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PubMed2002

Risk of calcium oxalate nephrolithiasis in postmenopausal women supplemented with calcium or combined calcium and estrogen.

BACKGROUND: Recent studies showed that postmenopausal women lost less bone mass when supplemented with calcium or estrogen therapy. However, the safety of the treatments in terms of the risk of calcium oxalate stone formation is unknown. We therefore conducted this study to determine the alteration in calcium oxalate supersaturation after calcium supplement or after combined calcium and estrogen therapy in postmenopausal osteoporotic women. METHODS: Fifty-six postmenopausal women were enrolled in this study. All subjects were more than 10 years postmenopausal with vertebral or femoral osteoporosis by bone mineral density criteria. They were randomly allocated to receive either 625 mg of calcium carbonate (250 mg of elemental calcium) at the end of a meal three times a day (group A, n=26) or calcium carbonate in the same manner plus 0.625 mg/day of conjugated equine estrogen and 5 mg medrogestone acetate from day 1-12 each month (group B, n=30). The age (mean +/- S.E.M.) was 66.3 +/- 1.2 and 65.1 +/- 1.1 years, weight 54.1 +/- 1.2 and 55.3 +/- 2.1 kg, in group A and group B, respectively. Urine specimens (24-h) were collected at baseline and 3 months after treatment for the determination of calcium oxalate saturation by using Tiselius's index (AP(CaOx)) and calcium/citrate ratio. RESULTS: After 3 months of treatment, there was no significant alteration from baseline for urinary excretion of calcium, citrate and oxalate. Urinary phosphate excretion was significantly reduced (6.3 +/- 0.7 vs. 5.1 +/- 0.7 mmol/day for group A and 8.2 +/- 0.9 vs. 5.8 +/- 0.7 mmol/day for group B, P<0.05), whereas net alkaline absorption was significantly elevated (10.1 +/- 3.6 vs. 20.1 +/- 4.4 meq/day for group A and 4.8 +/- 3.2 vs. 19.9 +/- 3.6 meq/day for group B, P<0.05). Calcium/citrate ratio and AP(CaOx) determined at baseline were not different from the corresponding values after treatment in both groups; calcium/citrate: 10.1 +/- 3.1 vs. 10.1 +/- 2.5 for group A and 9.3 +/- 1.8 vs. 11.9 +/- 2.5 for group B and AP(CaOx): 1.1 +/- 0.1 vs. 1.3 +/- 0.2 for group A and 1.2 +/- 0.2 vs. 1.1 +/- 0.1 for group B. There were eight and nine patients with high AP(CaOx), or >2, at baseline and after treatment, respectively. CONCLUSIONS: Calcium supplement with a meal or combined calcium supplement and estrogen therapy is not associated with a significant increased risk of calcium oxalate stone formation in the majority of postmenopausal osteoporotic patients. Determination of urinary saturation for calcium oxalate after calcium and estrogen supplements, especially at the initial phase of treatment, may be helpful in the avoidance of nephrolithiasis.

Aged↗
PubMed1999

Antioxidant effect of short-term hormonal treatment in postmenopausal women.

OBJECTIVES: Recent studies have shown that estrogens alone or in association with progestins can exert an antioxidant effect on Low-Density Lipoprotein (LDL) and lipids of platelet membranes. It has been demonstrated that the oxidative modification of LDLs also involving the formation of lipid peroxides, exerts several biological effects that may contribute to the onset and progression of cardiovascular diseases. Therefore, the aim of our study was to evaluate the effect of short-term treatment with oral estrogens alone and estrogens plus progestin on endogenous and copper-induced serum levels of lipid peroxides in postmenopausal women. METHODS: Thirty-nine postmenopausal women were randomly divided into three groups: group I was treated with oral conjugated equine estrogens (CEE) for 21 days; group II received oral CEE for 21 days and, after 14 days of this treatment, 5 mg/day of medrogestone was added for 7 days; group III did not receive any therapy (controls). Endogenous and copper-induced serum levels of lipid peroxides were determined before and after 21 days of treatment in the two treated groups and in the control group. RESULTS: The serum endogenous levels of lipid peroxides in postmenopausal women did not change after short-term treatment with hormone replacement therapy. Moreover, copper-induced serum levels of lipid peroxides significantly decreased after therapy in both groups I and II. CONCLUSIONS: Our data show that hormone replacement therapy (HRT) inhibits lipid peroxidation and may play a role in preventing cardiovascular diseases.

Cardiovascular Diseases↗
PubMed2000

Prevention of postmenopausal bone loss by low and conventional doses of calcitriol or conjugated equine estrogen.

OBJECTIVES: Estrogen deficiency is the most common cause of postmenopausal osteoporosis and estrogen replacement is well known to retard postmenopausal bone loss. Calcium supplement alone is generally considered to be insufficient for the prevention of bone loss associated with estrogen deficiency while the role of calcitriol is unclear. In the present study we examined the efficacy different doses of estrogen or calcitriol in the prevention of postmenopausal bone loss in Thais. METHODS: The subjects consisted of 146 Thai women no more than 6 years postmenopausal. The subjects were randomly allocated to receive 750 mg supplemental calcium alone, calcium and conjugated equine estrogen (CEE) at 0.3 or 0.625 mg, calcium and calcitriol at 0.25 or 0.5 microg daily. Those receiving CEE also took 5 mg medrogestone for 12 days each month. BMD at L2-4 and femoral neck were measured at baseline 1 year and 2 years after treatments. Data were expressed as mean +/- S.E. RESULTS: Subjects on supplemental calcium alone had approximately 2.5% decreases in L2-4 (P < 0.05) and femoral BMD (P < 0.01) at 2 years. CEE (0.3 mg) resulted in 3.20 +/- 1.2% increase in vertebral BMD (P < 0.05) while no significant change in BMD was demonstrated at the femoral neck. Likewise, 0.625 mg of CEE induced 5.4 +/- 1.4% increase in vertebral BMD at 2 years (P < 0.001) without change in the femoral BMD. In regard to calcitriol, no significant change in vertebral or femoral BMD was demonstrated with either 0.25 or 0.5 microg calcitriol. CONCLUSION: We concluded that calcitriol is effective in the prevention of early postmenopausal bone loss in Thais. It represents an option for the prevention of osteoporosis in postmenopausal women who are contraindicated for estrogen replacement.

Absorptiometry, Photon↗
PubMed1992

[Bone density before and after the hormonal therapy of young women with hypergonadotropic hypogonadal amenorrhea].

Dual energy X-ray absorptiometry of bone density in the lumbar vertebral column was performed in 32 young women (mean age 24.6 [19-34] years) with hypergonadotropic hypogonadal amenorrhoea. There was a significantly lower bone density (0.74 +/- 0.27 g/cm2) than in a control group of 27 women of similar age (1.17 +/- 0.081 g/cm2; P less than 0.001). Subsequently 21 of the 32 women received cyclical hormone substitution therapy for 24 months (day 1-30: 0.625 mg conjugated oestrogens; additionally, on days 20-30: 5 mg medrogestone; followed by a seven-day pause). After 6 months bone density, compared with that of the 11 untreated women, had increased significantly (P less than 0.001). It is therefore recommended that young hypoestrogenemic women should receive early and continuous hormone substitution treatment.

Absorptiometry, Photon↗
PubMedDate not supplied

Monitoring bone effect of transdermal hormone replacement therapy by ultrasound investigation at the phalanx: a four-year follow-up study.

OBJECTIVE: A controlled 4-year follow-up study was conducted on a population composed of 112 healthy early postmenopausal women to evaluate the ability of ultrasound technology in detecting the effects of hormone replacement therapy (HRT) on bone. At the end of the study, 47 untreated and 25 treated women had been evaluated. Cyclic sequential estrogen/progestogen therapy, 50 microg/day of transdermal 17beta-estradiol (Rotta Research Laboratorium) plus 5 mg/day of medrogestone (Wyeth-Ayerst) was used. DESIGN: Ultrasound transmission through the distal metaphysis of hand phalanxes was measured by DBM Sonic. Beside amplitude-dependent speed of sound (AD-SoS), three new parameters could be calculated: pure speed of sound (pSOS), bone transmission time (BTT), and ultrasound bone profile index (UBPI). Ultrasound measurements were taken at baseline and after 1, 2, and 4 years. RESULTS: Among untreated women a significant decrease of all ultrasound parameters was observed at follow-up measurements. In the HRT-treated group we observed a significant increase of AD-SoS, pSoS, and BTT. We qualified as "responders" women in the treated group for whom AD-SoS, pSoS, and BTT increased by more than 2.77 times the coefficient of variation of the measurement, i.e., 95% variability. Women in the treated group were identified as responders at 4 years of follow-up by AD-SoS (56%), pSOS (56%), and BTT (60%). Ultrasound bone profile index declined in both groups, although to a lower extent among HRT-treated subjects. CONCLUSIONS: The 4-year data confirm the results obtained at 1 and 2 years of follow-up. This study demonstrates that bone tissue investigation by ultrasound at the phalanx can be used to monitor the effect of HRT, and thus it should be considered a potential technology for the management of menopause by gynecologists.

Administration, Cutaneous↗
PubMed1981

Effects of Colprone on in vitro release of androgens from the reproductive organs of the male rat.

Effects of medrogestone (6,17 alpha-dimethyl-4-,6-pregnadiene-3, 20-dione; Colprone) on the release of testosterone (T) and 5 alpha-dehydrotestosterone (5 alpha-DHT) in the reproductive organs of the male rat were tested in vitro. The minced testes released twice as much T into the medium when incubated in the presence of 50 mIU/ml of hCG. The release of T was inhibited significantly when 10 or 50 micrometers Colprone was added to the incubation medium. More 5 alpha-DHT was released into the medium from the testes mince in the presence of hCG, while the addition of 10 or 50 micrometers of Colprone inhibited 5 alpha-DHT release as compared to hCG controls. On the other hand, hCG failed to stimulate the release of T and 5 alpha-DHT from the minced caput and cauda epididymis and ventral prostate. The addition of Colprone (10--50 micrometers/ml) to the medium containing caput epididymis or ventral prostate resulted in a significant inhibition of T and 5 alpha-DHT. However, no significant change in the rate of T or 5 alpha-DHT release was recorded in medium containing cauda epididymis. In spite of its anti-androgenic effects reported by several investigators, Colprone in the present study has shown differential effects on T and 5 alpha-DHT release from different reproductive tissues of the male rat.

Animals↗
PubMed1981

Measurement of plasma progesterone and its O-methyloxime by gas chromatography-nitrogen detection.

A routine method for the quantitation of plasma progesterone, using only 1 ml of sample, has been developed based on gas chromatography-nitrogen detection of the O-methyloxime derivative. Simple solvent extraction of progesterone from plasma using cyclohexane as solvent and medrogestone as internal standard allows measurement at the 3 nmol/l level, while the coefficient of variation at 16, 64, and 127 nmol/l progesterone is 14, 7.5, and 6.5% respectively. Comparison with a radioimmunoassay gave a linear regression equation of Y = 0.84x + 1.4, Syx = 7.8, r = 0.9255 (n = 55).

Chromatography, Gas↗
PubMedDate not supplied

[Mechanism of action of progestins in the treatment of hormone-dependent breast cancer (author's transl)].

The in vitro interference of some gestagens with the binding of 3H-17-beta-oestradiol to cytosol specific receptors was investigated with a view to elucidating the mechanism of action of progestins in the treatment of human hormone-dependent breast cancer. A decrease (up to 85%) of oestradiol binding capacity was observed with high concentrations of progesterone, clogestone and medrogestone. These findings are in good agreement with those previously obtained by the same progestins in our laboratory on rat uterine estrogen receptors in vitro or in vivo. These results provide the support for the hypothesis that the mode of action of progestins in the therapy of mammary and perhaps uterine carcinomas is to some extent related to the inhibition of oestradiol binding to cytosol specific receptors.

Breast Neoplasms↗
PubMed2001

Effects of estrogen/medrogestone therapy on the apoprotein B-containing lipoproteins in postmenopausal women with type 2 diabetes mellitus under satisfactory and non-satisfactory glycemic control.

BACKGROUND: Information is lacking on the effects of hormone replacement therapy in women with diabetes, especially during moderate chronic hyperglycemia. OBJECTIVES: To study the effects of HRT on the lipid profile and the low density lipoprotein subclass distribution in women with type 2 diabetes under satisfactory and non-satisfactory glycemic control. METHODS: Fifty-four postmenopausal women after a 6 week run-in diet were randomized to receive either placebo (HbA1c < 8%, n = 13; HbA1c > 8%, n = 17) or HRT (HbA1c < 8%, n = 11; HbA1c > 8%, n = 13) for 12 weeks. HRT consisted of cyclical conjugated estrogens 0.625 mg/day plus medrogestone 5 mg/day. At the beginning and at the end of each treatment period the LDL subclass distribution was estimated by density gradient ultracentrifugation. RESULTS: At the baseline and during the study, the HbA1c level was significantly higher in hyperglycemic patients than in the near-normoglycemic controls (baseline 10.2 +/- 2.9 vs. 6.5 +/- 0.7%, P < 0.01). They showed a trend for higher total and LDL cholesterol, triglycerides and lower high density lipoprotein-cholesterol compared to near-normoglycemic controls, as well as significantly higher triglyceride concentrations in very low density lipoprotein, intermediate density lipoprotein and LDL-1 particles and cholesterol content in LDL-1 and -2 particles. HRT decreased LDL-cholesterol in both groups. In the normoglycemic patients a small increase in HbA1c was observed (6.5 +/- 0.7 vs. 7.4 +/- 1%, P = 0.04). In all cases, HRT did not modify the proportion of LDL represented by denser LDLs. CONCLUSIONS: HRT did not modify the LDL subclass distribution, even in the presence of moderate chronic hyperglycemia in women with type 2 diabetes.

Aged↗
PubMed1992

[Italian multicenter study for the verification of the efficacy and tolerability of short-term substitution hormone therapy using conjugated estrogens and progestagens administered orally in the postmenopausal a period].

Three hundred and sixty-three postmenopausal women received 6 months of cyclic hormone replacement therapy with conjugated estrogens in differing doses (0.625 mg and 1.25 mg) associated in a sequential pattern lasting 12 days with progestagens (medroxyprogesterone acetate or medrogestone) in 16 italian health centres. The results of the multicentre study confirm the efficacy of this conjugated estrogen-progestogen regimen in resolving climacteric syndrome, offering cardiovascular protection and vaginal trophic effect and preventing postmenopausal osteoporosis, as well as confirming its tolerability in relation to blood pressure, body weight, breast, endometrium, blood coagulation and hepato-renal function.

Administration, Oral↗
PubMed1991

[Compared action of norethindrone and various steroids on Müller ducts of the female chick embryo].

Treatment of female chick embryo with norethindrone (NET), a potent progesterone-like steroid, caused caudal agenesia and cephalic regression of Mullerian ducts as the normal regression induced by anti-Mullerian-hormone in the male embryo. The comparative study of five other progesterone-like steroids shows that only lynestrenol which is metabolized into NET at least in man, possesses the same properties as NET. The four others, i.e. medroxyprogesterone, medrogestone, norgestrienone and 17 alpha hydroxyprogesterone are only able to induce agenesia, an unspecific property, which was observed with many steroidal hormones, as norethandrolone here studied.

Animals↗
PubMed1980

A comparison of oestrogen-progestogen with clonidine in the climacteric syndrome.

Twenty-three cases of the climacteric syndrome were analysed in a double-blind study comparing the effect of conjugated equine oestrogen (Premarin) and medrogestone (Colpro) with clonidine (Dixarit) on various clinical parameters. The treatment lasted 20 weeks. Statistical analysis of the results indictaed that opposed oestrogen therapy was effective in reducing hot flushes (P < 0,05) whereas clonidine was not. The other variables tested did not attain statistical significance.

Climacteric↗
PubMed1995

[Estrogen replacement in postmenopause, blood coagulation and fibrinolysis: comparison of a new kind of transdermal estradiol treatment with oral therapy with conjugated estrogens].

Estrogen replacement therapy (ERT) appears to markedly reduce the risk of cardiovascular disease in postmenopausal women. There is evidence that estrogen effects on blood coagulation and fibrinolysis are important mediators of this beneficial effect. It is the acute phase reactants such as factor VII (F VII), von Willebrand factor (vWF) and fibrinogen (Fbg) as well as the main inhibitor of the fibrinolytic system, the plasminogen activator inhibitor (PAI 1), which have been shown to be associated with a particular predisposition or poor prognosis of cardiovascular disease. Additionally, the analysis of stabile reaction products of the coagulation cascade allows for an assessment of the loss of endothelial anticoagulant properties, i.e. endothelial injury. We compared the effects of oral versus transdermal ERT on these key parameters of the hemostatic system. 42 postmenopausal women were randomly assigned to receive either a novel transdermal system releasing 50 micrograms 17-beta-estradiol/24 hours or oral therapy with 0.6 mg conjugated estrogens combined with cyclic medrogestone 5 mg on day 11-21 for three treatment cycles. The study was performed according to the criteria of good clinical practise. We observed no adverse effects on the hemostatic system. Particularly, no increase of coagulatory reaction products, i.e. activity was found. Differences between groups were seen with regard to the extent of favourable effects: While the continuous transdermal ERT significantly reduced factor VII activity, oral ERT had no effect. However, oral ERT significantly reduced PAI 1 concentration by 40% suggesting an improved fibrinolytic capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗
PubMed1995

[Hormone substitution with premarin plus. Results of an Austrian multicenter treatment study].

Estrogen/progestin hormone replacement therapy in menopausal women has 2 important medical rationales. First of all, patients are relieved from the subjective symptoms almost fully. In addition patients benefit from prophylaxis of long term even life threatening sequelae of estrogen deficiency. This paper documents the results of a multicenter phase IV study, performed nationwide in Austria with 158 participating gynaecologists. Objective of this phase IV study was the analysis of efficacy and safety data of a new estrogen/progestin hormone replacement therapy scheme under almost practice conditions in the gynaecological context. The therapy supplied was Premarin plus, containing 28 coated tablets of 0.625 or 1.25 mg conjugated estrogens and in addition 12 tablets for the last cycle days containing 5 mg medrogeston. Thus, the dispensing gynaecologists had the option of an individual estrogen dose adjustment in case the low starting dose showed lack of efficacy. The results are based on the data of 1508 recruited female patients. A very high degree of representativeness is attributable to the high number of recruited patients. Overall judgement of the results shows a very high level of efficacy and a well tolerated scheme of hormone replacement therapy with the option of individual estrogen dose adjustments.

Austria↗
PubMed1998

[The effect of cyclic administration of progestagens on blood coagulation factors].

The relationship between thromboembolism and oral contraceptives has been discussed for 30 years. Recently, a new actuality for this problem has grown up. The estrogen component of the preparations seems to be the cause, but some authors also think of the progestogens as responsible for drug-related thromboembolic disorders. In 31 patients with mastopathy or mastodynia, who had been treated with 10 mg medrogeston of dydrogesteron for six cycles, there were no significant changes in the parameters of hemostasis and fibrinolysis. Especially, we did not find any indications to an activation of the coagulation system. There is no evidence for a thrombogenetic effect caused by the cyclic therapy with these progestogens.

Adolescent↗
PubMed1998

Treatment with progesterone analogues decreases macrophage Fcgamma receptors expression.

Macrophage Fcgamma receptors (FcgammaRs) are critical for host defense against infection and have an important role in immune cytopenias. Modulation of macrophage FcgammaRs expression is a potential therapeutic approach to immune disorders. Glucocorticoids and synthetic progesterone analogues decrease macrophage FcgammaRs expression. We assessed the effect of treatment with commonly employed progestins on the expression of macrophage FcgammaRs using an experimental model in the guinea pig. Eight clinically available progesterones, medroxyprogesterone acetate (P3), megestrol acetate (P4), medrogestone (P5), alylestrenol (P6), linestrenol (P7), didrogesterone (P8), norethisterone (P9), and gestonorone caproate (P10) and two endogenous progesterones, progesterone (P1) and 17 alpha-hydroxyprogesterone (P2), were studied. Following in vivo treatment of guinea pigs, we determined the clearance of IgG-sensitized erythrocytes in vivo, the binding of IgG-sensitized erythrocytes by isolated splenic macrophages, and splenic macrophage Fcgamma receptor cell surface expression. All progesterones impaired the clearance of IgG-sensitized erythrocytes by decreasing splenic macrophage Fcgamma receptor expression. P5, P6, P7, and P8 were less effective. Flow cytometry and fluorescence microscopy with monoclonal antibodies demonstrated that progesterones decreased the cell surface expression of FcgammaR2 more than that of FcgammaR1,2. Clinically employed progestins impair the clearance of IgG-coated cells by decreasing splenic macrophage FcgammaRs expression. Thus, progesterones are candidate drugs for the treatment of immune disorders.

Animals↗
PubMed1979

Steroid hormone regulations of uterine peroxidase activity.

Uterine peroxidase enzyme activity has been studied as a marker for estrogen action in the uterus to help clarify the mechanism of estrogen action and its modulation by antiestrogens and progestins. Estrogen-induced increases in peroxidase were found to closely parallel increases in uterine weight and DNA content in the castrate rat. In the cycling female rat, uterine peroxidase levels were highest during proestrus and estrus and the lower levels of metestrous and diestrous uteri could be raised to estrous levels by administration of estrogen. However, the estrous levels were not further increased by estrogen treatment. The antiestrogen, CI628, while a very weak inducer of uterine peroxidase, is an effective antagonist of the estrogen induction of the enzyme. The prolonged duration of this CI628-effected inhibition corresponds to the prolonged depletion of cytoplasmic estrogen receptor seen with CI628 treatment. Progesterone, R5020 and norethindrone were also found to be effective antagonists of estrogen-induced uterine peroxidase. Medrogestone and clogestrone, less potent progestins in the rat, were also less effective antagonists of peroxidase induction. Since progesterone was found to inhibit peroxidase induction due to both estrone and diethylstilbestrol, as well as estradiol, it is considered unlikely that this antagonism relates to progestin-induced increases in uterine 17 beta-hydroxysteroid dehydrogenase. Rather, it is proposed that progestins, acting through progestin receptor, may have a more direct role, possibly acting at the level of the genome to repress the expression of estrogen-induced products.

Animals↗
PubMed1994

Impact of hormone replacement therapy on postprandial lipoproteins and lipoprotein(a) in normolipidemic postmenopausal women.

In 43 normolipidemic postmenopausal women we studied fasting and postprandial (oral fat load with 50 g fat per square meter; blood sampling for 5 h) lipoprotein components and lipoprotein(a) levels before and with the administration of conjugated equine estrogens opposed by medrogestone (on days 11-21). Data was compared intraindividually; the second testing was performed during the last 5 days of the combined estrogen/progestogen phase of the third cycle. Fasting low-density lipoprotein (LDL) and total cholesterol concentrations decreased significantly; high-density lipoprotein (HDL) cholesterol, including subfractions HDL2 and HDL3, was not changed. Fasting triglyceride concentrations increased. All lipoprotein fractions measured showed a postprandial elevation with the exception of chylomicron cholesterol concentrations. There was a significant effect of hormone replacement therapy on the postprandial course of total cholesterol (decrease; P < 0.001), VLDL cholesterol (increase; P = 0.025), and the triglyceride proportion in the LDL plus HDL fraction (increase; P < 0.001). With hormone replacement therapy the postprandial curve of total triglycerides was increased only 1 h after the fat load while chylomicron triglyceride concentrations were lowered after 5 h. VLDL triglycerides were not influenced. In all patients with lipoprotein(a) levels above 10 mg/dl, this parameter decreased (about 25%). Although increasing fasting triglyceride concentrations, hormone replacement therapy does not bring about an exaggerated postprandial increase in triglycerides. Postprandial chylomicron clearance is evidently promoted. Hormone replacement therapy leads to a small increase in triglycerides in the LDL plus HDL fraction by inhibiting hepatic lipase activity. Moreover, the decrease in lipoprotein(a) levels may contribute to the antiatherosclerotic effect.

Dietary Fats↗