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PubMed1996

Tibolone versus conjugated estrogens and sequential progestogen in the treatment of climacteric complaints.

OBJECTIVE: Tibolone has been shown to alleviate climacteric symptoms. This study was designed to compare the effect of tibolone (Livial, 2.5 mg daily) on different climacteric complaints and its impact on the endometrium, determined by vaginal ultrasound, with that of conjugated estrogens (Premarin, 0.625 mg daily) continuously for 6 months in combination with the progestogen medrogestone (Colpron, 2 x 5 mg daily for 12 days each month). METHODS: One hundred and twenty-nine postmenopausal women were recruited and the severity of climacteric symptoms as well as endometrial thickness were recorded at the pre-trial examination and after 1, 3, and 6 months. RESULTS: With the exception of vertigo, mood depression, mood disorder, loss of libido, and dryness of skin, where tibolone was found to be more effective than conjugated estrogens/medrogestone, climacteric symptoms improved significantly in both groups over the 6-month study period. Endometrial thickness did not increase significantly in the tibolone group, whereas in the conjugated estrogens/medrogestone group there was a highly significant increase after 1 month and still a trend towards significance after 6 months. Recurrence of vaginal bleeding occurred significantly less frequently in the tibolone group than in the comparison group. CONCLUSION: Tibolone seems to offer a complete treatment of the climacteric complaints whilst avoiding some of the problems associated with classical hormone replacement therapy.

Climacteric↗
PubMed2003

Classification and pharmacology of progestins.

Besides the natural progestin, progesterone, there are different classes of progestins, such as retroprogesterone (i.e. dydrogesterone), progesterone derivatives (i.e. medrogestone) 17alpha-hydroxyprogesterone derivatives (i.e. chlormadinone acetate, cyproterone acetate, medroxyprogesterone acetate, megestrol acetate), 19-norprogesterone derivatives (i.e. nomegestrol, promegestone, trimegestone, nesterone), 19-nortestosterone derivatives norethisterone (NET), lynestrenol, levonorgestrel, desogestrel, gestodene, norgestimate, dienogest) and spironolactone derivatives (i.e. drospirenone). Some of the synthetic progestins are prodrugs, which need to be metabolized to become active compounds. Besides the progestogenic effect, which is in common for all progestins, there is a wide range of biological effects, which are different for the various progestins and have to be taken into account, when medical treatment is considered.

Female↗
PubMed2003

Differential effects of progestins on breast tissue enzymes.

There is substantial evidence that mammary cancer tissue contains all the enzymes responsible for the local biosynthesis of estradiol (E2) from circulating precursors. Two principal pathways are implicated in the final steps of E2 formation in breast cancer tissue: the 'aromatase pathway' that transforms androgens into estrogens and the 'sulfatase pathway' that converts estrone sulfate (E1S) into estrone (E1) via estrone sulfatase. The final step is the conversion of weak E1 to potent biologically active E2 via reductive 17beta-hydroxysteroid dehydrogenase type 1 activity. It is also well established that steroid sulfotransferases, which convert estrogens into their sulfates, are present in breast cancer tissues. One of the possible means of blocking E2 effects in breast cancer is to use anti-estrogens, which act by binding to the estrogen receptor (ER). Another option is to block E2 using anti-enzymes (anti-sulfatase, anti-aromatase, or anti-17beta-hydroxysteroid dehydrogenase (17beta-HSD). Various progestins (e.g. promegestone, nomegestrol acetate, medrogestone, 17-deacetyl norgestimate, dydrogesterone and its 20-dihydro derivative), as well as tibolone and its metabolites, have been shown to inhibit estrone sulfatase and 17beta-hydroxysteroid dehydrogenase. Some progestins and tibolone can also stimulate sulfotransferase activity. These various progestins may therefore provide a new option for the treatment of breast cancer.

17-Hydroxysteroid Dehydrogenases↗
PubMed2001

Effects of postmenopausal hormone replacement therapy on lipid, lipoprotein, and apolipoprotein (a) concentrations: analysis of studies published from 1974-2000.

OBJECTIVE: To establish reference estimates of the effects of different hormone replacement therapy (HRT) regimens on lipid and lipoprotein levels. DESIGN: Review and pooled analysis of prospective studies published up until the year 2000. SETTING: Clinical trials centers, hospitals, menopause clinics. PATIENT(S): Healthy postmenopausal women. INTERVENTION(S): Estrogen alone, estrogen plus progestogen, tibolone, or raloxifene in the treatment of menopausal symptoms. MAIN OUTCOME MEASURE(S): Serum high- and low-density lipoprotein (HDL and LDL) cholesterol, total cholesterol, triglycerides, and lipoprotein (a). RESULT(S): Two-hundred forty-eight studies provided information on the effects of 42 different HRT regimens. All estrogen alone regimens raised HDL cholesterol and lowered LDL and total cholesterol. Oral estrogens raised triglycerides. Transdermal estradiol 17-beta lowered triglycerides. Progestogens had little effect on estrogen-induced reductions in LDL and total cholesterol. Estrogen-induced increases in HDL and triglycerides were opposed according to type of progestogen, in the order from least to greatest effect: dydrogesterone and medrogestone, progesterone, cyproterone acetate, medroxyprogesterone acetate, transdermal norethindrone acetate, norgestrel, and oral norethindrone acetate. Tibolone decreased HDL cholesterol and triglyceride levels. Raloxifene reduced LDL cholesterol levels. In 41 studies of 20 different formulations, HRT generally lowered lipoprotein (a). CONCLUSION(S): Route of estrogen administration and type of progestogen determined differential effects of HRT on lipid and lipoprotein levels. Future work will focus on the interpretation of the clinical significance of these changes.

Anabolic Agents↗
PubMed1992

Hypergonadotropic hypogonadic amenorrhea (World Health Organization III) and osteoporosis.

OBJECTIVE: To assess the bone mineral density in World Health Organization (WHO) III women after hormone replacement therapy. DESIGN: We studied the bone mineral density of 41 women with premature ovarian failure (hypergonadotropic hypogonadic amenorrhea--WHO III) before and during hormone replacement therapy. SETTING: All WHO III women were recruited from the Outpatient Department of the First Department of Gynecology and Obstetrics, University of Vienna Medical School, Austria, a public University Hospital. PATIENTS, PARTICIPANTS: Forty-one patients, 30 healthy women. INTERVENTIONS: Twenty-eight of 41 WHO III women received cyclic hormone replacement therapy consisting of 0.625 mg conjugated estrogen (days 1 to 30) and 5 mg medrogeston (days 20 to 30) in addition, with a 7-day interval. MAIN OUTCOME MEASURE: The bone mineral density was evaluated by single photon absorptiometry and dual energy x ray absorptiometry every 6 months (single photon absorptiometry six times, dual energy x ray absorptiometry four times). RESULTS: The bone mineral density in young women with hypergonadotropic hypogonadic amenorrhea (WHO III) was lower than in age-matched controls. Hormone replacement therapy produced an increase in bone mineral density in 28 WHO III women, whereas bone mineral density remained quite constant in the women without therapy. CONCLUSION: Hormone replacement therapy increases the bone mineral density of women with hypergonadotropic hypogonadic amenorrhea. Hormones should be substituted early and consistently in affected patients.

Adult↗
PubMed1997

The effect of sequential three-monthly hormone replacement therapy on several cardiovascular risk estimators in postmenopausal women.

OBJECTIVE: To investigate the changes in plasma lipids and lipoproteins, low-density lipoprotein (LDL) oxidizability, and plasma homocysteine during postmenopausal sequential 3-monthly hormone replacement therapy. DESIGN: Open longitudinal prospective study. SETTING: Gynecological outpatient department of a university hospital. PATIENT(S): Thirty-nine healthy nonhysterectomized postmenopausal women. INTERVENTION(S): Oral conjugated estrogen, 0.625 mg/d, combined with oral medrogestone 10 mg/d during the last 14 days of each 84-day treatment cycle. The treatment was given for four treatment cycles of 84 days (1 year). MAIN OUTCOME MEASURE(S): Plasma lipids and lipoproteins, LDL oxidizability, and plasma homocysteine. RESULT(S): After 1 year of treatment plasma concentrations of total cholesterol and LDL cholesterol were 3.5% and 8.7% lower, respectively. High density lipoprotein cholesterol, apolipoprotein A-I, and triglycerides were 6.5%, 9.0% and 16% higher, respectively. Apolipoprotein B concentration remained unchanged. The results on LDL oxidizability were inconsistent. Plasma homocysteine decreased with 12.3% during the first 6 months of treatment in women with higher homocysteine concentrations at baseline. These values returned to baseline levels during the second half year of treatment. CONCLUSION(S): This sequential hormone regimen induced beneficial changes in the conventional lipid and lipoprotein risk estimators, whereas the observed changes in the other markers remained inconclusive and/or of minor importance.

Cardiovascular Diseases↗
PubMed2000

Preperitoneal lipoleiomyoma of the abdominal wall in a postmenopausal woman.

OBJECTIVE: Extrauterine leiomyomas are rare events. These tumors may be easily misdiagnosed as ovarian tumors at the clinical investigation. We present the first case of an otherwise healthy postmenopausal woman, hysterectomized 20 years ago, who developed a preperitoneal lipoleimoyoma in the 30-year-old scar of a Pfannenstiel incision. The patient received continuous hormone replacement therapy (HRT) for 5 years with 1.25 mg conjugated estrogen and 5 mg medrogeston per day. METHODS: In sections of the tumor, immunohistochemical reactions with antibodies against actin, desmin, vimentin, estrogen and progesterone receptors and factor VIII related antigen was performed. RESULTS: Histologic findings revealed cellular fascicles of spindle-shaped smooth muscle cells in a whorled arrangement. Mitotic figures were absent. Central degenerative changes and focal edema were observed. Between muscle fascicles, a significant amount of fat cells (20% of tumor volume) was visible. Leiomyocytes showed immunohistochemicaly positive reactions with actin, desmin, vimentin, and steroid hormone receptors. Based on these findings, the tumor was diagnosed as lipoleiomyoma. CONCLUSIONS: Origin of the tumor of smooth muscle cells of vessels located in the abdominal wall and development under influence of oral steroids seems most probable. HRT appears to promote the development of extrauterine leiomyomas in postmenopausal women.

Abdomen↗
PubMed1998

Change in body weight after hormone replacement therapy in postmenopausal women is dependent on basal circulating leptin.

OBJECTIVE: To address the effect of leptin in the modulation of change in body weight after hormone replacement therapy (HRT), we prospectively examined the responses of body weight and serum leptin after estrogen-progestin replacement in postmenopausal women. PATIENTS: Subjects consisted of 63 postmenopausal women aged 54-82 years on HRT for osteoporosis. DESIGN: Thirty three of the subjects received 0.3 mg of conjugated equine estrogen (CEE) (group 1) while 30 were on 0.625 mg of CEE daily (group 2). All subjects also took 5 mg of medrogestone acetate and 750 mg elemental calcium supplement daily. MEASUREMENTS: Fasting serum leptin was measured by RIA at baseline, 1 and 3 months after treatment. Data were expressed as mean +/- S.E.M. RESULTS: Serum leptin was highly related to body weight both at baseline (r = 0.40, P < 0.001) and after 3 months of HRT (r = 0.42, P < 0.001). When divided the subjects into three equal groups according to baseline leptin levels, it was found that serum leptin significantly decreased in subjects with high baseline leptin at 3 months (-9.4 +/- 5.7%, P < 0.05) while it increased in subjects whose baseline leptin levels were in the lowest tertile at 1 month (33.2 +/- 8.3%, P < 0.001) and 3 month (27.8 +/- 8.3%, P < 0.01). In regards to body weight, those with leptin in the highest tertile demonstrated a reduction of body weight at 3 (-1.9 +/- 0.6%, P < 0.05) and 12 months (-3.2 +/- 0.5%, P < 0.05) after HRT while those whose serum leptin levels were in the lowest and middle tertiles did not demonstrate change in body weight. By repeated measured analysis of variance, it was found that the decrease in body weight in subjects with high serum leptin was independent of the doses of estrogen. CONCLUSION: Postmenopausal hormone replacement does not cause weight gain. However, it results in a small reduction in body weight particularly in subjects with higher basal leptin concentrations.

Aged↗
PubMed1999

The effects of six months of treatment with a low-dose of conjugated oestrogens in menopausal women.

OBJECTIVE: Hormone replacement therapy (HRT) is usually prescribed as medium- to high-dose formulations. Little is known, however, about dose-dependency of oestrogen effects on plasma hormone levels, markers of cardiovascular risk in lipid metabolism and the haemostatic system, or markers of bone turnover. SUBJECTS AND DESIGN: In an open trial, three groups of 12 or 13 healthy, non-obese postmenopausal women received conjugated equine oestrogens (CEE) for 6 months at doses of 0.3 mg/day (group 1), 0.6 mg/day (group 2) or 1.25 mg/day (group 3). From day 1 to day 10, CEE was administered alone, and from day 11 to day 21, in combination with 5 mg of medrogestone. Each treatment cycle was followed by a pause of 7 days. Fasting blood samples were obtained before treatment as well as on days 10, 21 and 28 of the first, third and sixth months on treatment. All results obtained on day 10 were grouped together as phase A, on day 21 as phase B, and on day 28 as phase C. MEASUREMENTS: Plasma concentrations of oestradiol (E), dehydroepiandrosterone sulphate (DHEA-S), total testosterone (T), FSH, PRL, sex hormone binding globulin (SHBG), type I procollagen propeptide (PICP) and the cross-linked carboxyterminal telopeptide of type I collagen (ICTP), total cholesterol, HDL-cholesterol, triglycerides (TG), apolipoprotein (apo) A-1, apo B, lipoprotein(a)[Lp (a)], fibrinogen, factor VIIc and plasminogen activator inhibitor 1 (PAI-1) were evaluated with commercially available kits. RESULTS: Dose-dependently, the three regimens increased E, SHBG and factor VIIc activity and decreased FSH, DHEAS, cholesterol, LDL-cholesterol and apoB. HDL-cholesterol and apoA-1 were slightly decreased in group 1 but increased in groups 2 and 3. The high CEE dosage in group 3 resulted in a significant increase of TG and decrease of Lp(a) and PAI-1. Markers of bone turnover were not significantly changed by any CEE dosage. CONCLUSIONS: Six months of treatment with 0.3 mg/day of conjugated equine oestrogen significantly lowers serum levels of total cholesterol and LDL-cholesterol without causing the adverse increases of triglycerides or factor VIIc, which were observed at higher doses. However, this low-dose treatment did not yield the maximal LDL-cholesterol lowering effect. Moreover, the positive effects of HRT on HDL-cholesterol, apolipoprotein A-I, lipoprotein (a) and plasminogen activator inhibitor-1 required at least the medium dose of 0.6 mg conjugated equine oestrogens per day. Therefore, further studies are needed to determine which dose of conjugated equine oestrogens has the optimal effect on cardiovascular risk and bone turnover.

Biomarkers↗
PubMed2003

Androgens and antiandrogens.

The role of androgens in women's health has been generally neglected. Currently available assays are lacking in sensitivity and reliability at the lower ranges. Circulating androgens as prohormones for other steroids (e.g., androgens) have an ubiquitous role on diverse physiological and behavioral systems. Clinical assessment of both androgen production and androgen availability can be achieved by measurement of two or three essential values. These include either total T and sex-hormone binding globulin (SHBG), free T and SHBG, or free T and total T. The free testosterone index (total T/SHBG) correlates well with free or bioavailable T and can be used as a substitute. DHEA-S is the most useful measure of adrenal androgen production in women. Androgen insufficiency in women is not a specific consequence of natural menopause, but may occur secondarily to the age-related decline in both adrenal and ovarian androgen production. Since estrogen effects are also strongly linked to mood, psychological well-being, and sexual function in women, the diagnosis of androgen insufficiency should only be made in women who are adequately estrogenized. Before initiating a trial of androgen replacement therapy, a comprehensive clinical assessment should be performed in all cases. Approved androgen replacement therapy is not yet available in most countries for treatment of female sexual dysfunction. This would include T supplements or DHEA. Several new progestins have been synthesized in the last decade. Dienogest is a hybrid progestin that is derived from both the pregnane and the estrane groups with a 17alpha-cyanomethyl radical; drospirenone is derived from spirolactone. Somehow, the molecules available have demonstrated antiandrogenic properties. Cyproterone acetate (CPA) is the most potent antiandrogenic progestin, followed by dienogest, drosperinone, and chlormadinone acetate. Nomegestrol acetate and medrogestone also exert some antiandrogenic properties and are similar to chlormadinone acetate in antiandrogenic potency. While androgens act positively on libido in women, antiandrogenic properties in doses used in HRT do not appear to have a negative effect. Progestins used in HRT have varying pharmacological properties that are associated with different adverse effects. The new progestins with antiandrogenic properties avoid many of the androgenic side effects related to testosterone-derived progestins. They also have the potential of not counteracting beneficial estrogen effects, for example, on the cardiovascular system or mental tone.

Aged↗
PubMed1994

Pulse amplitude and frequency modulation of parathyroid hormone in early postmenopausal women before and on hormone replacement therapy.

Although the pathophysiology of postmenopausal osteoporosis has been investigated extensively, it is still not established in what respect PTH is related to the events. Recently, consistent data on the pulsatile secretion of PTH in man have been published. In this study intact PTH was measured in six early postmenopausal women before and after 6 months of hormone replacement therapy (HRT; 0.6 mg conjugated estrogens and 5 mg medrogestone). In addition to parameters of calcium metabolism and bone mass and to control HRT, intact PTH was measured in blood drawn over 6 h every 2 min. With HRT there was a 30% reduction in PTH secretion. Both the amount secreted per pulse (baseline, 26.8 +/- 6.9 ng/L; HRT, 21.4 +/- 7.6 ng/L; P < 0.05) as well as the basal secretion (baseline, 232.6 +/- 117.6 ng/L.h; HRT, 145.5 +/- 80.0 ng/L.h; P < 0.01) were reduced, whereas the pulse count per h remained constant (baseline, 5.1 +/- 2.2; HRT, 5.1 +/- 1.3). Power spectrum analysis showed a shift in spectral maxima consistent with these findings. Ionized and total calcium were slightly, but nonsignificantly, reduced with treatment. In summary we conclude that in early postmenopausal women, HRT reduces the secretion of PTH by reducing both the basal secretion and the amount secreted per pulse. It is conceivable that some of the known effects of HRT on bone metabolism might be mediated by the modulation of PTH secretion.

Calcium↗
PubMed1979

Interaction of synthetic progestagens with renal mineralocorticoid receptors.

Progesterone increases urinary sodium excretion at least in part by competition for renal mineralocorticoid receptors. In contrast, synthetic progestagens do not increase sodium excretion or even cause a slight sodium retention. We therefore compared the ability of progesterone and 12 progesterone like compounds to displace [3H]aldosterone from binding at cytoplasmic mineralocorticoid receptors in rat kidney. All synthetic progesteronelike steroids were less active than progesterone in competing with [3H]aldosterone for the receptor binding: progesterone 100%, 11 beta-OH progesterone 50%, 17 alpha OH-progesterone 24% and 16 alpha-methyl-progesterone 3%. Derivates of 17 alpha OH-progesterone (medrogestone 5%, dydrogestone 4%, medroxy progesterone-acetate 2% and chlormadinone-acetate 0.5%) were more potent than 19-nor-testosterone derivates: ethisterone 1%, norethisterone less than 1%, norethindrone less than 1%, norethyl-nodrel less than 1%, and ethynodiol-diacetate less than 1%. The decreased affinity of synthetic progestins for mineralocorticoid receptors explains in part the lack of natriuretic activity of these compounds.

Aldosterone↗
PubMed1991

[Lipoprotein metabolism in menopause. Effect of hormonal substitution therapy].

Oral administration of conjugated estrogens, estradiol valerate and micronized estradiol--but not the percutaneous application--in the postmenopause modifies the plasmic lipoprotein profile by lowering, dose-dependently, LDL and elevating HDL (HDL2). In parallel, the cardiovascular mortality is decreased by 50-66%, with smokers also benefiting to the same extent. On account of the increased risk for endometrial carcinoma associated with postmenopausal estrogen monotherapy, combination with a lowest-dose gestagen is imperative. However, the very numerous synthetic gestagens can antagonize the favorable effects of the estrogen on lipoprotein metabolism. This applies in particular to the gestagens of the 19-nortestosterone type, such as norethisterone acetate and, in particular, levonorgestrel, but less so the 17-hydroxyprogesterone derivatives medroxyprogesterone acetate and medrogestone with their very low androgenic effect.

Aged↗
PubMed1994

Hormone replacement therapy and estrogen-dependent cancers.

Until a few years ago, every treated breast cancer was an absolute contraindication to hormonal replacement therapy (HRT). However, the very high five-year survival rate in stage I breast cancer observed today brings more and more apparently healthy early postmenopausal women who have been treated for breast cancer in the past and who are suffering from heavy vasomotor symptoms due to estrogen deficiency to gynecological consultation. Usually well informed, the same group of women starts to worry about an increased risk of postmenopausal osteoporosis and of cardiovascular diseases. What attitude should be adopted today? Our approach should be differentiated and respect the staging, the estrogen-receptor status, and the presence or absence of axillary lymph-node metastasis of every patient. In estrogen receptor-negative women, there is no contraindication to continuous combined HRT by a fixed estrogen-progestin combination. In estrogen receptor-positive and lymph-node-negative patients, treatment by a nonaromatizable progestin, such as medrogestone or medroxyprogesterone acetate (MPA), can be introduced to relieve the patient from her postmenopausal syndrome. After 2-3 years of a favorable evolution of the treated cancer, the substitution might be shifted to a fixed-combined continuous HRT. Because estrogen receptor-positive and lymph-node-positive patients today are usually receiving adjuvant treatment with tamoxifen, they profit already from prophylaxis for postmenopausal osteoporosis and, very likely, from decreased cardiovascular risk. If women out of this group continue to suffer from heavy vasomotor symptoms, MPA might be added. However, it must be stressed that every administration of sexual steroids to women who have been treated for breast cancer has to be started only in full agreement with the treating oncologist concerned with the case and only after having obtained the informed consent of the patient. The new ethical dilemma will be our attitude to quality of life in relation to life prolongation.

Breast Neoplasms↗
PubMed1997

[Postmenopausal hormone substitution and its effects on the climacteric syndrome, body weight and blood pressure].

The effect of 0.6 mg conjugated equine estrogens in combination with sequential medrogestone (5 mg from day 11 to 21) on climacteric symptoms, blood pressure and weight were investigated in 46 postmenopausal women. The climacteric symptoms were quantified by a modified Kuppermann-Index. After a 3 months' treatment the index decreased from 20.58 to 8.47 (p < 0.001). 28 patients (65%) showed a 50% and more reduction of climacteric symptoms. 40 patients (93%) reported an improvement of their complaints. The body weight remained stable. One patient had to interrupt the treatment due to a cerebral ischemic disease (PRIND). The systolic blood pressure was decreased by 7% and the diastolic by 16% under treatment (p < 0.001). 11 patients with borderline or not treated hypertension returned to normal ranges. 3 of the 4 patients treated with antihypertensiva came off the medicines.

Blood Pressure↗
PubMed1982

Estradiol and progesterone receptor concentrations and 17 beta-hydroxysteroid-dehydrogenase activity in estrogen-progestin stimulated endometrium of women with gonadal dysgenesis.

Four hypergonadotrophic women between 25 and 37 years of age with gonadal dysgenesis were treated sequentially with estrogens and a progestin. The hormonal environment induced by this therapy was similar to that of ovulating women, as demonstrated by serum levels of estradiol, endometrial histology and pituitary gonadotropin secretion before and after LH-RH double stimulation. The concentrations of estradiol and progesterone receptors (ER and PR) and the activity of the 17 beta-hydroxysteroid-dehydrogenase (17 beta-HSD) were determined in endometrial curettings obtained from the above patients at 5 different days of their 28-day artificial cycles. The results were correlated to the histology of the endometrium and the serum concentrations of estradiol at the corresponding days of the cycle. The cytoplasmic ER and PR concentrations in the endometrium were 3-6 times higher during the estrogen than progestin phase of the induced endometrial cycle. For the activity of the 17 beta-HSD, the contrary was the case, being 6-10 fold higher during the progestin phase. A 22-day administration of estrogens only did not lead to a rise in enzyme activity or decrease in receptor content as observed under progestin influence after day 14. Since ER and PR concentrations and 17 beta-HSD activities were similar to those in the endometrium of normally ovulating women, these results confirm experimentally the present concept concerning the dependence of the cytoplasmic ER and PR content and 17 beta-HSD activity on female sex hormone action.

11-beta-Hydroxysteroid Dehydrogenases↗