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PubMedDate not supplied

[Testicular feminization syndrome. Prenatal diagnosis: observations apropos of 2 sisters].

The anatomo-clinical aspects and the physiopathology of the feminizing testicle syndrome, are now better known. The prenatal diagnosis of this familial genetic ailment through the determination of the fetal sex by ultrasonography and the study of fetal karyotypes by amniotic fluid analysis or biopsy of trophoblast, is currently possible. Risk groups must be defined in order to ensure a better care for these children.

Adult↗
PubMed1985

Testicular feminization syndrome. An unusual case with high estrogen levels.

In an unusual case of testicular feminization, the patient had a high estrogen and low testosterone level. The source of this female hormone excess may have been functioning gonadal stroma of either female or male derivation. All other aspects of the case were consistent with classic examples of the syndrome.

Adult↗
PubMed1978

Feminizing adrenocortical carcinoma with Cushing's syndrome and pseudohyperparathyroidism.

A patient with adrenocortical carcinoma had three major endocrine abnormalities attributable directly to the tumor: hypercortisolism (Cushing's syndrome), hyperestrogenism (feminization), and hypercalcemia (pseudohyperparathyroidism). There were higher levels of immunoreactive parathyroid hormone in venous effluent from the tumor or its abdominal metastases compared to that found in the veins draining the parathyroid glands. This, together with the presence of normal parathyroid glands on autopsy, established the diagnosis of pseudohyperparathyroidism as the cause of hypercalcemia in this patient.

17-Hydroxycorticosteroids↗
PubMed1981

Testicular feminization of the mouse: paucity of peroxisomes in Leydig cell of the testis.

The testes of mice with the X-linked testicular feminization (Tfm/y hermaphrodite) mutation are very small and cryptorchid. The spermatogenesis in the adult Tfm/y hermaphrodite mouse testes is arrested, and the testosterone biosynthesis is significantly reduced due to deficiency of 17-keto-steroid reductase, the enzyme essential for the conversion of androstanedione to testosterone. In this study the distribution of peroxisomes in the Leydig cells of adult Tfm/y hermaphrodite mice was investigated because of the suggestion that peroxisomes may participate in lipid metabolism and/or androgen biosynthesis is steroidogenic cells. Aldehyde-fixed testicular tissue of Tfm/y hermaphrodite mice was processed for the cytochemical localization of peroxisome catalase to facilitate identification of these organelles in the Leydig cells. Testes from Blo/y and CSa strain normal adult mice served as controls. Testicular Leydig cells of normal adult Blo/y and CSa mice contained abundant smooth endoplasmic reticulum (SER) in the form of complex interconnected tubules and double-walled membranous vesicles. Numerous peroxisomes, often in continuity with SER channels or in close association with lipid droplets, were observed in Leydig cells of normal males. In contrast, the peroxisomes in the Leydig cells of adult Tfm/y hermaphrodite mouse testes were either undiscernible or greatly reduced in number and size. SER in these cells was sparse, whereas mitochondria were numerous. In addition, abundant clusters of lipid droplets were encountered in a majority of Leydig cells of Tfm/y hermaphrodite mouse testes. Peroxisome and SER paucity in Leydig cells of Tfm/y hermaphrodite mice may be a reflection of reduced testosterone production. Whether excessive accumulation of lipid in the Leydig cells of Tfm/y hermaphrodite mouse testes is due to reduced utilization of cholesterol for the biosynthesis of testosterone or to impaired lipid metabolism due to reduction in peroxisome population in these cells remains to be ascertained.

Animals↗
PubMedDate not supplied

[Malignant tumour of adrenal with feminizing syndrome and primary hyperaldosteronism (author's transl)].

Feminizing tumour of adrenals are rare. Gynecomasty, abdominal tumour are the more frequently observed symptoms. The described case in a 38 years aged man is of special interest because of association with primary hyperaldosteronism. Studies in vivo and in vitro are reported. In vitro studies shown a high 18 hydroxylation biosynthetic activity of tumoral fragment and a great synthesis of polar phenolsteroids with testosterone as precurseurs.

Adrenal Cortex Neoplasms↗
PubMed1979

Cytotoxic activity of 1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2-dichloroethane (mitotane) and its analogs on feminizing adrenal neoplastic cells in culture.

Mitotane [1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2-dichloroethane], an antineoplastic agent for inoperable adrenal carcinoma, was studied for its cytotoxic activity on a clonal line of feminizing human adrenal neoplastic cells (Fang-8 cells) in culture. At concentrations higher than 1.68 X 10(-4) M, mitotane produced a dose-related toxic effect on the cells. The effect of the drug was specific to Fang-8 cells because the same treatment produced little or no toxicity on lines of rat pituitary GH3 cells and human skin fibrocytes. The effect of mitotane to Fang-8 cells was a reversible one. Electron microscopic pictures revealed that the drug was causing mitochondrial degeneration. In this testing system, several isomers and analogs of mitotane were found equally or more toxic than was mitotane itself. The dichloro- or trichloroethylene structure was essential for the cytotoxic activity while the chloro substituents on phenyl rings appeared to be unimportant. This system appears to be useful in elucidating the biochemical mechanism of mitotane action on adrenal cancer.

Adrenal Gland Neoplasms↗
PubMed1994

[Bilateral gynecomastia revealing malignant feminizing adrenocortical carcinoma].

We report here a new case of feminizing adrenocortical carcinoma revealed by a bilateral gynecomastia in a 50 year old man. The malignant character was already suspected on clinical and hormonal data. It was confirmed by the pathology. The op'DDD treatment of three weeks was of too short duration to allow any opinion on its efficacy.

Adrenal Cortex Neoplasms↗
PubMed1977

[Feminizing adrenal cortex carcinoma in a 66-year-old man].

Feminizing tumors of the adrenal cortex in man are very rare. The case is reported of a 66-year-old man who had a carcinoma of the right adrenal cortex which produced various steroid fractions. In the primary tumor and in the second reccurrence the estrogens were dominant. In electron microscopy the tumor cells are poorly differentiated. They may be attributed to the fasciculo-reticular layer and show no signs specific for their secretory activity. The patient died 2 1/2 years after onset of the disease. The case is discussed in the light of the pertinent literature.

Adrenal Cortex Hormones↗
PubMed1980

Peutz-Jeghers syndrome with feminizing sertoli cell tumor.

A case involving a 6-year-old boy with Peutz-Jeghers syndrome and an unilateral feminizing Sertoli cell tumor is described. Endocrinologic studies revealed consistently high plasma and urine levels of estrogens and normal levels of testosterone and dihydrotestosterone. The increased levels of estrogens did not show changes that could be correlated with exogenous gonadotropin administration, thus indicating an autonomous nature. The histopathologic studies of nontumorous testicular tissue revealed changes in the seminiferous tubules which suggested that estrogens, directly or indirectly, may have had both stimulating and atrophying effects. It is concluded that gonadal tumors are in additional manifestation of the Peutz-Jeghers syndrome gene in both male and female patients.

Androgen-Insensitivity Syndrome↗
PubMed1984

Presidential address. Fatti Maschii Parole Femine.

The current role of the Society of Surgical Oncology has demonstrated leadership in the field of surgical oncology in both word and deed, as exemplified by the motto of the State of Maryland, adopted from the 1632 family seal of Lord Baltimore, "Fatti Maschii Parole Femine." The current emphasis on the need for clinical research on human cancers, and the education of surgeons in all aspects of various cancers is well founded in the writings and the addresses of Dr. James Ewing, the Society's founder. Our goals as a society for the next decade have been precisely defined and, as in all important national programs, made current and interfaced with corresponding priorities of the American Cancer Society and the National Cancer Institute. The Society, in three project areas, is: (1) assessing current progress in surgical oncology, as well as future manpower needs; (2) studying on a comprehensive basis the surgical practices in cancer patient management; and (3) surveying academic centers concerning the nature of current education and training of academic surgeons in clinical research. The Training Committee currently reviews and recognizes 2-year postresidency multidisciplinary training at several institutions, and the James Ewing Foundation has expanded its fiscal support of educational activities. This annual meeting marks an historic first signified by the conjoint sessions being held with other international surgical oncology societies.

Education, Medical, Graduate↗
PubMed1985

Characterization of a feminizing testicular Leydig cell tumor by hormonal profile, immunocytochemistry, and tissue culture.

A patient with gynecomastia and a nonpalpable testicular Leydig cell tumor is presented. Estradiol and progesterone levels were elevated whereas serum testosterone was reduced. Following removal of the tumor the hormonal values returned to normal with reduction of gynecomastia. Tumor tissue was maintained in culture for 9 days during which high estradiol levels as well as lesser quantities of testosterone and progesterone were demonstrated in the culture medium. Elevation of progesterone supports a block of 17 alpha-hydroxylase activity caused by increased endogenous estradiol. This is the first case of a cultured feminizing testicular Leydig cell tumor in which hormone production was demonstrated. The freshly removed tumor as well as the cultured tissue material were studied by immunocytochemical methods and biochemical analysis of cytoskeletal proteins. These methods revealed vimentin as the exclusive type intermediate sized filament in both. This is the first demonstration of vimentin in a Leydig cell tumor, in agreement with its occurrence in normal Leydig cells.

Adult↗
PubMedDate not supplied

Ethanol-induced increase in cytosolic estrogen receptors in human male liver: a possible explanation for biochemical feminization in chronic liver disease due to alcohol.

The hepatic cytosolic estrogen receptor content was measured in liver samples from patients with normal livers and from patients with nonalcoholic cirrhosis, alcoholic cirrhosis and alcoholic hepatitis. The estrogen receptor content of normal liver was 5.2 +/- 3.5 fmoles per mg of cytosolic protein. Levels which were not significantly different from this were found in the samples from patients with nonalcoholic cirrhosis (2.1 +/- 2.0 fmoles per mg of cytosolic protein). The cytosolic estrogen receptor content in the livers of patients with alcoholic cirrhosis who were abstaining was 4.2 +/- 3.6 fmoles per mg of cytosolic protein, but it increased to 10.4 +/- 4.9 fmoles per mg of protein in the livers of patients with alcoholic cirrhosis who were drinking, to 17.3 +/- 8.7 fmoles per mg of protein in the livers of patients with alcoholic hepatitis with cirrhosis and to 22.7 +/- 15.7 fmoles per mg of protein in the livers of patients with alcoholic hepatitis without cirrhosis. Alcohol abuse appeared, therefore, to induce an increase in the estrogen receptor content of human liver, especially in patients who were drinking and had histological evidence of acute liver damage (alcoholic hepatitis). The increase in hepatic estrogen receptor which we have observed may be involved in the molecular mechanisms underlying the feminization of the liver in alcoholic males.

Aged↗
PubMed1993

Bone and mineral metabolism in the androgen-resistant (testicular feminized) male rat.

Androgens have important effects on bone in vivo, possibly by direct activation of the androgen receptors in osteoblasts. To test this hypothesis, calcium homeostasis, bone mass, and bone turnover were evaluated in mature (4-month-old) androgen-resistant (testicular feminized, TFM) male rats. Data were compared with data from both female and male littermates of the same age and strain. Compared to normal males, TFM had similar serum testosterone, twofold higher estradiol and estrone, and sixfold higher androstenedione concentrations. Compared to normal females, TFM rats showed lower estradiol but also elevated concentrations of androstenedione and estrone. Despite similar free 1,25-(OH)2D3 concentrations, both TFM and male rats maintained higher serum calcium and phosphate concentrations than their female littermates. Serum IGF-I concentrations in TFM rats were decreased compared to male rats (-12%) or female rats (-27%). Serum osteocalcin concentrations, however, were twofold higher in TFM rats than in females but not significantly different from males. Femoral length, diameter, and cortical thickness were intermediate between those of males and females. The cancellous bone density of the femur and cancellous bone volume of the proximal metaphysis of the tibia, however, were not significantly different between groups. The ash weight of the tibia was also not significantly different, and the ash weight of the four distal lumbar vertebrae ranged between male and female values. Bone mechanical properties as measured by torsional strength and energy absorption of the femur were lower in TFM than in females but not different from males.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgen-Insensitivity Syndrome↗
PubMed1986

Androgenic induction of DNA synthesis in prostatic glands induced in the urothelium of testicular feminized (Tfm/Y) mice.

It has been shown previously that wild-type urogenital sinus mesenchyme can induce the formation of prostate-like glandular structures in urinary bladder epithelium derived from adult Tfm (testicular feminization) mice. Total DNA synthesis within these tissue recombinants has been shown biochemically to be androgen sensitive. To determine which tissue (epithelium or stroma) accounts for this androgen-dependent DNA synthesis, an autoradiographic study was performed with tissue recombinants composed of rat wild-type urogenital sinus mesenchyme (UGM) associated with bladder epithelium from either wild-type (BLE) or Tfm mice (Tfm BLE). Both types of recombinants were grown under the kidney capsule of male athymic nude mice for 4 weeks. The hosts were then castrated, and 2 weeks later were treated with either testosterone propionate (TP), TP plus cyproterone acetate (CA), or oil vehicle for 3 days. DNA synthetic activity was measured through analysis of labelling index (LI) after incorporation of 3[H]-thymidine in vivo. For both UGM + BLE and UGM + Tfm BLE recombinants thymidine incorporation in epithelial cells greatly exceeded that of the stromal cells. TP stimulated epithelial LI to a similar degree (about 50- to 200-fold greater than controls) in both UGM + BLE and UGM + Tfm BLE recombinants; CA antagonized the effect of TP. Nuclear 3H-DHT binding was observed autoradiographically within the epithelial cells of the induced epithelium of UGM + wild-type BLE recombinants, but not within epithelium of UGM + Tfm BLE recombinants. Wild-type mesenchymal cells in both tissue recombinants showed specific nuclear 3H-DHT uptake. Thus, the proliferative effect of androgens upon prostatic epithelium is not a direct effect mediated by intra-epithelial androgen receptors, but rather it appears to be elicited indirectly via regulatory influences from androgen-receptor-positive stromal cells.

Androgens↗
PubMed1994

A substance secreted by rat Sertoli cells induces feminization of embryonic chick testes in vitro.

Male and female gonads from 7- to 9-day-old chick embryos were cultured for 6 days in Sertoli cell-conditioned medium or in serum-free medium to investigate the possible effect of substances secreted by rat Sertoli cells on chick gonad development. Histological analysis showed that whereas all female gonads proceed through normal ovarian development in both culture media, most of male gonads showed clear feminization only when cultured in Sertoli cell-conditioned medium; male gonads cultured in serum-free medium developed as normal testes. Because the only substance detected in our conditioned medium with the potential to cause these effects was sex-specific antigen (Sxs), our results provide further evidence that Sxs antigen may play a role in sexual differentiation in birds, and probably in mammals.

Androgen-Insensitivity Syndrome↗
PubMed1990

Maternal meiosis II nondisjunction in a case of 47,XXY testicular feminization.

An 11-year-old patient with incomplete testicular feminization and a 47,XXY karyotype is described. The patient had female external genitalia, clitoromegaly, and some features of Klinefelter's syndrome, including speech delay and delayed intellectual development. DNA analysis using X chromosomal DNA sequences suggest that the supernumerary X chromosome in the patient resulted from maternal nondisjunction during meiosis II. The M II error thereby provides the basis for homozygosity of a mutation in the androgen receptor locus.

Androgen-Insensitivity Syndrome↗
PubMed1975

Testicular lipids in mice with testicular feminization.

Morphological, histochemical and biochemical studies of the testis of mice with testicular feminization (tfm/y) reveal a large accumulation of lipids in Leydig cells and in Sertoli cells. In Leydig cells of tfm/y mice, lipid droplets do not exhibit the special relationship with smooth endoplasmic reticulum that exists in normal adult Leydig cells. Compared to the surgically-cryptorchid control, the tfm/y testis contains more lipid in Leydig cells but less in Sertoli cells. There are also quantitative differences in testicular lipids in tmf/y and normal testes but no significant differences were noted between tfm/y and surgically-cryptorchid testes. The testes of both the genetically defective and surgically-cryptochid animals contain increased amounts of total lipids and phospholipids, and of free and esterified cholesterols. Exogenous testosterone has no effect on lipids or other characteristics of these cells. The present results suggest that the increased lipids in tfm/y mice result from a genetic disorder that asserts itself (1) in Leydig cells where it is associated with, and is probably a result of, impaired lipid metabolism and steroidogenesis, and (2) in Sertoli cells where it is perhaps attributable to arrested spermatogenesis and impaired steroidogenesis.

Androgen-Insensitivity Syndrome↗