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At least 19 recordsLinked to original sources
PubMed2004

[Disorders of sex differentiation caused by exogenous hormones].

Transplacental and lactogenic exposure of fetus and neonate to exogenous hormones and endocrine disrupters can cause a range of abnormalities of the reproductive system including sex differentiation and sex maturation. Sex differentiation is critically dependent on the normal action of androgens and can be disturbed by unbalanced androgen/estrogen ratios. Androgenic substances masculinize female fetus. Progestogens act both as androgen antagonists, demasculinizing males, and as androgen agonists, masculinizing females. Transplacental exposure of male fetus to synthetic estrogen diethylstilbestrol is recognized to have led to increases in the incidence of cryptorchidism, hypospadia and decreased sperm counts. A growing number of endocrine disrupters have been found to possess either weak estrogenic, anti-androgenic or other hormonal activities. Increased exposure to environmental endocrine disrupters can cause male pseudohermaphroditism.

Animals↗
PubMed1990

[Alternative solutions in the treatment of patients with combined benign endometrial and myometrial pathology].

The study included 96 women with combined benign hyperplastic uterine conditions. Half of them underwent a radical uterine resection and were examined at 3.1 +/- 0.2 years following the operation. The rest were randomly selected as matched pairs and were evaluated at 4.3 +/- 0.13 years following multicomponent treatment including hormones (n-26) and cryohormonal treatment (n-22). Analysis of results revealed a complex pathogenesis of this disease of the reproductive tract, presenting as severe postoperative vegetoneurotic disorders. Potential of an adequate conservative treatment in preserving specific female functions was determined.

Adult↗
PubMed1985

[Estrogen metabolism and hormone substitution in the climacteric].

Report about the metabolism of estrogens in the postmenopausal period and the hormone replacement therapy. The indications and contraindications for the estrogen- and estrogen-progesterone-therapy were discussed. Osteoporosis in the aging women constitutes a major public health and socio-economic importance than the climacteric syndrome.

Adult↗
PubMed1979

Cancer of the breast. Endocrine and hormonal therapy.

Additive hormonal therapy remains the treatment of choice for disseminated breast cancer in postmenopausal women. Patients with hormone-dependent tumors receive excellent and long-lasting palliation from alterations in the hormonal milieu. Now that hormone receptor assays are clinically available, responses can be accuratedly predicted in a large percentage of cases. Tables 11--6 is a summary of additive hormonal therapy in postmenopausal patients. Endocrine ablative therapy remains of primary importance in premenopausal women because of the superior results, but androgens or antiestrogens may be helpful when patients are not surgical candidates. Castration continues to be the initial approach, with adrenalectomy or hypophysectomy reserved for promising candidates. In postmenopausal women the initial choice is estrogens. The exceptions are those patients with metastases limited to bone, when androgens excel because of an equivalent objective response and superior subjective and metabolic effects. Patients who respond to estrogens and then progress are observed for a rebound regression following the discontinuation of estrogen therapy. Whereas some who do not respond to androgens will respond to estrogens, the converse does not appear to be true (Kennedy, 1974). Currently progestins are the secondary hormonal agent of choice in postmenopausal women, but they may be displaced by antiestrogens as more data become available. In general, if a patient's tumor lacks estrogen receptors or the patient fails to respond to an adequate trial of endocrine or hormonal therapy, one should proceed directly to cytotoxic chemotherapy. A suggested plan for the integration of endocrine with hormonal therapy and both with other forms of palliation is diagrammed at the end of Chapter 12.

Adrenal Cortex Hormones↗
PubMed2000

Progestins and androgens increase expression of Spot 14 in T47-D breast tumor cells.

Enhanced expression of fatty acid synthase and other lipogenic enzymes has been observed in a subset of breast cancers with poor prognosis. This phenomenon has been related to amplification of a gene on chromosome region 11q13 encoding Spot 14, a putative regulator of lipogenic enzyme expression. In this paper we demonstrate that the induction of lipogenesis by progestins and androgens in the breast cancer cell line T47-D is accompanied by a marked increase in the expression of Spot 14. These data corroborate the correlation between Spot 14 expression and increased lipogenesis. Moreover they show that apart from gene amplification there is another steroid-regulated pathway that may enhance Spot 14 expression and lipogenesis in tumor cells.

Breast Neoplasms↗