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At least 361 records · Page 20Linked to original sources
PubMed1976

Steroid metabolism in the gonads of a patient with testicular feminization. II. Metabolism of c19- and c18-steroids in vitro.

The metabolism of C19- and C18-steroids, in particular, the aromatization of androstenedione and testosterone, the interconversion of androgens to estrogens and the 5alpha-reductase activity of a right abdominal (r) and a left inguinal (l) testis of a patient with testicular feminization, are reported. Aromatization and 5alpha-reductase activity were also evaluated in tissue from the left ductus diferens (ld). The following results were obtained: 1. aromatization of androstenedione to estrone 2.52% (r), 0.02% (l), 0.94% (ld); 2. aromatization of testosterone to estradiol 0.58% (r), 2.88% (l); 3. conversion of androstenedione to testosterone 95.65% (r), 98.07% (l); 4. conversion of testosterone to androstenedione 33.14% (r), 53.65% (l); 5. conversion of estrone to estradiol85.29% (r), 100% (l), 6. conversion of estradiol to estrone 33.12% (r), 32.33% (l); 7.5alpha-reduction of testosterone to 5alpha-dihydrotestosterone 12.01% (r), 13.64% (l) and 4.10% (ld). A lack of 5alpha-reductase activity was not found in the tissues examined as stated in the literature. Estrogen production in these testes was demonstrated by the aromatization of androstenedione and testosterone to estrone and estradiol and is reflected in the difference of the estradiol concentration measured in spermatic and peripheral blood of the same patient (168 versus 33 pg/ml).

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1992

[Male pseudohermaphroditism. Testicular feminization syndrome].

Male pseudohermaphroditism--testicular feminization syndrome is a rare genetic entity with considerably familial predisposition. Of the 9 cases, 7 except 2 children were confirmed surgically. Clinical manifestations of the disorder were primary amenorrhea, infertility and a mass in groin. We suggested that orchiectomy is necessary after puberty. The genetic pattern, clinical characteristics, diagnosis and treatment of the condition were briefly discussed with a review of the literature.

Androgen-Insensitivity Syndrome↗
PubMed2004

Androgen insensitivity syndrome in a thoroughbred mare (64, XY--testicular feminization).

A Thoroughbred mare was presented for stallion-like behavior. Reproductive and ultrasonographic evaluation, testosterone assays, and karyotyping confirmed a diagnosis of androgen insensitivity syndrome (64, XY--testicular feminization). Surgery to remove abdominal testicles was successful in alleviating the behavioral abnormality. This condition is discussed with reference to the current literature.

Androgen-Insensitivity Syndrome↗
PubMed1992

[A case of male pseudohermaphroditism with incomplete testicular feminization syndrome].

A 19-year-old female visited our hospital because of primary amenorrhea. She was genetically (46XY) male. Her breasts were poorly developed. She had no pubic or axillary hair. The phenotype was female, and the vagina had a short and closed end. Plasma testosterone (T) and 5-alpha dihydrotestosterone (DTH) were low. However, DHT was elevated by ex vivo T load. The testis, which was atropic, epididymis and vas deferens, which were well developed, were found and resected by operation. The amount of androgen receptors of the skin tissue of the external genitalia was normal. These findings suggested that male pseudohermaphroditism with incomplete testicular feminization syndrome may have been caused by androgen resistance syndrome due to the disorder of androgen receptor complex, genetic information or post receptor.

Adult↗
PubMed1992

[The complete testicular feminization syndrome: apropos 2 new cases].

Two additional cases of complete testicular feminization syndrome or Morris syndrome are described. The patients had consulted for primary amenorrhea. Patient work up revealed a female phenotype, hormone profile and 46,XY karyotype. They were submitted to abdominal surgical exploration and orchidectomy of the cryptorchid male gonads. The potential etiologic factors, pathogenesis, incidence and clinical features of this syndrome are discussed. Furthermore, the surgical treatment and outcome are described, highlighting the incidence of gonadal malignancy if these are not removed early.

Adult↗
PubMed2005

47,XXY female with testicular feminization and positive SRY: a case report.

BACKGROUND: Males with a 47,XXY karyotype have the clinical phenotype of Klinefelter syndrome. A few 47,XXY cases with a female phenotype have been reported. These individuals have positive SRY (testis-determining factor). The genetic explanation of this phenomenon is unclear. CASE: A 34-year-old woman presented with testicular feminization and a 47,XXY karyotype. Cytogenetic analysis and fluorescence in situ hybridization suggested that the Y chromosome had a normal structure; the polymerase chain reaction was positive for SRY. CONCLUSION: This is the third reported case of 47,XXY with afemale phenotype in spite of the presence of a Y chromosome and the normal SRY. This suggests that the phenotypic sex in these patients might be due to the involvement of other sex-determining genes.

Adult↗
PubMedDate not supplied

Feminizing adrenocortical adenoma presenting as heterosexual precocious puberty: report of one case.

We report on a case of a 2 2/12-year-old boy with heterosexual precocious puberty secondary to a feminizing adrenocortical adenoma. The boy, with no previous history of disease or treatment, presented with bilateral gynecomastia and pubic hair development (Tanner III breasts and Tanner II pubic hair). Plasma estradiol and testosterone were 410.9 pg/ml and 126.2 ng/dl respectively. Basal plasma LH and FSH levels were within the normal range. Bolus i.v. injection of GnRH showed unresponsiveness of LH and FSH. Abdominal echography and abdominal magnetic resonance imaging revealed a well-defined mass at the left suprarenal region (measuring 4.0 x 2.7 x 3.6 cm in size). After removal of the adrenal tumor, the estradiol and testosterone levels fell to normal in 2 weeks. The gynecomastia and pubic hair regressed with time. The pathology of the tumor showed compact pattern with polygonal cells containing moderate eosinophilic cytoplasm without mitotic figure. These findings were consistent with an adrenocortical adenoma secreting estradiol and testosterone as the cause of the patient's heterosexual precocious puberty.

Abdomen↗
PubMed1991

Role of gonadal dysgenesis in gonadoblastoma induction in 46, XY individuals. The Leuven experience in 46, XY pure gonadal dysgenesis and testicular feminization syndromes.

To stress the importance of gonadal dysgenesis in the genesis of gonadoblastoma in the presence of the Y-chromosome, the authors report their experience on 7 patients with 46, XY Pure Gonadal Dysgenesis (PGD) and 14 patients with complete or incomplete forms of Testicular Feminization (TF) syndrome. The diagnostic criteria and the clinical and pathological findings are reviewed. Four patients with PGD were found to be affected by bilateral (1 patient) or unilateral (1 patient) gonadoblastomas, and by extragonadal (1 patient) or gonadal (1 patient) dysgerminoma, whereas no gonadal tumors were encountered in testes of patients with complete (CTF) or incomplete (ITF) forms of TF, underlining the pathogenic role of the gonadal dysgenesis.

Adolescent↗
PubMed1991

Urinary excretion of histamine and methylhistamine in testicular feminizing syndrome.

Histamine is implicated in several reproductive functions. Correlation between histamine metabolism and sex hormones has been a matter of interest for many years. Urinary histamine excretion has been studied under various experimental conditions in different species. In man it was reported, that the urinary excretion of histamine and/or methylhistamine in women was correlated to the excretion of oestrogen. Very little is known about the condition in man with intersex. The case reported here shows that histamine and methylhistamine excretion in urine in a patient with testicular feminizing syndrome is unaffected by castration.

Adult↗
PubMedDate not supplied

[Biochemical and endocrine heterogeneity in the complete form of testicular feminization syndrome].

A familial variant of male pseudohermaphroditism different from the classical form of the complete testicular feminization syndrome was studied. The three affected 46, XY sibling (16,18 and 20 years old) exhibited female phenotype identical to that of a 17 years old patient with the classical form, included as a control. The major endocrine and biochemical differences observed in this family, as compared with the classical form, includes: a. Markedly elevated serum levels of LH and FSH; b. Non-elevated serum testosterone levels; c. Poor testicular hCG responsiveness; d. Abnormally elevated baseline and hCG-stimulated androstenedione: testosterone ratio; e. Slight pituitary responsiveness to androgens; f. presence of residual androgen uptake by cultured fibroblasts derived from genital skin. These differences were more evident in the two older patients. All subjects presented a lack of nitrogen retention following testosterone administration. These results were interpreted as demonstrating a testicular impairment of testosterone biosynthesis in the older subjects of this family, which resulted in an unusual gonadotropin profile. The altered androstenedione: testosterone ratio suggests a secondary partially decreased activity of testicular 17-hidroxysteroid dehydrogenase, as demonstrated in TFM mice and rats. The overall data indicate an age-dependent variability in the expression of androgen insensitivity in this family, thus demonstrating the wide biochemical heterogeneity of the androgen resistant syndromes.

Adolescent↗
PubMed1990

[Ingestion of diethylstilbestrol during pregnancy. Its responsibility in the testicular feminization syndrome].

We report the cases of two women who had testicular feminization with remnants of Müllerian ducts and whose mothers had received diethylstilbestrol (DES) during the first trimester of pregnancy. At laparotomy, masses were removed which had the microscopic appearances of testes and Fallopian tubes, and were confirmed as such at histology. There were three possible explanations for these genetic abnormalities: deficient antimüllerian hormone (AMH) secretion (or lack of sensitivity of Müllerian ducts to AMH); early testicular descent with regression of Müllerian ducts beyond the efficacy margin of AMH; exposure to DES in utero during the first trimester of pregnancy. In these two women, the most likely explanation seems to be the last one.

Adult↗
PubMed1989

Testicular feminization syndrome. Four case reports with a brief review of the literature.

Four cases of testicular feminization syndrome in Ethiopian patients are described. All four patients had normal female breasts, scanty pubic and axillary hair and absent internal genital organs. Three had bilateral inguinal or labial masses. The main features of their clinical presentation and histological studies are briefly discussed with a review of the literature.

Adult↗
PubMed1989

Testicular feminization in a cat.

Testicular feminization, caused by an inherited defect of the androgen receptor, was diagnosed in a domestic cat. Individuals affected with this syndrome are genetic males that have testes but fail to undergo masculinization because the internal and external genitalia cannot respond to androgens. The affected cat had the external appearance of a sexually normal female, but during surgery for ovariohysterectomy, only 2 abdominal gonads were found. Müllerian (uterus) or wolffian (epididymides) derivatives were not present. Only testicular tissue was found in histologic sections of the gonad. A normal male chromosome constitution (38,XY) was found in karyotypes prepared from lymphocyte cultures. High affinity binding of dihydrotestosterone was undetectable in fibroblasts cultured from genital skin of the affected cat, indicating that the cytosolic androgen receptor was nonfunctional. Pedigree analysis indicates that this is an X-linked disorder in cats, as it is in other mammals. Accurate diagnosis and genetic counseling are advocated to reduce the prevalence of the disorder.

Androgen-Insensitivity Syndrome↗
PubMed1989

Testicular feminization syndrome: a case study of four generations.

This report deals with the complete form of testicular feminization in four generations of a single kindred. The four siblings who have had orchiectomy had no evidence of testicular malignancy. Because all four of the postpubertal patients have the complete form of the disorder, the prepubertal member is being managed expectantly, awaiting the onset of female secondary sexual characteristics at puberty. Other carriers may be identified as reproductive function continues.

Adolescent↗
PubMed1988

[Endocrinological and electron microscopical studies on the complete form of testicular feminization syndrome].

A 23-year-old patient with a complete form of testicular feminization syndrome (Tfm) was examined endocrinologically and morphologically by electron microscopy. 1. Serum testosterone, DHEA and estrone concentrations and the urine 17-KS concentration were higher than in adult males. Furthermore, serum pituitary gonadotropins, especially LH, were increased. 2. We found that testicular venous testosterone, estrone, estradiol and progesterone were remarkably increased compared with their peripheral concentrations, and that circulating concentrations decreased rapidly after gonadectomy. The electron microscopic study showed active steroidogenesis in Leydig cells. We believe that these results prove that these steroids are produced in Leydig cells. 3. We found that the administration of 10,000 IU/day of hCG for 2 days increased serum gonadal steroids but that of 225 IU/day of hMG for 2 days did not, that LH responded strongly to LH-RH but FSH response was weak, and that after gonadectomy serum LH immediately increased but FSH did not change for at least 24 hours. From these results, we assume that FSH is not related to steroidogenesis and that the mechanisms regulating serum LH and FSH are different. 4. The seminiferous tubules were occupied by two kinds of cells. Both kinds were Sertoli cells, one of which was numerous and of low electron density indicating an immature type, and the other was of high electron density indicating a mature type. Spermatogonia were not detected.

Adult↗
PubMed1988

[A case of testicular feminization].

A 21-year-old female visited the gynecological clinic because of primary amenorrhea. The patient was a phenotypic female with scanty pubic hair, short and blind-ending vagina and bilateral inguinal soft masses. The patients was referred to our clinic. The serum luteinizing hormone level was 27.1 mIU/ml, follicle stimulating hormone level was 8.8 mIU/ml, and testosterone level was 11 ng/ml. Chromosomal analysis of peripheral lymphocytes revealed the karyotype 46, XY. The pathological specimens of bilateral inguinal masses showed atrophic testis without spermatogenesis and with Sertoli's cell nodular hyperplasia. The diagnosis of testicular feminization was established.

Adult↗
PubMed1978

[Gonadotropin secretion in patients with testicular feminization].

FSH and LH were functionally examined in 5 women with feminizing testis and compared with the peripheral sex steroid hormones. The oestradiol levels were found decreased, while those of testosteron were elevated. FSH disclosed no significant differences while the basal levels of LH and its stimulatory response to LH-RH were increased in the patients.

Adolescent↗