Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:APRD00691 (EE2)
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Plasma levels of gonadotropins, PRL, T4, and adrenal and gonadal steroids were measured in two groups of 7- to 9-yr-old and 10- to 11-yr-old obese prepubertal girls, and were compared to those found in groups of nonobese girls of the same age. The data found in normal weight subjects confirm the data reported in the literature, showing a significant rise between the 7- to 9- and 10- to 11-yr groups, of FSH, pregnenolone, dehydroepiandrosterone, testosterone, and estradiol plasma levels, while LH, PRL, T4, cortisol, progesterone, 17-hydroxyprogesterone (17P), and androstenedione remained constant. In the obese subjects, pregnenolone and dehydroepiandrosterone levels are notably higher than in the normal girls, in the same range as those found in adult women; furthermore, they show no rise between the two age groups. The obese prepubertal groups had significantly higher progesterone, androstenedione, and PRL levels in comparison with those observed in girls of normal weight, but 17-hydroxyprogesterone, cortisol, testosterone, LH, and T4 were similar in both groups. Estradiol levels were markedly depressed in the obese girls; FSH levels were higher in the younger girls than in normal subjects. These data indicate that in prepubertal obesity, maturation of adrenal gland function (chiefly the delta 5 pathway), is notably enhanced, whereas gonadal secretion of estradiol is impaired in the presence of high levels of FSH and PRL.
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PMID:Plasma levels of gonadotropins, prolactin, thyroxine, and adrenal and gonadal steroids in obese prepubertal girls. 16 19

Although there is a critical need for effective contraception in the immediate postpartum period for women who are not breastfeeding, this need must be balanced against the inherent risks. The most effective form of contraceptive protection--oral contraceptives (OCs)--can present an increased risk of thromboembolism in the period after delivery. The thrombotic changes associated with pregnancy, and the statistics and vascular damage following a delivery, can combine to create greater potential for thromboembolism after delivery than during pregnancy. Reported here is the case of a 21-year-old woman who, 4 weeks postpartum, developed pain and swelling in the right lower calf and mottled discoloration extending from the proximal thigh to the toes. A diagnosis of deep venous thrombosis was made and heparin was administered. In the hospital, the patient experienced pleuritic chest pain and diaphoresis. A ventilation-perfusion scan indicated a pulmonary embolism. 1 week after delivery, the patient had initiated use of Triphasil. Although this woman had other risk factors (obesity, light cigarette smoking, and a sedentary life-style), OC use in the immediate postpartum period may have been the final factor precipitating the thromboembolic event. It is recommended that OC use should be delayed until at least 2 weeks postpartum in women without other risk factors for thromboembolism and until 4-6 weeks postpartum in those with such factors.
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PMID:Oral contraceptives in the immediate postpartum period. 201 Jul 44

The relationships between blood levels of estrogen and lipoprotein lipids and apoproteins were evaluated in 120 women early in the climacteric. Among women who were 1-year amenorrheic, not taking hormone replacement therapy, and with follicle-stimulating hormone levels greater than 720 ng/ml, serum estradiol levels were positively related to concentrations of the high density lipoprotein 2 cholesterol (HDL2c) subfraction. There was a substantial decrease in HDL2c and apoprotein (apo) A-I in women whose estradiol levels decreased to less than or equal to 2.5 pg/ml from the first to the second postmenopausal examination. In a sample of women evaluated during the perimenopause (3-months' amenorrheic), those with the highest concentrations of estradiol or estrone showed a (nonsignificantly) higher level of HDL2c and a lower level of low density lipoprotein cholesterol (LDLc) than did those with the lowest concentration of estradiol or estrone. Estradiol levels declined dramatically between the perimenopausal and the postmenopausal examinations, and this was accompanied by a decrease in HDL2c and a nonsignificant increase in LDLc. HDL2c levels fell substantially in those women whose estradiol decreased below the sensitivity of the assay. The change, however, was not statistically significant. Estrone is the primary postmenopausal estrogen, and levels are directly related to obesity, as are levels of insulin. The interrelationship among obesity, conversion of estrone to estradiol at the tissue level, and insulin (or insulin sensitivity) is probably the primary determinant of HDLc concentration among postmenopausal women.
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PMID:Relationship of endogenous sex steroid hormones to lipids and apoproteins in postmenopausal women. 212 88

A fictitious patient with obesity, hirsutism and polycystic ovary syndrome is discussed by 3 British general practitioners to illuminate management of this type of case. The patient is 24 years old, expects to marry next year, has irregular menses averaging 6 weeks apart, and is requesting an explanation for her irregular periods as well as oral contraception. The 1st physician would exclude hypothyroidism, then evaluate polycystic ovary syndrome by assaying testosterone, LH, FSH and prolactin, next find out the significance of the patient's questions in her mind and finally prescribe a triphasic pill. The 2nd doctor would withhold the pill on the grounds that it might compromise future fertility if she has a primary endocrine imbalance. She would check rubella status, assay progesterone, LH, FSH, prolactin and testosterone on Day 19 of the cycle, and probably prescribe Marvelon oral contraceptives. The 3rd doctor would use a hirsutism score, investigate the polycystic ovary syndrome by ultrasound and an essay of sex hormone binding globulin and the LH:FSH and prolactin, next find out the significance of the patient's questions in her mind and finally prescribe a triphasic pill. The 2nd doctor would withhold the pill on the ground that it might compromise future fertility if she has a primary endocrine imbalance. She would check rubella status, assay progesterone, LH, FSH, prolactin and testosterone on Day 19 of the cycle, and probably prescribe Marvelon oral contraceptives. The 3rd doctor would use a hirsutism score, investigate the polycystic ovary syndrome by ultrasound and an assay of sex hormone binding globulin and the LH:FSH ration between Days 2-6 of the cycle, and rule out congenital adrenal hyperplasia with an assay for 17-alpha-OH-progesterone. Since the patient might be anovulatory because of obesity, major long-term weight lose is a priority. Prescription of pills would depend on family history, smoking, and the degree of hirsutism and endocrine status. The most likely prescription would be a reverse sequential of cyproterone acetate 50 or 100 mcg from Days 5-15, and ethinyl estradiol 30 mcg on Days 2-25.
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PMID:Contraception and irregular menses. 259 23

To clarify the independent relationships of obesity and overweight to cardiovascular disease risk factors and sex steroid levels, three age-matched groups of men were studied: (i) 8 normal weight men, less than 15% body fat, by hydrostatic weighing; (ii) 16 overweight, obese men, greater than 25% body fat and 135-160% of ideal body weight (IBW); and (iii) 8 overweight, lean men, 135-160% IBW, but less than 15% fat. Diastolic blood pressure was significantly greater for the obese (mean +/- SEM, 82 +/- 2 mmHg) than the normal (71 +/- 2) and overweight lean (72 +/- 2) groups, as were low density lipoprotein levels (131 +/- 9 vs. 98 + 11 and 98 + 14 mg/dl), the ratio of high density lipoprotein to total cholesterol (0.207 +/- 0.01 vs. 0.308 +/- 0.03 and 0.302 +/- 0.03), fasting plasma insulin (22 +/- 3 vs. 12 +/- 1 and 13 +/- 2 microU/ml), and the estradiol/testosterone ratio (0.076 +/- 0.01 vs. 0.042 +/- 0.02 and 0.052 +/- 0.02); P less than 0.05. Estradiol was 25% greater for the overweight lean group (40 +/- 5 pg/ml) than the obese (30 +/- 3 pg/ml) and normal groups (29 +/- 2 pg/ml), P = 0.08, whereas total testosterone was significantly lower in the obese (499 +/- 33 ng/dl) compared with the normal and overweight, lean groups (759 +/- 98 and 797 +/- 82 ng/dl). Estradiol was uncorrelated with risk factors and the estradiol/testosterone ratio appeared to be a function of the reduced testosterone levels in obesity, not independently correlated with lipid levels after adjustment for body fat content. Furthermore, no risk factors were significantly different between the normal and overweight lean groups. We conclude that (a) body composition, rather than body weight per se, is associated with increased cardiovascular disease risk factors; and (b) sex steroid alterations are related to body composition and are not an independent cardiovascular disease risk factor.
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PMID:Body composition, not body weight, is related to cardiovascular disease risk factors and sex hormone levels in men. 365 69

In order to study the effect of obesity or underweight on gonadotropins and steroid hormone levels, serum concentrations of FSH, LH. Testosterone, Estradiol, Estrone, 17-OH-Progesterone and SHBG were measured by RIA in obese, underweight and control women, all menstruating in the follicular phase. Serum concentrations of all parameters measured did not differ significantly in the underweight and control groups. All obese women had higher levels of estrone than the control group, and only obese patients with a body mass index above 39 showed a lower SHBG level than that of the control group. The data suggest that the increased levels of estrone could play a role in the amenorrhea of obese women.
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PMID:[Influence of body weight on gonadotrophins and steroid hormone levels in menstruating women]. 379 88

Estradiol benzoate (EB) treatment of male and female C57BL/6J ob/ob mice for 32 days led to decreased body weight (20%), percentage body fat (8%) and carcass protein content (12%) when compared with non-EB-treated obese control mice. Estradiol reduced the caloric intakes of both genders by 25-35%, but did not affect body temperature regulation. Circulating glucose and insulin concentrations were also lowered by estrogens, although hyperinsulinemia persisted. Since post-treatment body weight changes correlated with daily food intakes (r = 0.81) rather than to rectal temperatures (r = -0.19), it appears that hypophagia provided a greater contribution to the estrogen-mediated reductions of growth and carcass fat than did altered energy expenditure for thermoregulation. While these data show that EB treatment does reduce the severity of some metabolic disturbances in a genetic model of type II diabetes, long-term estrogens do not appear to offer substantial advantages in the treatment of obesity or diabetes when compared with the effects of caloric restriction alone.
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PMID:Effects of estrogen on food intake, body weight, and temperature of male and female obese mice. 390 58

120 women with carcinoma of the breast were matched in a matched pairs analysis to 120 women as a control group. The estrogen use patterns for these women were determined after the matching and the relative risk (RR) of developing breast cancer during estrogen use was determined. The RR of developing breast cancer was increased significantly among patients who used conjugated estrogens. The RR did not increase as the length of estrogen use increased. Estradiol use caused a non-significant increase in the RR of developing breast cancer. Nulligravidity, hypertension, and obesity did not increase the RR of developing breast cancer during estrogen use.
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PMID:[Estrogen therapy in carcinoma of the breast (author's transl)]. 624 9

The cases are described of 3 female adolescents evaluated at the Cincinnati Adolescent Clinic for delayed or incomplete secondary sexual development due to primary ovarian failure. All 3 patients had normal blood leukocyte and ovarian tissue karyotypes. The clinical, laboratory, and pathological findings are discussed with emphasis on distinguishing chromosome incompetent ovarian failure (CIOF-Turner's syndrome) from chromosome competent ovarian failure (CCOF). The patients included a 15 1/2 year old black female who sought evaluation of obesity and lethargy, a 17 1/2 year old white female with secondary amenorrhea in whom oral provera failed to induce menstrual flow, and a 17 1/2 year old black female with scanty, infrequent menses who achieved a normal amount and duration of menstrual flow with Norinyl 1 + 80. Hypoestrogenization should be suspected in cases of incomplete breast development for age, thin vaginal mucosa with a prepubertal pattern of the vaginal cytology, scant cervical mucus without ferning, and lack of withdrawal bleeding after progesterone administration. If any decrease in ovarian steroid production is clinically suspected in an adolescent with primary or secondary amenorrhea associated with delayed or incomplete puberty, serum gonadotropin levels should be measured. A single elevated follicle stimulating hormone (FSH) level in the menopausal range is diagnostic of primary ovarian failure in an adolescent. If the FSH is low or normal, hypothalamic or pituitary disease would be suspected. A blood leukocyte karyotype is the next diagnostic procedure for patients with primary ovarian failure to distinguish between CCOF and CIOF. If the blood karyotype is XO or a variant without a Y cell line, no further cytogenic workup or visualization of the gonads is needed, but girls with blood karyotype of XX or a mosaic pattern with 1 cell line with a Y chromosome should undergo laparoscopy and gonadal biopsy. A unilateral testis should be removed to avoid malignant changes in later years. Patients with CCOF may have other endocrine dysfunction, particularly autoimmune disease. Other possible diagnoses include resistant ovary syndrome, pure gonadal dysgenesis, premature menopause, or infectious, chemical, or other causes of ovarian failure. The incidence of CIOF is greater than that of CCOF among patients with primary ovarian failure. Optimal treatment requires medical and psychosocial intervention.
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PMID:Chromosomally competent ovarian failure at adolescence. 631 54

The objective of this study was to examine the relation of endogenous sex hormones to subsequent height loss in postmenopausal women, in whom height loss is usually a surrogate for osteoporotic vertebral fractures. This was a prospective, community-based study. The site chosen was Rancho Bernardo, an upper middle class community in Southern California. A total of 170 postmenopausal women participated, aged 55-80 years. None of them were taking exogenous estrogen between 1972 and 1974. Plasma was obtained for sex hormone and sex hormone-binding globulin (SHBG) assays. Estradiol/SHBG and testosterone/SHBG ratios were used to estimate biologically available hormone levels; bioavailable (non-SHBG-bound) testosterone was measured directly in 60 women. Height loss was based on height measurements taken 16 years apart. Height loss was strongly correlated with age (p = 0.001). These women lost an average 0.22 cm/year in height. Neither estrone nor estradiol levels were significantly and independently related to height loss. Both estimated bioavailable testosterone (testosterone/SHBG ratio) and measured bioavailable testosterone levels predicted future height loss (p = 0.02 and 0.08, respectively) independent of age, obesity, cigarette smoking, alcohol intake, and use of thiazides and estrogen. We conclude that bioavailable testosterone is an independent predictor of height loss in elderly postmenopausal women. The reduced height loss is compatible with a direct effect of testosterone on bone mineral density or bone remodeling.
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PMID:Low bioavailable testosterone levels predict future height loss in postmenopausal women. 761 Sep 37


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