophoresis, with beta-actin as an internal control. RESULT(S): Estradiol stimulated VEGF isoforms 121 and 165. The progestins studied increased mRNA for VEGF isoforms 121 and 165 at all doses. Medroxyprogesterone acetate resulted in the greatest increase in both VEGF 121 and 165 compared with norethindrone and levonorgestrel. CONCLUSION(S): Estradiol and progestins increased VEGF 121 and 165 isoform mRNA in Ishikawa cells in vitro. We hypothesize that differences in VEGF expression may be associated with the irregular bleeding during progestin use in clinical situations.

Adenocarcinoma↗

PubMed1992

Inhibitory effect of medroxyprogesterone acetate on angiogenesis induced by human endometrial cancer.

OBJECTIVE: The purpose of this study was to investigate the effect of medroxyprogesterone acetate on angiogenesis induced by endometrial cancer and to elucidate the possible mechanisms by which it inhibits the growth of the cancer. STUDY DESIGN: Tumors were obtained from 29 patients with endometrial adenocarcinoma, and angiogenesis was assayed in corneas of white rabbits. RESULTS: Transplantation of tumor tissues into rabbit corneas induced angiogenesis in 70.4% of the corneas, but their transplantation with a pellet of medroxyprogesterone acetate induced angiogenesis in only 21.5% of the corneas. This compound also inhibited angiogenesis induced by acidic fibroblast growth factor and transforming growth factor-alpha. CONCLUSION: Inhibition of angiogenesis may be one mechanism by which medroxyprogesterone acetate inhibits the growth of endometrial adenocarcinoma, and its inhibition of neovascularization induced by adenocarcinoma may be through its direct action on endothelial cells.

Adenocarcinoma↗

PubMed1988

Reduction of the intraperitoneal inflammation associated with endometriosis by treatment with medroxyprogesterone acetate.

An intraperitoneal inflammatory exudate has been repeatedly observed in infertile women without mechanical compromise of the pelvic viscera, particularly with endometriosis. This is manifested by increases in the peritoneal fluid volume, leukocyte number, and proteolytic enzyme concentrations. We tested the hypothesis that the stimulus responsible for eliciting this intraperitoneal inflammation is retrograde menstruation by measuring the peritoneal fluid volume and leukocyte count in 16 infertile women with endometriosis before and after ovulation suppression with medroxyprogesterone acetate, 30 mg/day for 4 months. Medroxyprogesterone acetate therapy significantly reduced the peritoneal fluid volume (22.5 +/- 4.1 versus 6.8 +/- 0.9 ml mean +/- SE, p less than 0.0001), the peritoneal fluid leukocyte count (30.7 +/- 6.5 versus 7.1 +/- 0.7 x 10(6) cells per patient, p less than 0.0001), and American Fertility Society score (23.2 +/- 5.1 versus 15.4 +/- 4.1, p less than 0.0002). We conclude that medroxyprogesterone acetate treatment reduces the intraperitoneal exudate associated with endometriosis. These results support the contention that the stimulus eliciting the intraperitoneal inflammation in infertile women with endometriosis is retrograde menstruation.

Adult↗

PubMed2000

Depot medroxyprogesterone acetate and basal serum prolactin levels in lactating women.

OBJECTIVE: To study the effect of depot medroxyprogesterone acetate on basal serum prolactin levels in lactating women. METHODS: We compared basal serum prolactin levels in 25 lactating women after depot medroxyprogesterone acetate injection and in 25 lactating women of similar age who were using a copper T380A intrauterine device (control group). This sample size was required in order to have 95% power to detect a significant difference. Basal prolactin levels were evaluated by time-resolved fluoroimmunoassay three times (6 weeks postpartum and 3 and 6 weeks after beginning either contraceptive method). RESULTS: At 6 weeks postpartum, before beginning either contraceptive method, the mean prolactin levels in the study and control groups were 991.31 and 948.75 mU/L, respectively (P =.850, 95% confidence interval [CI] -407.57, 492.70). Three weeks later, the mean prolactin levels in the study and control groups were 1156.12 and 860.10 mU/L, respectively (P =.116, 95% CI -76.20, 668.26). At the last follow-up, the mean prolactin levels in the study and control groups were 1127.83 and 710.97 mU/L, respectively (P =.026, 95% CI 51.97, 781.73). There were no significant within-group differences at 6 weeks postpartum before contraception and at 6 weeks after beginning contraception in the study and control groups (P >.05, 95% CI -327.99, 243.02 and -46.76, 522.33, respectively). CONCLUSION: Contraception with depot medroxyprogesterone acetate in lactating women produced higher basal prolactin levels than contraception with copper T380A intrauterine device.

Contraceptive Agents, Female↗

PubMed1999

Bone density effects of continuous estrone sulfate and varying doses of medroxyprogesterone acetate. Ogen/Provera Study Group.

OBJECTIVE: To establish the optimum oral daily dose of medroxyprogesterone acetate with estrone sulfate for 2 years to maintain bone density. METHODS: A multicenter, double-blind study involved 568 postmenopausal women given estrone sulfate, 1.25 mg, and randomized to receive 2.5, 5, or 10 mg of medroxyprogesterone acetate. Bone density analyses of the lumbar spine and femoral neck were done at baseline and 12 and 24 months. RESULTS: There was a significant increase from baseline to 24 months in mean lumbar spine (4.0% +/- 0.27%) and femoral neck (3.2% +/- 0.28%) bone density, with no significant differences between the treatment groups. Factors most influencing bone density changes were baseline bone density and treatment duration. Significant increases were seen in the spine over 2 years; in the hip, those occurred in the first 12 months only. In both sites, lower baseline bone density resulted in greater increases. In the spine only, no previous hormone replacement therapy, higher body mass index, more than 2 years postmenopause, and nonsmoking resulted in greater gains. Once those covariates and center-to-center variations were corrected for, in the spine, the 10-mg group had smaller increases than the other groups. Changes were unrelated to age, parity, calcium, and alcohol intakes in either site. CONCLUSION: Daily estrone sulfate, 1.25 mg, with 2.5, 5, or 10 mg medroxyprogesterone acetate was effective for preventing bone loss in postmenopausal women.

Adult↗

PubMed1996

The nuclear channel system in endometrial adenocarcinoma exposed to medroxyprogesterone acetate.

The nuclear channel system (NCS), giant mitochondria and subnuclear glycogen form a triad of ultrastructural features observed in normal human endometrial epithelium in response to progestational steroids. Both the giant mitochondria and subnuclear glycogen have been described in endometrial adenocarcinoma, but the NCS has not. This article reports the development of the NCS in adenocarcinoma treated with medroxyprogesterone acetate. Previous studies suggest that the NCS in normal tissue is a response to the acyl group in the 17-beta position of the D-ring of some progestational steroids, such as medroxyprogesterone acetate. Medroxyprogesterone acetate was administered to 12 postmenopausal women with endometrial adenocarcinoma. Hysterectomies were performed 8 to 20 days after treatment. Pretreatment specimens were also obtained on 8 of the 12 patients. Using standard electron microscopy procedures, light microscopy on plastic semithin sections was first used to confirm the presence of tumor. Thin sections of malignant endometrium were prepared and evaluated ultrastructurally for progestational alterations. Abnormal giant mitochondria and subnuclear glycogen were found both before and after treatment. The third element of the triad, the NCS, was not observed in any of the available pretreatment biopsies, but was seen in three of the treated specimens. Thus it appears that the NCS is a response to the given progesterone therapy.

Adenocarcinoma↗

PubMed2001

Medroxyprogesterone acetate alone or synergistic with chemotherapy suppresses colony formation and DNA synthesis in C6 glioma in vitro.

We have studied the effects of medroxyprogesterone acetate (MPA) on C6 glioma growth in vitro in order to prove the hypothesis that it could arrest growth and induce drug sensitisation in a glial tumour as it does in breast cancer cells. Plating, thymidine-labelling index, ultra-structure, and soft agar colony growth were determined after incubation with MPA, and/or cisplatin, procarbazine and methotrexate (MTX). MPA (microg/ml) reduced the thymidine-labelling index by 41 and 73% at 48 and 96 h, respectively, and decreased colony growth by 61%. Soft agar colony inhibition by MPA was almost as potent as MTX (0.3 microg/ml), but the latter drug showed very high cytotoxicity. Electron microscopy revealed that in medroxyprogesterone treated cells myeloid bodies developed, but MTX treatment caused mainly necrosis. Medroxyprogesterone increased procarbazine and cisplatin-induced colony growth and S-phase inhibition, but reduced MTX-induced thymidine-labelling inhibition. In conclusion, progesterone may inhibit growth and sensitize to drugs.

Antineoplastic Agents↗

PubMed2004

Anaphylaxis from medroxyprogesterone acetate.

BACKGROUND: More than 30 million women in more than 90 countries use depot medroxyprogesterone acetate as an injectable contraceptive agent, and it is thought to be very safe. However, it should be recognized that serious and potentially life-threatening adverse effects can occur. CASE: A 40-year-old para 2 went into anaphylactic shock after receiving 150 mg of depot medroxyprogesterone acetate intramuscularly. She was not taking any other medication, and there was no history of allergy to food or cosmetics. She responded fully to immediate resuscitation. A repeat episode occurred when she received another dose 12 weeks later. CONCLUSION: Although thought to be very safe, life-threatening adverse effects can occur with depot medroxyprogesterone acetate, and practitioners should be prepared for such eventuality.

Adult↗

PubMed1985

Growth inhibition of fibroblasts by progesterone and medroxyprogesterone in vitro.

This study was carried out to evaluate in vitro the beneficial effects observed in various aggressive fibromatoses (mediastinal, retroperitoneal, paraneoplastic fibrosis and desmoid tumors) after treatment with progesterone. Primary cultures of fibroblasts were prepared from fetuses of Swiss strain mice. Continuous fibroblast lines LM and Vero were also used. Moreover, cultures of non-fetal human fibroblast from skin and lung were employed. Epithelial tumor cell line HeLa was used as a control. All cultures were incubated with various doses of progesterone at concentrations from 1.4 X 10(-4) to 1.4 X 10(-3) M. Human cells and monolayers of fetal murine fibroblast were submitted to the action of medroxyprogesterone solution at the same concentrations as used for progesterone. Other steroids (estrone, estriol, testosterone and prednisolone) were used at the identical concentrations in the same vehicles. Progesterone affected all lines of fibroblasts studied and destroyed them within either 2-4 or 24-48 h depending on the steroid concentrations used. Medroxyprogesterone had a comparable effect on human cell lines and monolayers of fetal murine fibroblasts provided that the same ratio between the hormone concentration and the time of exposure was maintained. With higher medium concentrations shorter times of incubation were required for the destruction of fibroblast. However, to observe a degree of lysis similar to that elicited by progesterone, it was necessary to use 4 times higher concentrations of medroxyprogesterone. No effect on HeLa epithelial cells was observed nor were the controls affected by the steroids or diluents used at the appropriate concentrations. Results from incubation studies using monolayers of murine fibroblast and 14C-progesterone suggested that the cells were destroyed by the progesterone and not by a bioproduct of its metabolism.

Animals↗