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Results for “Medroxyprogesterone Acetate”

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PubMed1980

Endogenous serum testosterone in males after different doses and routes of administration of medroxyprogesterone acetate.

The effects of different doses and routes of administration (oral and IM) of medroxyprogesterone acetate on endogenous testosterone secretion were studied in healthy male volunteers. There were three treatment groups. Serum testosterone levels, measured by radioimmunoassay before, during and after different doses of medroxyprogesterone acetate, were significantly lowered (p < 0.05) in these subjects. A tendency to return toward pretreatment values was noted within three to six weeks after the last dose of medroxyprogesterone acetate. The IM route of administration suppressed the testosterone levels for the longest period of time. No indication of drug-induced toxicity, as judged by vital signs, systemic side effects, standard laboratory evaluations and some special clinical evaluations, was found during treatment or in the period immediately following the course of therapy. No serious or untoward side effects were encountered.

Administration, Oral↗

PubMed1989

Deoxyribonucleic acid content and medroxyprogesterone acetate treatment in metastatic renal cell carcinoma.

High dose medroxyprogesterone treatment was given to 20 patients with metastatic renal cell carcinoma. Distant metastases occurred before the perifascial nephrectomy in 11 patients and following nephrectomy in 9. Tumor deoxyribonucleic acid content was analyzed by flow cytometry in 8 fresh samples from each primary tumor. Four patients had homogeneously diploid primary tumors, 5 had tumors with diploid and aneuploid samples, and all 8 tumor samples were aneuploid in 10 patients. Deoxyribonucleic acid analysis was unsuccessful in 1 patient. One patient with a diploid primary tumor died of an intercurrent disease. Three patients (16 per cent) had objective remissions and 1 had a long-lasting stable disease. Of the 4 patients with any response to medroxyprogesterone acetate treatment 3 had diploid primary tumors, and 1 had 8 diploid and 2 aneuploid samples in the primary tumor. The remaining 14 patients showed no response to treatment and had progressive disease (11 of these patients died within 14 months). All 14 patients had aneuploid primary tumors. The results indicate that tumor ploidy might be related to response to medroxyprogesterone acetate treatment. Deoxyribonucleic acid content seems to be an important parameter to consider in planning treatment of metastatic renal cell carcinoma.

Aneuploidy↗

PubMed1989

Endocrine manipulation of meningiomas with medroxyprogesterone acetate. Effect of MPA on growth of primary meningioma cells in monolayer tissue culture.

Intracranial meningiomas from patients treated with medroxyprogesterone acetate as well as from untreated patients were studied in monolayer tissue culture with trials of in vitro hormonal modulation with medroxyprogesterone acetate. The following conclusions were drawn from investigations which comprise 37 cell culture assays: (a) tissue cultures of meningiomas inherit the disadvantages of loss of the progesterone receptor and frequent transformation to cells resembling fibroblasts after three to four passages. For these reasons, drug testing as well as the establishment of cell cultures that exhibit the characteristics of meningioma are impeded; (b) the progesterone receptor-content of the solid tumors does not reflect the response to medroxyprogesterone acetate-therapy in vitro; (c) medroxyprogesterone acetate-pretreated meningiomas showed sufficient in vitro growth in 38%, and untreated meningiomas grew well in 56% of the cases; (d) medroxyprogesterone acetate-induced inhibition or delay of growth was observed in 35%. These findings have resulted in criticism with respect to the value of meningioma tissue cultures for trials of hormonal manipulation and it is thought that another method, which consists of immunostaining of cycling cells, and has been tested in another study, may be superior to cell culture assays with respect to evaluation of the effect of hormonotherapy in meningiomas. Medroxyprogesterone acetate holds an interesting position because it reduces cell growth in some meningiomas in vitro.

Antigens, Surface↗

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↗

PubMed1981

The effect of depot-medroxyprogesterone acetate on the fetus and nursing infant: a review.

Data from published studies of the quantity of medroxyprogesterone acetate and/or its metabolites in the milk of lactating women receiving Depo-Provera for contraception is extrapolated into the amount of drug ingested daily by a theoretically average infant. Comparisons are made with the results of similar studies in animals. Fetal metabolism of medroxyprogesterone acetate is reviewed. Embryonic and fetal development of the human reproductive system is discussed. Results of studies of the effects of steroidal hormones, particularly medroxyprogesterone acetate, on mental development and sexual dimorphic behavior after exposure in utero are presented. It is concluded that the very small amount of drug and/or its metabolites ingested by the nursing infant via breast milk is highly unlikely to have any significant effect on the nursing infant.

Animals↗

PubMed1995

Phasic serum lipid excursions occur during cyclical oral conjugated oestrogens but not during transdermal oestradiol sequentially combined with oral medroxyprogesterone acetate.

BACKGROUND AND OBJECTIVE: Recent data indicate that oral medroxyprogesterone acetate (MPA) has limited unfavourable, neutral or even favourable effects on serum lipid fractions when added to oestrogen replacement therapy. The purpose of this study was to evaluate the serum lipid fractions at the beginning and at the end of each phase of a sequentially combined replacement cycle comparing the oral and the transdermal routes of oestrogen administration. DESIGN: Randomized study with a matched control group. Oral conjugated oestrogens (OCE, 0.625 mg) or transdermal oestradiol (TE 50 micrograms) was taken from day 1 to day 25 and MPA (5 mg) added on days 14 to 25. Serum lipids were evaluated on days 1, 14 and 25 of monthly replacement cycles. PATIENTS: The early post-menopausal women in the control group (n = 11) and in the treatment groups (OCE/MPA, n = 15; TE/MPA, n = 17) were evaluated every 3 months for 12 months and every 6 months for another 12 months. MEASUREMENTS: Serum levels of triglycerides (TG), cholesterol (C) fractions and apolipoproteins (Apo) and their respective ratios were measured at months 1, 3, 6, 9, 12, 18, 24. Menopausal symptoms and uterine bleedings were evaluated in parallel and an endometrial biopsy was performed at the end of the 12th and 24th months of treatment. RESULTS: After 14 days of OCE, C, LDL-C, and Apo B were decreased and TG, HDL-C and Apo A1 were increased. The sequential addition of MPA accentuated the reduction of LDL-C and Apo B but attenuated the elevation of TG, HDL-C and Apo A1. These changes tended to revert toward baseline during the period free of medication. By contrast, at the end of 14 days of TE there was a non-significant reduction in TG and LDL components and a limited increase in HDL-C and Apo A1. During the subsequent addition of MPA there was no significant decrease in TG, LDL-C or Apo B but an elimination of the increase in HDL components. These combined changes resulted in a significant reduction in the LDL-C/HDL-C ratio and a significant elevation in the Apo A1/Apo B ratio only in the OCE/MPA group. CONCLUSION: Overall, oral conjugated oestrogens induced favourable intragroup changes in cholesterol fractions whereas transdermal oestradiol maintained serum lipids at levels not different from baseline. The sequential addition of oral medroxyprogesterone acetate attenuated the beneficial elevation of HDL, did not affect the beneficial effect of oestrogens on ratios of cholesterol fractions and attenuated the unfavourable effect of oral conjugated oestrogens on triglycerides. The partial loss of beneficial effects on lipoproteins during cyclical interruption of hormone therapy would be an argument in favour of the evaluation of continuous regimens of oestrogen/progestagen replacement.

Administration, Cutaneous↗

PubMedDate not supplied

Additional effects of medroxyprogesterone acetate on mammary tumors in oophorectomized, estrogenized, DMBA-treated rats.

Although hormone replacement therapy not only relieves vasomotor symptoms but also reduces cardiovascular disease and osteoporosis, long-term estrogen therapy increases the risk of endometrial and/or mammary cancer. We investigated the effects of conjugated estrogens with or without medroxyprogesterone acetate in oophorectomized, 7,12-dimethylbenz(a)anthracene-treated rats. Chemically induced mammary carcinogenesis was completely suppressed by the simultaneous oophorectomy, but conjugated estrogens replacement with or without medroxyprogesterone acetate markedly stimulated mammary carcinogenesis in the ovariectomized rats. The chronic administration of conjugated estrogens and medroxyprogesterone acetate markedly reduced the activities of thymidylate synthetase and thymidine kinase and bromodeoxyuridine-immunoreactive (S-phase) cells in mammary tumors. These results indicate that the treatment using conjugated estrogens with or without medroxyprogesterone acetate may promote the mammary carcinogenesis in postmenopausal women but the chronic administration of medroxyprogesterone acetate may alter the development of established mammary cancer.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2005

Can medroxyprogesterone acetate alter Toll-like receptor expression in a mouse model of intrauterine inflammation?

OBJECTIVE: Activation of the innate immune receptors, Toll-like receptors 2 and 4, are critical for a host inflammatory response to both Gram-positive and Gram-negative organisms. These receptors can initiate and modulate the inflammatory response. Differential regulation of Toll-like receptors may be one of the mechanisms by which intrauterine inflammation signals parturition. Likewise, progestational agents may have the ability to modify this effect. These studies were performed to elucidate the effect of intrauterine inflammation and medroxyprogesterone acetate on Toll-like receptor expression in the uterus, cervix, and placenta in a mouse model of intrauterine inflammation. STUDY DESIGN: On day 15 of gestation, CD-1 mice were randomized to pretreatment with medroxyprogesterone acetate or vehicle before intrauterine infusion with lipopolysaccharide or sterile saline solution. Six hours after intrauterine infusion, uterine, cervical, and placental tissues were harvested. RNA and protein were extracted. Quantitative polymerase chain reaction was performed for Toll-like receptor 2 and 4 messenger RNA. Western blot analysis was performed with Toll-like receptor 4-specific antibodies. RESULTS: Intrauterine inflammation up-regulated Toll-like receptor 2 and 4 messenger RNA in uterus, cervix, and placenta. Pretreatment with medroxyprogesterone acetate decreased the lipopolysaccharide-induced up-regulation of Toll-like receptor 2 and 4 messenger RNA in the cervix and placenta. Medroxyprogesterone acetate treatment, in the presence of lipopolysaccharide, was unable to prevent the lipopolysaccharide-induced increase in Toll-like receptor 4 messenger RNA and protein in the uterus. Medroxyprogesterone acetate treatment alone in pregnant mice significantly increased Toll-like receptor 4 messenger RNA expression in the uterus. CONCLUSION: Intrauterine inflammation has a differential effect on Toll-like receptor 2 and 4 expression. The observed up-regulation of Toll-like receptor 2 in the uterus in response to intrauterine lipopolysaccharide may be a mechanism to augment the inflammatory response and may serve to promote parturition in the setting of inflammation. Consequently, the ability of medroxyprogesterone acetate to suppress lipopolysaccharide-induced up-regulation of Toll-like receptor 2 messenger RNA may be one of the mechanisms by which progestins are able to decrease preterm birth.

Animals↗

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↗

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↗

PubMed2005

Cytogenetic findings, Trp53 mutations, and hormone responsiveness in a medroxyprogesterone acetate induced murine breast cancer model.

Medroxyprogesterone acetate (MPA)-induced mammary carcinomas express high levels of estrogen (ER) and progesterone receptors (PR) and when transplanted in syngeneic mice they show a progestin-dependent (PD) growth pattern. By successive transplantation, progestin-independent (PI) variants were generated and showed a different response to antihormone therapy. A diploid chromosome number (2n=40) was found in three of five PD tumors, with numbers in the triploid to tetraploid range in the other two. Some PI tumors were diploid, but most were aneuploid (8 of 12 tumors). The most frequent alterations found in PD and PI tumors were gains of chromosomes 3, 4, and 6 and losses of chromosomes 16 and X. Chromosomes 4 and 7 were involved in translocations in three of the four tumor families studied. single-strand conformation polymorphism analysis revealed a point mutation on the Trp53 gene in one of the PD tumors; this showed a stable diploid karyotype, suggesting that mutated Trp53 is not uniquely involved in chromosome instability. We have shown that hormone independence may be acquired without changes in ploidy, suggesting that the increase in ploidy is favored by successive transplantation. In our model, diploid tumors responded to hormone treatment but aneuploid tumors were either responsive or not.

Aneuploidy↗

PubMed1999

Androgen receptor agonist activity of the synthetic progestin, medroxyprogesterone acetate, in human breast cancer cells.

Medroxyprogesterone acetate (MPA), which is frequently used as second line hormonal therapy for the treatment of metastatic breast cancer, binds with high affinity to the progesterone receptor (PR). However, the androgenic side-effects of MPA suggest that it may also activate androgen receptor (AR) regulated pathways. Treatment of the human breast cancer cell lines MDA-MB-453, ZR-75-1 and T47-D with high dose (100 nM) MPA resulted in 26-30% inhibition of cell growth, which was partially reversed by co-treatment with a 10-fold excess of the synthetic antiandrogen, anandron. Scatchard analysis demonstrated specific, high affinity (non-PR) binding of [3H]MPA to cytosols prepared from the PR-/AR+ MDA-MB-453 and PR+/AR+ ZR-75-1, but not the PR-/AR- BT-20 breast cancer cell lines. Competition of [3H]MPA binding to MDA-MB-453 cytosols by equimolar concentrations of androgens (5alpha-dihydrotestosterone (DHT), R1881) and the antiandrogen, anandron was consistent with binding of MPA to the AR. In ZR-75-1 cell cytosol fractions, DHT, R1881 and anandron only partially competed out [3H]MPA binding, suggesting that androgens displace [3H]MPA binding to AR but not to PR. Induction by MPA of AR transactivation was demonstrated in MDA-MB-453 and ZR-75-1 cells, and in the CV-1 cell line transfected with a full-length AR. In these cell lines the increased activity of the androgen responsive reporter gene (MMTV-CAT) by 1 nM MPA was fully (MDA-MB-453, CV-1) or partially (ZR-75-1) inhibited by co-culture with 1 microM anandron. These findings indicate that MPA is an AR agonist and suggest that the in vivo effects of MPA in breast cancer patients may in part be mediated by the AR.

Androgen Antagonists↗

PubMed1988

In vitro growth regulation of endometrial carcinoma cells by tamoxifen and medroxyprogesterone acetate.

The growth inhibitory effects of medroxyprogesterone acetate (MPA) and tamoxifen (TAM) were tested on three long-established endometrial carcinoma cell lines (HEC-1, KLE, and RL95-2) and on UM-EC-1, a new endometrial carcinoma cell line established in our laboratory. MPA and TAM were used in growth experiments either alone, simultaneously, or sequentially. The MCF-7 breast cancer cell line was used as a control. None of the endometrial carcinoma cell lines showed significant sensitivity to 0.1-10 microM MPA. In contrast, 10 days exposure to 5 microM TAM induced 83 and 70% growth inhibition in HEC-1 and KLE cultures, whereas the growth of UM-EC-1 was inhibited by 99.7% and RL95-2 cultures by 100%. TAM-induced growth inhibition was reversible since all cell lines resumed logarithmic growth when TAM was removed from the culture medium. Addition of 17 beta-estradiol (E2) to the culture medium did not accelerate recovery, and reversal of TAM-induced growth inhibition was not seen when TAM and E2 were added simultaneously. This is consistent with our finding that, except for MCF-7, these cell lines did not show detectable estrogen receptor (ER) activity in assays performed at the time of these experiments. When treated sequentially with TAM and MPA, all cell lines resumed logarithmic growth when medium containing TAM was replaced with medium containing MPA. Simultaneous exposure to 5 microM MPA and 5 microM TAM resulted in a slight additive growth inhibitory effects only in KLE cultures. Our results show that MPA does not have growth inhibitory effects in these endometrial carcinoma cell cultures, whereas TAM exerts a potent inhibitory effect that is not reversed by estrogen and may thus be mediated through a mechanism different from blockade of ER. In vitro results with the UM-EC-1 cell line correlated with the clinical response of the cell line donor. Her disease progressed during postoperative MPA therapy, but subsequently she responded to TAM therapy.

Aged↗

PubMed1986

Effects of medroxyprogesterone acetate in obstructive sleep apnea.

We studied the effects of medroxyprogesterone acetate, a respiratory stimulant, on the incidence and duration of episodes of apnea and disordered breathing in 13 nonhypercapnic men with obstructive sleep apnea. Nocturnal polysomnography was done before and after four weeks of treatment with medroxyprogesterone acetate (60 mg/day) and one week after cessation of treatment. There were no significant (p less than 0.05) differences in the mean frequency of apneic episodes per hour of sleep before (31.3 +/- 5.7 [+/- SE]), during (26.8 +/- 6.6), or after (23.6 +/- 7.0) treatment, or in the mean number of disordered breathing episodes per hour of sleep before (19.4 +/- 5.6), during (21.4 +/- 5.8), or after (23.1 +/- 6.3) the period of treatment. Medroxyprogesterone did not alter significantly the total time of apnea or the total time for disordered breathing, expressed as percentages of total sleep time. Arterial oxygen desaturation during apnea and disordered breathing did not change with treatment. Medroxyprogesterone increased the minute ventilation and occlusion pressure responses to hypercapnia measured in the awake state; however, the results of this study demonstrate that medroxyprogesterone does not improve the breathing disorders during sleep in the nonhypercapnic patient with obstructive sleep apnea.

Adult↗

PubMed1985

Short-term effects of tamoxifen, medroxyprogesterone acetate, and their combination on receptor kinetics and 17 beta-hydroxysteroid dehydrogenase in human endometrium.

The interactions of an antiestrogen (tamoxifen) and a progestin (medroxyprogesterone acetate) on endometrial 17 beta-hydroxysteroid dehydrogenase activities were studied in short-term experiments (four to 96 hours) in normally menstruating women at the follicular phase and were related to simultaneously measured concentrations of cytosol and nuclear estrogen and progestin receptors. Tamoxifen effected a decrease in the activity of 17 beta-hydroxysteroid dehydrogenase. This was associated with an apparent translocation to and retention of estrogen receptor in the nucleus without any significant changes in cellular progestin receptor. Medroxyprogesterone acetate administration led to a rapid increase in endometrial 17 beta-hydroxysteroid dehydrogenase activity, and depletion of cytosol and total cellular progestin receptor. Combination of the drugs led to effects that could be addressed to the individual drugs separately, and under the experimental conditions the effects of medroxyprogesterone acetate were uninfluenced by simultaneous tamoxifen administration. Put together with the authors' previous findings on the same parameters during long-term (three-week) medroxyprogesterone acetate administration, it seems possible that potentiation of progestin effects on endometrial carcinoma is not to be expected during long-term simultaneous antiestrogen-progestin treatment. It is therefore likely that the favorable effects of combining these two drugs in long-term treatment are due to their different endocrine action mechanisms.

17-Hydroxysteroid Dehydrogenases↗

PubMed1992

Use of injectable progestin (medroxyprogesterone acetate) in adolescent health care.

To assess medroxyprogesterone acetate (DMPA) prescription practices in adolescent health care practices, an anonymous questionnaire was distributed to 160 American and Canadian physicians attending the 1991 meetings of either the Society for Adolescent Medicine or the North American Society for Pediatric and Adolescent Gynecology. Of 54 (33.7%) physicians who responded, 33 (61.1%) reported prior prescription of an injectable progestin (DMPA) as a form of birth control. Of those, 15 (45.5%) had prescribed it to 10 or more adolescents. Twelve (57%) pediatricians but only 3 (25%) gynecologists reported prescribing DMPA to 10 or more adolescents (p = 0.074). Female physicians were more likely to have prescribed DMPA to adolescents than male physicians (p = 0.009). Mental retardation was considered the strongest "potential indication" for DMPA administration by 48 physicians responding to a 5-point Likert scale. The study suggests that physicians with interest or expertise in Adolescent Medicine are using DMPA as a form of birth control for selected young women in spite of the lack of Food and Drug Administration approval. A centralized DMPA registry is suggested to monitor adverse outcomes in users.

Adult↗

PubMed1984

Return of ovulation following a single injection of depo-medroxyprogesterone acetate: a pharmacokinetic and pharmacodynamic study.

The effect of a single dose of 150 mg of depo-medroxyprogesterone acetate (DMPA) on pituitary, ovarian and endometrial function was assessed in relation to the peripheral levels of the compound in 8 women. The levels of medroxyprogesterone acetate (MPA), follitropin (FSH), lutropin (LH), prolactin, estradiol (E2) and progesterone ( Prog .) were measured 3 times a week during a pretreatment (control) cycle and then daily during postinjection weeks 14-17, 22-25 and 30-33. An endometrial biopsy specimen was obtained during postinjection weeks 17, 25 and 33. In three out of 8 subjects the daily hormone assays carried out during postinjection weeks 30-33 indicated anovulatory periods; in these subjects peripheral blood was drawn daily during postinjection weeks 46-49 and a fourth endometrial biopsy was taken during week 49.

Adult↗

PubMed1998

The influence of transdermal oestradiol replacement therapy and medroxyprogesterone acetate on serum lipids and lipoproteins.

AIMS: The objective of this study was to examine the effects of continuous transdermal oestradiol with or without sequential oral medroxyprogesterone acetate on serum lipids and lipoproteins in menopausal women. METHODS: Sixty-two healthy menopausal women, attending at two menopause clinics in Western India, were recruited for this study over a period of 1 year. Group 1 included 38 hysterectomised women being treated with continuous transdermal oestradiol only (50 microg daily). Group 2 included 24 menopausal women with an intact uterus being treated with transdermal oestradiol (50 microg daily) and medroxyprogesterone acetate (10 mg daily for the first 12 days of each calendar month). Women maintained on 50 microg oestradiol throughout 6 months (group 1: n = 22; group 2: n = 16) were reviewed for changes in serum lipids and lipoproteins at the end of 6 months (group 1), and between days 8 and 12 of the seventh month (combined phase of treatment) (group 2). RESULTS: In group 1, there was a small reduction in the concentrations of total cholesterol (-5.5%, P = 0.04) and a small but not significant reduction in LDL-cholesterol (-5.7%, P = 0.16). In group 2, there were no significant changes in total cholesterol (-4.2%, P = 0.43) and LDL-cholesterol (-3.9%, P = 0.57). HDL-cholesterol levels did not change significantly with unopposed transdermal oestradiol (+3.0%, P = 0.53), or with additional sequential medroxyprogesterone acetate (-3.8%, P = 0.32). Serum triglyceride concentrations decreased significantly in both the groups (-13.9%, P = 0.01, and -13.4%, P = 0.008, respectively). Serum lipid changes did not differ between the groups. CONCLUSIONS: Transdermal oestrogen therapy appears to be of particular benefit for women with hypertriglyceridaemia. There were no significant adverse effects of medroxyprogesterone acetate on serum lipids and lipoproteins.

Administration, Cutaneous↗