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)

In vivo and in vitro studies were conducted on a male pseudohermaphrodite. Levels of gonadal steroids in peripheral blood suggested low activity of steroidogenesis which was consistent with the high levels of gonadotropins found. In vitro incubation studies with testosterone, human chorionic gonadotropin (hCG) and follicle-stimulating hormone (FSH) indicated that both gonadotropins increased the endogenous accumulation of testosterone (P less than 0.05) and the rate of conversion of testosterone to androstenedione (P less than 0.025). Estradiol accumulation was increased only in the presence of hCG. These data suggest that the aromatase and 17 beta-hydroxysteroid dehydrogenase enzyme systems in the gonads of this patient may be influenced by gonadotropins.
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PMID:An unusual case of male pseudohermaphroditism. 49 36

The steroid hormone estradiol, and the glycoprotein hormones follicle-stimulating hormone (FSH) and luteinizing hormone (LH), are known to be essential for the growth and differentiation of follicles in the ovary. The present study was conducted to determine quantitatively the effects of estradiol, FSH and LH on proliferation of different ovarian cell types (granulosa and theca cells). The immature female hypophysectomized rate sequentially primed with estradiol, FSH and LH was used as the experimental model. Proliferation was assessed by examining changes in total DNA, incorporation of 3H-thymidine into DNA and labeling index in specific cell types. Estradiol and FSH each acted on follicles at different stages of development to stimulate proliferative activity of both granulosa and theca cells. Continued administration of either hormone caused a decrease in the proliferative activity of both cell types. These observations have been interpreted to indicate that estradiol and FSH can each alter the length of the specific phases of the cell cycle. A luteinizing dose of LH caused a cessation of proliferation in luteinizing granulosa cells while stimulating a limited proliferation of theca cells. Absence of the appropriate hormonal stimulus caused both granulosa and theca cells to stop proliferating and the follicles to undergo atresia. These results indicate that, depending upon the state of differentiation of granulosa and theca cells, estradiol, FSH and LH can stimulate or inhibit the ability of these cells to proliferate.
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PMID:Hormonal regulation of ovarian cellular proliferation. 56 19

Two formulations of a low-dose oral contraceptive (Microgynon: 150 microgram of levonorgestrel [NG] +30 micrograms of ethynylestradiol [EE2]) were studied. The first was the "conventional" pill; the second was a "paper" pill prepared by evaporation of aliquots of a solution of the component steroids onto squares of edible cellulose separated by perforations, similar to a sheet of postage stamps. The effects of the two formulations on plasma levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), 17beta-estradiol (E2), and progesterone were compared. Samples of blood were obtained from five women during a treatment period on the "conventional" pill and from five on the "paper" pill. When possible, blood samples were also obtained from a "control" cycle of each of these female subjects. Plasma LH, FSH, E2, and progesterone levels were determined by specific radioimmunoassay methods during control and treatment periods and NG and EE2 levels during treatment periods. Eight-hour plasma profiles for NG and EE2 at the beginning and in the later stage of the treatment periods were obtained and these samples were also analyzed for LH, FSH, E2, and progesterone. Results showed that with one exceptcrogynon were equally effective in suppressing ovulation. As in a previous study, FSH levels appeared to be one of the most sensitive indices of suppression.
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PMID:Comparison of plasma hormone changes using a "conventional" and a "paper" pill formulation of a low-dose oral contraceptive. 64 48

A study was undertaken to determine the effects of a low-dose oral contraceptive comprising 150 mug of D-norgestrel and 30 mug of 17alpha-ethynyl estradiol (Microgynon) on the plasma levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), 17BETA-ESTRADIOL, AND PROGESTERONE AND ON THE PHYSICAl properties of cervical mucus. Samples of blood and cervical mucus were obtained from three women during a treated cycle and the immediately-following "withdrawal" cycle. Specific radioimmunoassay methods were used to determine LH, FSH, 17beta-estradiol, and progesterone levels in treated and withdrawal cycles, and D-norgestrel and 17alpha-ethynyl estradiol in samples obtained during treated cycles. The concentration of synthetic steroids was also measured in blood samples obtained before and 1 hour after ingestion of the contraceptive to determine the maximal daily variation. The results indicated that the contraceptive action of this combined low-dose oral contraceptive is mediated through suppression of ovulation and by rendering the cervical mucus impenetrable to sperm. Plasma FSH levels appeared to be one of the most sensitive indices of suppression. Determination of D-norgestrel and 17alpha-ethynyl estradiol showed that 3 to 4 days were required to reach maximal plasma levels and that daily fluctuations were considerable. Withdrawal of the pill resulted in an immediate return to ovulatory cycles in all three subjects studied.
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PMID:Studies on low-dose oral contraceptives: cervical mucus and plasma hormone changes in relation to circulating D-norgestrel and 17alpha ethynyl-estradiol concentrations. 95 31

We report results from 2 years of therapy with the long-acting form of the gonadotropin-releasing hormone (GnRH) analog leuprolide acetate, which was previously reported in short-term trials to be efficacious in the treatment of central precocious puberty. Thirteen girls and two boys, aged 1.9 to 9.7 years, who satisfied clinical criteria including GnRH-stimulated luteinizing hormone (LH) greater than 10 IU/L (mean radioimmunoassay LH, 29.1 +/- 5.54 IU/L), received depot leuprolide, 6 to 15 mg intramuscularly every 4 weeks. Estradiol (or testosterone), insulin-like growth factor I, and GnRH-stimulated gonadotropins were obtained at baseline, at 2 months, and at 6-month intervals with bone age determinations. Pubertal progression ceased in all patients, and menses did not occur. Mean increase in height during therapy was 5.77 +/- 2.0 cm/yr. Predicted adult height increased over baseline by 5.52 +/- 1.16 cm at 18 months. Mean estradiol values in the girls declined from 3.3 +/- 0.6 to 0.60 +/- 0.03 ng/dl, with no overlap of baseline and treatment values. The mean basal LH value was unchanged by therapy; mean basal and peak LH values for all follow-up GnRH stimulation tests were 4.05 +/- 0.57 and 4.95 +/- 0.70 IU/L, respectively. Basal and peak follicle-stimulating hormone (FSH) values were suppressed from 4.10 +/- 0.62 and 10.06 +/- 1.34 IU/L, respectively, to generally undetectable levels (< 1). Comparison with untreated control patients suggested that basal LH did not completely return to prepubertal levels, whereas FSH levels were suppressed below prepubertal levels. Estradiol, FSH, and LH levels reached their nadir by 2 months; in contrast, mean serum levels of insulin-like growth factor I progressively declined from +0.57 +/- 0.19 SD score to -0.06 +/- 0.22 SD score at 24 months. Two girls were withdrawn from the study because of reactions at injection sites, with apparent sterile abscess formation in one patient. This study provides evidence that (1) long-term treatment with depot leuprolide is characterized by immediate and sustained laboratory and clinical suppression, (2) GnRH-stimulated LH and random FSH and estradiol concentrations are useful laboratory measures of efficacy, and (3) the progressive increase in predicted adult height is temporally associated with decreased serum levels of insulin-like growth factor I and striking deceleration of bone age advancement.
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PMID:Two-year results of treatment with depot leuprolide acetate for central precocious puberty. 834 41

Two experiments were conducted in July with adult Dorset x Leicester x Suffolk rams to determine whether increases of 150 or 300% in estradiol (E2) concentration in peripheral blood (from 6.3 +/- 0.8 pg/mL in control rams) would affect testosterone secretion directly as well as indirectly via the hypothalamic-pituitary axis. After 4 days of estradiol treatment (experiment 1) provided with subcutaneous polydimethylsiloxane implants filled with crystalline estradiol, luteinizing hormone (LH) and testosterone secretions were reduced by 50% (p < 0.05) in both groups of rams because of subtle decreases in pulse frequencies and amplitudes. Estradiol treatments were also associated with decreases in mean follicle-stimulating hormone (FSH) concentration (30-50% in both groups, p < 0.05) and increases in mean prolactin concentration (35% in low-E2 group; 105% in high-E2 group, p < 0.05), but testicular responsiveness to an LH challenge (single intravenous dose, 10 micrograms NIH-LH-S25) remained normal. When along with estradiol treatment, 10-micrograms doses LH were given every 80 min (experiment 2), testosterone secretion increased by 265% (p < 0.05) in both treated and control rams. Relative to day -1, secretion on day 4 was characterized by higher (p < 0.05) pulse frequencies and baseline concentrations and lower (p < 0.05) pulse amplitudes; values for all characteristics were similar to those for Dorset x Leicester x Suffolk rams in the breeding season. Interestingly, the decreases in mean FSH concentration brought about by estradiol and (or) LH treatments were not any greater than in experiment 1, and estradiol's ability to elevate mean prolactin concentration was blocked completely.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Moderate increases in peripheral blood estradiol concentration in the adult ram do not directly inhibit testosterone secretion. 149 Feb 56

Patients with testicular cancer treated with cisplatin can undergo feminization that is understood poorly. Rat model studies recently showed that cisplatin can feminize in part the profile of hepatic steroid-metabolizing enzymes and circulating hormone levels. This study was undertaken to determine whether cisplatin similarly might contribute to the perturbations in gonadotropin or steroid hormone levels that can occur in patients undergoing cisplatin-based treatment for testicular cancer. Analysis of serum free testosterone, total testosterone, and androstenedione levels revealed that these hormones were not altered significantly in patients during a 38-week period of cisplatin-based treatment and follow-up. Estradiol levels were elevated before chemotherapy and were reduced to normal levels during treatment. This reduction was attributed to the cytotoxic effect of chemotherapy on the tumors and the resultant reduction in serum chorionic gonadotropin levels. Serum dihydrotestosterone (DHT) levels were normal before chemotherapy but progressively became elevated during treatment with cisplatin in five of ten patients examined. The rise in DHT may relate to the previously described increase in hepatic androgen 5 alpha-reductase activity in cisplatin-treated rats. Levels of the gonadotropins, luteinizing hormone, and follicle-stimulating hormone (FSH) were normal before cisplatin-based treatment was administered; however, FSH was elevated selectively during chemotherapy. This selective induction of FSH may reflect an effect of cisplatin on the hypothalamic secretion of gonadotropin-releasing hormone. Taken together, these findings suggest that cisplatin contributes to the perturbation of steroid and peptide hormone levels in patients with testicular cancer and perhaps in others undergoing cisplatin-based chemotherapy.
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PMID:Hormonal perturbations in patients with testicular cancer treated with cisplatin. 156 77

Changes in serum concentrations of gonadotropins and gonadal steroids during the periovulatory period were monitored in green, Chelonia mydas, and loggerhead, Caretta caretta, sea turtles. Turtles were from natural populations that nest on a coral island on the Great Barrier Reef. After nesting, each turtle was transferred to a holding tank and held for a maximum of 8 days. A time series of blood samples was obtained from each of five sea turtles (three C. mydas and two C. caretta) starting immediately after nesting and then at approximately 12-hr intervals until the time of release. Prior to release back into the ocean, each turtle was examined by laparoscopy to verify that ovulation had occurred. Serum concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), progesterone (PRO), and testosterone (T) in both species exhibited significant changes during this period. Surges of FSH, LH, and PRO were evident within approximately 20 to 50 hr after each turtle had nested. The significant change in FSH concentration during the periovulatory period is the first such report for a reptile. Coincident with maximal concentrations of FSH, LH, and PRO was a decline in T concentrations in both species. Estradiol-17 beta concentrations were near or below assay sensitivity in the C. mydas, whereas those in the C. caretta were detectable but exhibited no significant changes. The dynamic changes in FSH, LH, PRO, and T concentrations are consistent with the hypothesis that these hormones facilitate specific physiological events during ovulation and egg production.
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PMID:Serum gonadotropins and gonadal steroids associated with ovulation and egg production in sea turtles. 162 99

In a combined phase I-II study the hormonal effects of Toremifene were investigated in 15-15 patients at two dose levels: 60 mg and 300 mg per os, daily. Serum estradiol, progesterone, testosterone, follicle-stimulating hormone, luteinizing hormone, prolactin, human growth hormone were monitored by radioimmunoassay and sexual hormone binding globulin by immunoradiometric assay prior to treatment and at the 2nd, 8th and 12th weeks. The influence of Toremifene upon the hypothalamo-hypophyseal axis was also controlled by a tirotropin releasing hormone functional test using 400 micrograms tirotropin releasing hormone injection iv. Estradiol, progesterone, follicle-stimulating hormone, luteinizing hormone and prolactin decreased proving the antiestrogenic activity of the drug. Sexual hormone binding globulin significantly (p less than 0.002) increased by week 12 at both doses, probably due to a direct effect of Toremifene upon the liver. The increase in sexual hormone binding globulin suggests the partial estrogenic effect of the drug. The tirotropin releasing hormone induced prolactin release was also suppressed. On the basis of hormonal changes and the clinical response of patients 60 mg of Toremifene proved to be as effective as 300 mg.
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PMID:[The anti-estrogenic effect of 4-chloro-1,2-diphenyl-1-(4-[2-(N,N-dimethylamino)ethoxy]phenyl)1-butene (Toremifene) on the endocrine regulation in breast cancer patients]. 182 56

The concentrations of the gonadotropins, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were measured in the luteal phase of the cycle in patients undergoing ovarian hyperstimulation. In nonconception cycles, FSH and LH were increased in the late luteal phase compared with conception cycles in which both gonadotropins were suppressed. Estradiol (E2) and progesterone concentrations increased in pregnancy cycles and may be the sole cause for the decreased gonadotropin concentrations as shown by equivalent concentrations of LH and FSH in both pregnancy and nonpregnancy cycles after matching for E2 concentrations. Subjects who subsequently had twin pregnancy or a spontaneous abortion were compared with those with a successful ongoing singleton conception. There were no significant differences relative to LH and FSH between the three groups, although in twin pregnancy FSH tended to be lower at day 16 from oocyte recovery. It is concluded that suppression of LH and FSH in hyperstimulated pregnancy cycles occurs after the time of the rising human chorionic gonadotropin concentrations in plasma.
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PMID:Decrease in luteal gonadotropin concentration in conception cycles after in vitro fertilization/gamete intrafallopian transfer. 189 87


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