Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042755 (masculinization)
 2,562 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of Danazol, a synthetic 2,3 isoxazol derivative of 17 alpha-ethinyl testosterone, was assessed in three girls and two boys with sexual precocity. Progression of sexual development ceased during administration of Danazol; the effect upon growth rate and skeletal maturation was equivocal. Serum estrogen and progesterone concentrations in the girls were lower during treatment; serum testosterone and dehydroepiandrosterone levels in the boys were also lower. Serum and urinary luteinizing hormone concentrations were inconsistently suppressed. No effect upon follicle-stimulating hormone levels could be demonstrated. Although Danazol appears to inhibit sexual development, this study indicates that the pituitary-gonadal axis is not completely suppressed. Growth rate is not reverted to normal, and virilization may occur among girls. Because undesirable side effects may outweight desirable results, careful consideration is recommended before Danazol is prescribed in the management of sexual precocity.
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PMID:The effect of danazol in sexual precocity. 17 12

Androgen insensitivity was demonstrated in two male siblings with partial masculinization of the external genitalia. They had a previously undescribed defect characterized postpubertally by high plasma testosterone and luteinizing hormone concentrations with low serum follicle-stimulating hormone levels. Studies in skin fibroblasts showed normal androgen receptor affinity and capacity for 5alpha-dihydrotestosterone (DHT), normal nuclear retention of the receptor-DHT complex, and normal conversion of testosterone to DHT.
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PMID:Male pseudohermaphroditism with partial androgen insensitivity. 83 6

Pituitary content or concentration of follicle-stimulating hormone (FSH), prolactin and growth hormone in the genetically androgen insensitive male rat pseudohermaphrodite is intermediate between normal male and female rats, while pituitary luteinizing hormone (LH) concentration and serum FSH levels are the same as in the normal male. The concentration of serum LH, prolactin and growth hormone indicated no sexual dimorphism. Although the pseudohermaphrodite is genetically male with a female phenotype, our results suggest some degree of masculinization of the hypothalamic-pituitary system.
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PMID:Pituitary hormone secretion in the genectically male rat pseudohermaphrodite. 111 35

The role of estrogens on gonadotropin secretion was assessed in two siblings with incomplete virilization syndrome type I due to partial androgen insensitivity (Reinfenstein's syndrome). Serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured before and after 100 micrograms LH-releasing hormone (RH) intravenous (IV) stimulation, as well as during long-term clomiphene citrate (CC) administration. Serum testosterone (T) and estrogens were determined before and during daily administration of human chronic gonadotropin (hCG) and also during the CC treatment. Basal levels of LH were elevated in both patients: 12.5 +/- 1.1 mIU in patient A and 19.8 +/- 1.8 mIU/ml in patient B. Conversely, FSH levels were within normal limits. Administration of LH-RH in both subjects induced a rise in LH levels, while FSH concentration showed no increase. The CC administration resulted in a significant (P less than 0.005) increment in serum LH levels without changes in FSH concentration. An important increase of serum T and estradiol (E2) levels was noted during CC administration; thus, in patient A those levels augmented from 20 to 48 ng/ml for T and from 78 to 220 pg/ml for E2; and patient B showed an increment from 20 to 35 ng/ml for T, and from 55 to 180 pg/ml for E2. The daily administration of hCG was followed by an increment in both T and E2 levels, which was of lesser degree for estrone concentration. These results suggest that endogenous estrogens, particularly E2, modulate LH secretion in patients with partial androgen insensitivity; however, it appears that estrogens had no physiologic effect on FSH secretion.
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PMID:Modulation of luteinizing hormone secretion by estrogens in patients with Reifenstein's syndrome. 250 38

Neonatal female hamsters were exposed to doses of testosterone propionate or estradiol benzoate that would lead to behavioral masculinization and defeminization at adulthood. At Days 20, 30, or 40 of life, ovaries were removed and incubated in Kreb's Ringer bicarbonate for 4 h with or without the addition of 1 X 10(-9) M testosterone as a substrate. Incubation medium was assayed by radioimmunoassay (RIA) for the accumulation of estradiol. Ovaries from steroid-exposed animals aromatized testosterone to estradiol at a greatly increased rate compared to ovaries from oil-injected control animals. Serum from treated animals contained androgen, which could act as substrate for aromatization in vivo. Neonatally estrogenized females exhibited elevated circulating estradiol levels. Increased aromatizing ability could be due to early antral follicle formation as a result of elevated luteinizing hormone (LH) and/or follicle-stimulating hormone (FSH). Implications of increased aromatization ability of ovaries in the process of behavioral sexual differentiation are discussed.
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PMID:Neonatal steroid exposure increases in vitro aromatization ability of peripubertal hamster ovaries. 358 Apr 53

Gonadectomy of male rats was performed at 0, 6-7 (6h), 12-13 (12h), or 24 h postnatally in order to examine the influence of testosterone exposure on sexual differentiation of the brain. The indices examined were: the volume of the sexually dimorphic nucleus of the preoptic area (SDN-POA) and luteinizing hormone (LH) and follicle-stimulating hormone (FSH) titers following estradiol benzoate (EB) and progesterone (P) administration. Control animals were sham-operated at 0 h and gonadectomized at 29 days of age (sham). A decrease in the percentage of males with elevated plasma LH levels following P was found with increasing delay before gonadectomy. Significant (P less than 0.001) differences existed in the amplitude of plasma LH titers 5 h following P administration between sham, 0 h, and 6 h groups. Follicle-stimulating hormone was also elevated in all neonatally gonadectomized male groups following P administration, but there was no difference between the groups. Volume of the SDN-POA was significantly (P less than 0.001) smaller in all gonadectomized males when compared to that of sham-operated males, but no differences existed between males gonadectomized at the different hours postpartum. In female rats gonadectomized at 0 h (F0h), LH levels were elevated 5 h following P, but only to a magnitude of 36% of that of sham-operated controls (P less than 0.001). Volume of the SDN-POA of the F0h group was significantly reduced (P less than 0.05) when compared to that of sham females. Thus, in males, the presence of the tests prenatally may be responsible for the initiation of masculinization of LH release mechanisms and the SDN-POA, but both require further androgen exposure for their completion. In addition, the LH and FSH regulating systems show a differential sensitivity to the steroid hormone environment during development that shapes the animal's response to steroid as an adult.
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PMID:Differential effects of the perinatal steroid environment on three sexually dimorphic parameters of the rat brain. 392 34

We studied four patients with Robinow's syndrome. New findings included the following: (1) normal pubertal virilization with persistence of micropenis; (2) elevated basal serum follicle-stimulating hormone levels and a hyperresponse of serum luteinizing hormone to gonadorelin hydrochloride (Factrel) stimulation among postpubertal male patients, suggesting partial primary hypogonadism; (3) normal 5 alpha-reductase and androgen receptor activity in genital skin fibroblasts; and (4) normal to borderline adult height.
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PMID:Robinow's syndrome. Partial primary hypogonadism in pubertal boys, with persistence of micropenis. 612 75

In women with preexisting virilization, it is advisable to prescribe contraceptive agents that do not provoke a further increase in free circulating androgens. This study evaluated the influence of 3 gestagens without androgenic effects on the endogenous sex hormone equilibrium and sex hormone-binding globulin (SHBG) concentrations. 122 women were administered 4 different combined contraceptives for up to 6 cycles. The estrogen component of each of the 4 preparations was estradiol estrogen (EE), while the gestagens were desogestrel (in 2 formulations in 2 different dosages), cyproterone acetate, and chlormadinone acetate. Most subjects had irregular cycles before treatment, and exhibited seborrhea, acne, and hirsutism. Luteinizing hormone, follicle-stimulating hormone, estrone, estradiol, progesterone, free testosterone, and dehydropeiandrosterone-sulfate levels were significantly reduced in all 4 treatment groups during tablet intake. However, SHBG concentrations increased in a highly significant manner during treatment. The elevation of SHBG is an expression of increased hepatic synthesis induced by EE. Concentrations of circulating SHBG determine the balance between estrogens and androgens. Since SHBG binds androgens better than estrogens, it effectively monitors androgenic activity. Because of their role in significantly lowering the active fraction of androgens, the preparations studied are considered appropriate contraceptives for androgenized women.
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PMID:Effects of various combined oral contraceptives on sex steroids, gonadotropins and SHBG. 668 15

Male rats were castrated at 26 days of age and treated with 0.05, 0.1, 1.0 and 2.0 micrograms/kg of BW of estradiol for 4 days starting with the day of castration. On the morning of Day 30 of life they were sacrificed and serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were determined. A significant reduction of LH and/or FSH occurred only with the 1.0 and 2.0 micrograms/kg of BW dose of estradiol. This was in sharp contrast to results in female rats at the same age in which 0.2 microgram/kg of BW of estradiol suppressed the post-castration rise of gonadotropins. This change in threshold sensitivity to the suppressive effects of estradiol may be one component of the changes accompanying the masculinization of the hypothalamus. The 1.0 and 2.0 micrograms/kg of BW doses of estradiol then were used in combination with 0.1, 0.5, 1.0, 2.0, 4.0 and 8.0 mg/kg of BW of progesterone. The addition of progesterone to the treatment regimen resulted in either no change or a suppression or stimulation of FSH and LH, depending upon the dose of progesterone used. With the 2 micrograms/kg of BW dose of estradiol, 1.0 mg/kg of BW of progesterone resulted in a surge of both FSH and LH, irrespective of whether it was given in combination with estradiol or a single injection following 4 days of estradiol treatment. This, to our knowledge, is the first demonstration of a gonadotropin surge induced by progesterone in the estrogen-primed castrated male rat.
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PMID:Induction of luteinizing hormone, follicle-stimulating hormone surge in the estrogen-primed castrated male rat by progesterone. 681 10

A 26-year-old woman with secondary amenorrhea, temporal balding, and clitoromegaly was found to have both the gonadotropin-resistant ovary syndrome and hilus cell hyperplasia. Simultaneous sampling of peripheral and ovarian venous blood revealed excess ovarian testosterone secretion to be the probable cause of the patient's virilism. The marked response of the ovary to stimulation by luteinizing hormone (LH) coupled with the lack of ovarian follicular development suggested that an isolated resistance of the ovarian follicle to follicle-stimulating hormone (FSH) was present in this patient. The administration of a daily pharmacologic dose of dexamethasone for 14 days was followed by the patient's first menstrual period in 13 years, raising the possibility that autoimmunity may have been involved in this patient's ovarian resistance to FSH stimulation.
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PMID:Ovarian and adrenal steroidogenesis in a virilized patient with gonadotropin-resistant ovaries and hilus cell hyperplasia. 739 11


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