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PubMed1999

[Effectiveness and tolerance of a gonadotropin releasing hormone (goserelin) in treatment of symptomatic endometriosis].

Endometriosis is one of the most common benign gynecological diseases, affecting an estimated 10-15% of all premenopausal women. In this open multicentric prospective study, we investigated the effectiveness and tolerance of a gonadotropin releasing hormone agonist (goserelin) for the treatment of symptomatic endometriosis. One hundred and thirteen patients were included in the study. During the treatment, we documented a relevant reduction in the rAFS score and in the additive diameter of the implants. In addition, we noted a reduction in pelvic pain and an improvement of symptoms on pelvic examination. These effects were also reported during the follow up visits (24 weeks). Only 12 patients had intolerable side effects (hot flushes, sweating during the night, vaginal dryness, depression), which could be managed with transdermal 17 beta estradiol, without reducing therapeutic effectiveness. In conclusion, gonadotropin releasing hormone analogs proved to be an excellent treatment for symptomatic endometriosis and are generally well tolerated.

Adolescent↗
PubMed1990

Cholesterol ester cycle in rat liver: effects of estradiol and progesterone.

The regulation of the enzymatic synthesis and hydrolysis of cholesteryl esters by female sex hormones has been investigated in rat liver. When the effects of estradiol and progesterone were studied in "in vitro" incubations of hepatic microsomes, a dual effect was observed. Progesterone inhibited both microsomal cholesterol ester hydrolase and acyl-CoA: cholesterol acyltransferase activities in a concentration-dependent manner; however, the presence of estradiol stimulated cholesterol ester hydrolysis while it inhibited cholesterol ester formation. The administration of pharmacological doses of estradiol for three consecutive days resulted in decreased cytosolic and microsomal cholesterol esterase activities followed by an increased microsomal cholesteryl esters content whereas acyl-CoA: cholesterol acyltransferase and other microsomal parameters remained unchanged. Examination of the effects of the short-term treatment with pharmacological doses of progesterone showed that treatment was less effective in changing the hepatic pattern of the cholesteryl esters cycle, since only cytosolic cholesterol ester hydrolase activity diminished slightly. Neither cytosolic nor microsomal cholesterol esterase or acyl-CoA: cholesterol acyltransferase were consistently affected by the administration of therapeutical doses of estradiol or progesterone for 21 days, although both the free cholesterol-phospholipid and the total cholesterol-phospholipid molar ratios decreased moderately. The effect of the hormonal vehicle, propylene glycol, on some microsomal lipid parameters is finally discussed.

Acyl Coenzyme A↗
PubMed2004

17Beta-estradiol confers a protective effect against transforming growth factor-beta2-induced cataracts in female but not male lenses.

Transforming growth factor-beta2 (TGF-beta2) induces anterior subcapsular cataracts, with a marked increase in cytoskeletal and extracellular matrix proteins, such as alpha-smooth muscle actin (alphaSMA). It has been shown that 17beta-estradiol (E2) can prevent TGF-beta2-induced cataracts in lenses from ovariectomized female rats. The purpose of the current study was to extend this finding by testing whether E2 can prevent TGF-beta2-induced cataracts and inhibit the induction of alphaSMA gene expression in normal male and normal, non-ovariectomized female rats.Sex-specific differences were observed in 17-week-old rat lenses incubated in 0.15 ng ml(-1) TGF-beta2 and in 10(-8)M E2 plus TGF-beta2. TGF-beta2 induced approximately twice as many anterior subcapsular plaques and 1.5 times the level of alphaSMA transcripts in male lenses compared to female lenses. Notably, E2 inhibited plaque formation and the induction of alphaSMA transcripts in female rat lenses but not in male rat lenses. E2 also inhibited the induction of alphaSMA in TGF-beta2-incubated lenses from ovariectomized female rats.E2 prevented lens opacification and the induction of alphaSMA gene expression in female, but not male, lenses. This sex-specific difference may have implications for studies on the therapeutic use of estradiol for treatment of secondary cataract.

Actins↗
PubMed1985

Treatment of hot flashes with transdermal estradiol administration.

A randomized prospective double blind study was performed to assess the ability of a transdermal therapeutic system (TTS) delivering estradiol (E2) to suppress hot flashes (HFs) in symptomatic postmenopausal women. Patients were given placebo or E2 in four doses for a 20-day period, and serum gonadotropin and estrogen levels and the occurrences of HFs were measured. Administration of placebo had no measurable effect on either estrogen or gonadotropin levels or the occurrence of HFs. A dose-response relationship was found between the rate of E2 administered and the circulating level of E2, with 25, 50, 100, and 200 micrograms/24 h dosages raising the mean E2 concentrations from mean baseline levels of 5-8 pg/ml to 18, 38, 73, and 100 pg/ml, respectively. Estrone levels also increased with TTS application, but to a lesser extent than did E2 levels. Dose-response reductions of FSH and LH with increasing amounts of E2 administration occurred, but gonadotropin levels were not lowered in any of the patients into the ranges found in premenopausal women. TTS application significantly suppressed the occurrence of HFs at the 50 micrograms/24 h dosage and higher. A significant negative correlation (r = 0.6045; P less than 0.001) between E2 levels and the rates of occurrence of HFs was found during hormone administration. Based on this regression, 50% and 100% reductions of HFs should occur at 61 and 122 pg/ml E2. These data indicate that the transdermal delivery of E2 with these systems significantly reduced the occurrence of HFs and allowed definition of the therapeutic range of hormone replacement in terms of lost ovarian function, as reflected by circulating E2 levels.

Administration, Topical↗
PubMed1996

The effect of hormone replacement therapy on bone mass in patients with ovarian failure due to bone marrow transplantation.

BACKGROUND: Long permanent remissions in malignant hematopoietic disorders can often be achieved by autologous bone marrow transplantation (ABMT) or by allogenic bone marrow transplantation (BMT). Previous studies have shown that such therapies may induce osteoporosis due to iatrogenic ovarian failure. The administration of hormone replacement therapy (HRT) in these women could prevent the adverse effects of long-term ovarian failure without remarkable side effects. The aim of this study was to evaluate how the bone mass is affected by HRT in patients undergoing ABMT or BMT adjusting the results for age, weight, and height. SUBJECTS AND METHODS: Thirteen women with previous ABMT/BMT were treated with a standard dose (0.625 mg/day) of conjugated equine estrogen (CEE) or with 50 micrograms/day of 17-beta-estradiol in transdermal therapeutic systems (TTS) plus 5 mg/day of medroxyprogesterone acetate sequentially added to the last 12 days of estrogen therapy. Bone mass was measured prior to and 12 months following HRT. Blood samples were collected before therapy and during the 6th and 12th treatment months. RESULTS: The mean time elapsed between bone transplantation and HRT initiation was 13.0 months (range 3-26 months). Before treatment nine patients were osteopenic and after HRT bone mass increased in all cases. Following ABMT/BMT, hepatic hyperenzymemia was detected in three patients. After 6 and 12 months of treatment no significant changes were observed in hepatic enzymes. CONCLUSION: Although hepatic hyperenzymemia is commonly considered as a contraindication for HRT, our results suggest that HRT is safe for these patients and that such therapy should be initiated after transplantation in women to prevent adverse effects of long-term ovarian failure.

Administration, Cutaneous↗
PubMed1999

Long-term postmenopausal hormone replacement therapy effects on bone mass: differences between surgical and spontaneous patients.

BACKGROUND: Hormone Replacement Therapy (HRT) begun soon after spontaneous menopause or oophorectomy minimizes or even reverses the loss of bone that occurs normally during those years. The persistence of this HRT protective effect at long-term on bone density, however, is not well documented. AIM: to evaluate the effects of 5 years of HRT in postmenopausal women on bone mineral density of the lumbar spine. SUBJECTS AND METHODS: The 5-year prospective study enrolled 154 postmenopausal women, of them 136 completed the first year and were considered electible to continue the follow-up. These 136 postmenopausal women were allocated to two groups according their origin: surgical (n=68) and spontaneous (n=68). HRT was prescribed and bone mineral density (BMD) was measured at the lumbar spine prior to commencement of therapy, and then yearly for the duration of the study. All patients received a continuous therapy with standard dose (0.625 mg/day) of conjugated equine estrogen (CEE) or 50 microg/day of 17-beta-Estradiol in transdermal therapeutic systems (TTS). Subjects who experienced natural menopause also received 5 mg/day of medroxyprogesterone acetate sequentially added to the last 12 days of estrogen therapy. Treated groups were compared with two non-treated control groups (surgical n=77; spontaneous n=53). RESULTS: Our data showed that HRT increased the BMD of women who had experienced spontaneous menopause. Comparison with a control group revealed that HRT also protected against bone loss in women who had undergone surgical menopause. CONCLUSION: Long term hormone replacement therapy increases bone mineral density in women who have experienced natural menopause, and protects against bone loss in surgically postmenopausal women.

Absorptiometry, Photon↗
PubMed2000

Elevation of tail skin temperature in ovariectomized rats in relation to menopausal hot flushes.

Menopausal hot flushes (HFs), which manifest as an increase in skin temperature, most frequently occur after menopause and cease with the passage of time. We designed this study to elucidate the characteristics of the elevation of tail skin temperature (TST) in ovariectomized (OVX) rats, which is relevant to human symptoms of HFs. First, we measured TST and rectal temperature (RT) and investigated the time course of their changes up to 20 wk after ovariectomy. The TST in OVX rats (28.4 +/- 0.3 degrees C) was significantly (P = 0.0035) elevated from 2 to 7 wk after the ovariectomy compared with that in sham-operated (Sham) rats (27.0 +/- 0.2 degrees C), whereas the RT in OVX rats was elevated from 8 to 20 wk. We next examined the therapeutic effects of estradiol (E(2)) on the elevation of the TST by continuous subcutaneous infusion. E(2) treatment (1.0 microg/day) completely (P = 0.0232) inhibited the elevation of the TST (28.4 +/- 0.3 degrees C for Sham rats, 29.3 +/- 0.3 degrees C for OVX rats, 28.2 +/- 0.4 degrees C for OVX + E(2) 1.0 microg/day rats). These results demonstrated that the elevation of TST in OVX rats was exhibited soon after the estrogen removal and diminished with time and that it was normalized with continuous E(2) replacement. These characteristics are similar to the symptoms of menopausal HFs in women.

Animals↗
PubMed1986

Estrogen induction of liver proteins and high-density lipoprotein cholesterol: comparison between estradiol valerate and ethinyl estradiol.

The effects of ethinyl estradiol and estradiol valerate were compared in 135 postmenopausal women during estrogen replacement therapy. Subfractions of high-density lipoprotein (HDL) cholesterol and its apolipoproteins and the serum levels of 2 estrogen-sensitive liver proteins were followed during 3 cycles of unopposed treatment with either ethinyl estradiol 10 or 30 micrograms or estradiol valerate 2 mg daily. Estrogen therapy induced significant and dose-dependent changes in all serum factors except HDL3 cholesterol. The effects of 10 micrograms of ethinyl estradiol upon the lipoproteins were 1.5-2.5 times greater than those of 2 mg of estradiol valerate. Sex-hormone-binding globulin and the pregnancy zone protein were the most sensitive markers for the estrogenic effect and these 2 liver-derived plasma proteins were also much more sensitive to ethinyl estradiol than to estradiol valerate. Although satisfactory therapeutic effects were achieved with both estrogens, the marked influence of ethinyl estradiol on liver protein synthesis should make estradiol valerate the first choice in clinical replacement therapy.

Adult↗
PubMed1999

[Hormone substitution therapy. Side-effects and compliance of various therapeutic regimens].

BACKGROUND: The aim of this study is to evaluate the tolerability and long-term compliance of four Estrogen Progestin treatments (HRT) for menopause. METHODS: One hundred and ten symptomatic menopausal women were divided into four groups according to therapeutic regimens: A) Estradiol (E2) transdermal treatment 50 micrograms (TTS 50) continuously administered (cont.) plus Medroxyprogesterone Acetate (MPA) 10 mg/die for twelve days a month: 35 women. B) Conjugated Equine Estrogens (CEE) 0.625 mg/die cont. plus MPA for twelve days a month: 25 women. C) Estradiol transdermal 50 micrograms (cont.) plus MPA 2.5 mg/die cont.: 26 women. D) CEE 0.625 mg/die cont. plus MPA 2.5 mg/die cont.: 24 women. RESULTS: Menopausal symptoms were significantly reduced with all treatments. During the first year group C and D patients showed irregular bleeding (group C: 46%, group D: 61%). After 24 months the bleeding frequency was reduced (group C: 11%, group D: 13%). Mastodynia was the more frequent side-effect in particular among women who were utilizing cont.comb. regimens. The total percentage of drop out (D.O.) after 2 years was more than 30% (Group A: 31%, Group B: 33%, Group C: 39%, Group D: 35%). The most frequent reasons for abandoning HRT (79% of all DO) were not linked to therapy side-effects. 19% of DO switched to other hormonal regimens.

Administration, Cutaneous↗
PubMed1996

Effects of progestogen on lipids, lipoproteins and apolipoproteins during transdermal estrogen replacement therapy with and without medroxyprogesterone acetate.

OBJECTIVE: To assess whether the effects on plasma lipids and lipoproteins after oophorectomy differ in patients who receive transdermal estrogen replacement therapy (ERT) with and without progestin. STUDY DESIGN: Twenty-five healthy, normal-weight, regularly menstruating women who underwent hysterectomy and bilateral oophorectomy for benign diseases received, for one year, transdermal therapeutic systems containing estradiol with daily delivery of 50 micrograms cyclically for 24 days per month plus 2.5 mg/d of oral medroxyprogesterone acetate (MPA) sequentially for the last 12 days of each cycle. After the first year the patients ceased to take MPA. We determined the levels of cholesterol (CHOL), high density lipoprotein (HDL)-CHOL, low density lipoprotein (LDL)-CHOL, triglycerides (TG) and apolipoproteins (apo) A-I and B prior to oophorectomy, one month after surgery and during the 6th and 12th months on estrogen plus progestogen substitution and during the 18th and 24th months without progestogen addition. RESULTS: After oophorectomy, the patients showed increases in LDL, apo-B and atherogenic index, whereas after hormone replacement therapy the patients exhibited falls in plasma LDL, apo-B and atherogenic index and increases in HDL and apo A-I. No significant changes in total CHOL were observed after surgery or treatment, and TG were decreased. Plasma levels of lipids and lipoproteins during estrogen replacement therapy (ERT) without MPA were not significantly different from those observed during ERT plus MPA. CONCLUSION: Changes in lipids induced by transdermal ERT were not affected by low doses of MPA.

Administration, Cutaneous↗
PubMed1993

The role of lipoproteins in the distribution of tin etiopurpurin (SnET2) in the tumor-bearing rat.

The role of plasma lipoproteins in the distribution of the photosensitizing agent tin etiopurpurin (SnET2) was examined in male rats bearing the N-[4-(5-nitro-2-furyl)-2- thiazolyl1bdformamide-induced tumor. Treatment with 17 alpha-ethinyl estradiol resulted in the depletion of total plasma cholesterol by > 70% and a corresponding decrease in plasma lipoproteins. To both control and estradiol-treated animals, a therapeutic dose (1.5 mg/kg) of SnET2 was administered and biodistribution measured 24 h later. Estradiol treatment was not associated with differences in the distribution of SnET2 to liver, skin or tumor, or in the pattern of affinity of SnET2 to plasma albumin and lipoprotein. These results indicate that a substantial decrease in circulating lipoprotein levels does not alter patterns of SnET2 biodistribution.

Animals↗
PubMed1976

[Influence of ethinyl estradiol sulfonate on the decreased urinary bladder tonus in the menopause].

In 40 women with hypotonic urinary bladder the influence of 17alpha-Athinyl-3-isopropyl-sulfonyloxy-Ostradiol (Athinylöstradiol) (3 X 15 mug/die without weekend) was examined concerning the intravesical pressure; The cystotonometry has been done just before as well in intervalls of 2 months during half year's period of treatment. The authors used the fill-up-cystotonometry of Hartl. The intra-vesical pressure rose significantly by the influence of Athinylöstradiolsulfonat after 2 months treatment already. In comparison to the hypotonic value before treatment there was an average normotonic urinary bladder after application of Athinylöstradiolsulfonat past 4 and 6 months. Incidence on clinical relevance of these results.

Ethinyl Estradiol↗
PubMed2005

Ethinyl estradiol treats collagen-induced arthritis in DBA/1LacJ mice by inhibiting the production of TNF-alpha and IL-1beta.

We previously demonstrated the therapeutic effects of ethinyl estradiol (EE), an orally active estrogen and a component of birth control pills, in encephalitogenic autoimmune encephalomyelitis (EAE). In this study, we report the effectiveness of EE in treating collagen-induced arthritis (CIA) induced with bovine type II collagen (bCII) in DBA/1LacJ mice, a CIA susceptible strain. Both low and high doses of EE notably suppressed clinical and histological signs of CIA in a dose-dependent manner compared to vehicle-treated controls. Oral treatment with EE decreased proliferation and secretion of pro-inflammatory factors, TNF-alpha IFN-gamma, MCP-1 and IL-6 by bCII peptide-specific T cells, production of bCII-specific IgG2a antibodies, and mRNA for cytokines, chemokines and chemokine receptors in joint tissue. This is the first report demonstrating effective treatment of joint inflammation and clinical signs of CIA with orally administered ethinyl estradiol, thus supporting its possible clinical use for treating rheumatoid arthritis in humans.

Animals↗
PubMed1980

[Local therapy of androgenetic alopecia with 17 alpha-estradiol. A controlled, randomized double-blind study (author's transl)].

In a controlled, randomized double-blind study, 51 patients with androgenetic alopecia and increased hair loss (telogen rate greater than 20%) were treated by local application of hair lotions with and without 17 alpha-estradiol (0.025%) for a period of at least 6 months. Before and after therapy trichograms were taken and evaluated under standardized conditions. In 63% of the treated patients a reduction of the amount of telogen hairs appeared, whereas in the control group the same reduction was found in only 37% of the cases. Similarly, in the treated group only 11% of the patients worsened, in contrast to 50% of the control group who showed an increased telogen rate (greater than 10%). The amount of growing anagen hairs and of seborrhea did not change significantly in both groups. Side effects were not seen. These findings indicate that hair lotions containing 17 alpha-estradiol may have a therapeutic value in reducing androgenetic hair loss, if applied topically for a long period of time, similar to 17 beta-estradiol. However, no regrowth of new hair was found.

Administration, Topical↗