Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:APRD00691 (EE2)
 7,802 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors recall the antagonism between estradiol and parathormone. Estradiol tends to lower serum calcium and fix calcium in the bones as shown by one of us 25 years ago. The mechanism of this action of estrogen on calcium metabolism has been determined by numerous authors but some points are still not clear, e.g. the interferences between estrogen and calcitonin. Classically, parathormone is known to increase bony reabsorption and raise serum calcium. After the menopause the gradual reduction in estradiol secretion leads to post-menopausal osteoporosis. It is better to administer estrogens prophylactically to women after the menopause provided a cervical smear and mammography have been carried out to eliminate latent carcinoma of the breast or uterine cervix.
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PMID:[Calcium metabolism after the menopause]. 18 38

Eleven women with hyperprolactinemic amenorrhea were treated with a combined estrogen/progestogen preparation (Loestrin 30) for 3 months as hormone replacement therapy because of estrogen deficiency, with a view to protection against osteoporosis. Serum prolactin levels rose during the 1st month of treatment (p < 0.05) but did not rise significantly further during the 2nd and 3rd months. The levels rose in proportion to pretreatment levels by 28% (median), and fell significantly but not completely during the 1-week treatment-free intervals. After the study period, prolactin values appeared to remain stable in those women who continued longer on treatment, and returned to around pretreatment values in those who stopped. In one woman there was radiological evidence of pituitary tumor growth during treatment. This study shows that estrogen/progestogen treatment in standard contraceptive dosage usually leads to only moderate and non-progressive stimulation of pituitary activity in women with hyperprolactinemic amenorrhea, but occasional excessive growth of a prolactinoma can occur and treatment needs to be monitored. Women with relatively high prolactin levels seem to be at particular risk. Safer variations of estrogen therapy such as lower dosage or combination with a protective low dose of a dopamine agonist should also be considered.
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PMID:The effect of combined estrogen/progestogen treatment in women with hyperprolactinemic amenorrhea. 144 63

One reliable, controlled and convenient method of delivering parenteral estrogen replacement therapy is by means of a transdermal patch known as the Estraderm Transdermal System, which contains a 17-beta estradiol formulation. The primary side effect appears to be a localized skin irritation in about 15 percent of the women using this route. Most women find this irritation annoying but not enough to necessitate stopping therapy. Studies indicate that the patch provides amelioration of climacteric symptoms that is comparable to the oral estrogens. Preliminary research shows that parenteral estrogen is as effective as oral estrogen in decreasing the risk of osteoporosis. No adverse changes in lipid-lipoprotein levels have been found. A recent Swedish study found an increased relative risk of breast cancer with estradiol and with combined estrogen-progestin use for postmenopausal therapy. Thus, more research on the long-term hormonal replacement effects of the patch is indicated. One advantage of the transdermal delivery system is a first bypass of the liver, thus decreasing the possible risk of renin substrate elevation and the potential increase in blood pressure associated with oral estrogen therapy.
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PMID:Estrogen replacement therapy and the estraderm transdermal system. 234 64

Although osteoporosis is an age-related disorder, the accelerated bone loss observed in postmenopausal women may be preventable with early diagnosis and adequate estrogen replacement. In a prospective study, we investigated the effect of oral estrogen replacement using conjugated estrogens (Premarin, 0.625 mg) or micronized 17 beta-estradiol (Estrace, 1 mg) versus no estrogen in sequential single-photon bone density measurements over 3-year intervals in 397 postmenopausal women. Estradiol, 1 mg, and conjugated estrogens, 0.625 mg, were equally effective in regarding bone loss. The rate of bone loss was about the same for estrogen users regardless of age (51 to 80 years) and was approximately one third that of nonusers. Among nonusers a uniform accelerated rate of bone loss of 2.5% per year was noted between 56 and 70 years old, whereas between the ages of 51 and 55 years and after age 70 years, the rate of bone loss was significantly less. Ever users over age 65 years showed continued protection from bone loss as long as estrogen therapy was continued. Previous estrogen users who stopped estrogen after age 65 years lost bone more rapidly than women of similar age who had never taken estrogen. Thus to prevent accelerated bone loss in postmenopausal women, we recommend early and continued hormone replacement for life. Estrogen nonusers should be monitored at regular intervals to minimize accelerated bone loss.
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PMID:Estrogen therapy arrests bone loss in elderly women. 303 27

Estradiol (E2) plays a major role in maintaining women's skeletal integrity. Loss of bone mass is a regular occurrence with E2 deficiency, regardless of etiology. Estrogen-dependent bone loss follows a predictable pattern. Initially, it is quite rapid, preferentially affecting trabecular bone, which may decrease by 5-8% annually, whereas compact or cortical bone decreases by 1-3% annually. After 10-15 years of E2 deficiency, the rate of loss each year decreases; however, by that time, skeletal mass may be one-third to one-half of its youthful level. Because of the resultant skeletal fragility, even minimal trauma can produce fractures of the spine and wrist. After an additional 10-15 years of bone loss, hip fractures occur with alarming frequency. Timely restoration of E2 levels can prevent estrogen-dependent bone loss and can reduce significantly the risk of fracture. Studies show that 2 mg of E2 administered orally is an adequate dose; 1 mg will suffice if it is combined with a high dietary calcium intake. High calcium intake without estrogen is not effective in preventing the accelerated loss of bone that occurs in the years immediately after menopause. Long-term studies confirm that postmenopausal women who regularly use estrogen have greater bone mass and fewer osteoporotic fractures. Physicians should be encouraged to treat all estrogen-deficient women, particularly those who appear to be at higher risk for osteoporosis.
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PMID:Prevention of osteoporosis: treatment of estradiol deficiency. 317 36

Previous studies have suggested that estrogen may have an effect on cognitive and emotional function in women. Studies in rodents and non-human primates have demonstrated the presence of estrogen receptors in brain, and that estrogen can affect behavior in animals. Estrogen administration to ovariectomized rats increases choline acetyltransferase activity in certain regions of brain. Choline acetyltransferase activity is known to be significantly decreased in senile dementia-Alzheimer's type (SDAT). Based on these observations, we treated seven women with SDAT with low dosages of estradiol over a six week period. A battery of assessments was performed throughout the study period. Significant improvements in three women were noted on measures of attention, orientation, mood and social interaction. These estrogen-responsive women were characterized by dementia associated with an affective disorder, older age at onset, and evidence of osteoporosis. Side effects of estradiol therapy included withdrawal bleeding in one woman and transient breast tenderness in another. Estradiol therapy thus may benefit some postmenopausal women with SDAT. The occurrence of osteoporosis in the estrogen-responsive group suggests that SDAT in some women may be associated with or related to a systemic estrogen deficiency state. However, considering the potential for serious side effects as a result of estrogen therapy, the current risk to benefit ratio precludes the routine clinical use of estrogen for dementia until careful clinical research trials have been performed.
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PMID:Observations in a preliminary open trial of estradiol therapy for senile dementia-Alzheimer's type. 378 38

Premenopausal amenorrheic women may be at risk for the development of osteoporosis. In hyperprolactinemia, cortical bone mass is decreased and the magnitude of the decrease correlates with the severity of the estrogen deficiency. However, bone loss in women with amenorrhea from other causes has not been assessed. We have studied women with hypothalamic and hyperprolactinemic amenorrhea and premature ovarian failure. Bone mass in the peripheral cortical bone was only slightly decreased from age-matched controls, but spinal trabecular bone was decreased 20% to 30%. Estradiol levels were 20 to 80 pg/mL in these women, not different from normal early follicular levels. The decrease in bone mass in the spine did not correlate with serum estradiol at these levels. The hypothalamic amenorrhea group was made up of athletes in whom the bone mass decrease was an unexpected finding.
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PMID:Decreased spinal mineral content in amenorrheic women. 669 Aug 36

15 sterilized women participated in a clinical trial of the implant Implanon (Organon), a single ethylene vinyl acetate rod containing 60 mg 3-ketodesogestrel (3-KDG), the metabolite of desogestrel. The rod is 40 mm long, 2 mm in diameter and is packaged in its inserter. In this trial the implants were treated to simulate the 2nd year of use. The study subjects underwent intensive hormone and ultrasound monitoring for 72 hours after insertion, twice weekly for 6 weeks and at 6-month intervals. 13 women completed 6 months, 7 completed 12 months, and 5 continued the trial 24 months. There were no complications related to insertion or removal. 3-KDG levels rose to a steady state of 245 pg/ml by 72 hours, then fell to a mean of 17 pg/ml at 12 months. 90 pg/ml of 3-KDG is the critical serum level for anovulation. After removal, 3-KDG declined to 54 pg/ml in 3 days. Follicle development tended toward small follicles or those larger than 10 mm. There was no luteal activity, and LH, FSH and progesterone remained in the follicular phase range. Estradiol levels were not low enough to risk osteoporosis. There was no significant change in serum sex hormone binding globulin. Systolic blood pressure decreased significantly at 12 months; mean weight gain was 3.7 kg (range from loss of 4 kg to gain of 22 kg); a variety of bleeding irregularities were recorded by individual women.
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PMID:Release characteristics, ovarian activity and menstrual bleeding pattern with a single contraceptive implant releasing 3-ketodesogestrel. 846 16

The failure of follicular development that characterizes the menopause leads to a marked reduction in serum levels of estradiol and progesterone. As a result, the majority of women develop symptoms, including hot flushes, sleep disturbance, and vaginal dryness. Long-term consequences of ovarian insufficiency include genital atrophy, osteoporosis, and increased rates of myocardial infarction. Estradiol replacement (ERT) has proved effective in treating and preventing these problems. ERT has, however, led to increased risk of endometrial carcinoma. Consequently, treatment regimens now include progestins (HRT) to protect women who have a uterus. Progestins act by down-regulation of estradiol receptor activity, which is an advantage for preventing endometrial hyperstimulation, but a potential disadvantage when beneficial effects of estradiol are opposed. Current menopause health care includes assessment, treatment, and follow-up. Signs and symptoms of estradiol deficiency are evaluated during initial history-taking and physical examination. The MENSI (Menopause Symptom Index) has proved an efficient questionnaire for both initial assessment and monitoring of treatment effects. Vaginal cell maturation index (M.I.) can be helpful in determining need for hormonal treatment and for assessing response to treatment. A "therapeutic range" for ERT can be achieved with the availability of a variety of hormone preparations administered in different ways (oral, transdermal, skin gel, implants, etc.), thus avoiding the problems of both inadequate and excessive hormonal doses. This paper will describe a structured approach to the delivery of health care in the menopause.
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PMID:Hormone replacement therapy in the menopause. 916 Feb 17

Estrogens have a beneficial effect on atherosclerosis and osteoporosis after menopause, but their exact mechanism of action is still unknown. The aim of the present study was to investigate the effects of estradiol and its metabolites catechol estrogens on arachidonic acid metabolism in vitro. Estradiol had no effect on arachidonic acid metabolism up to 33 microM in A23187-stimulated human whole blood. All catechol estrogens (2-hydroxyestradiol, 2-hydroxyestrone, 4-hydroxyestradiol and 4-hydroxyestrone) had similar kinds of actions on arachidonic acid metabolism, being over ten times more potent inhibitors of leukotriene synthesis (IC50 values 0.044-0.16 microM) than thromboxane (IC50 values 0.99-2.1 microM) and prostaglandin E2 synthesis (IC50 values 0.84-5.5 microM). It is suggested that some of the protective actions of estrogens--e.g., on atherosclerosis and osteoporosis--may be related to the inhibition of leukotriene synthesis by catechol estrogens.
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PMID:Catechol estrogens as inhibitors of leukotriene synthesis. 941 36


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