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At least 73 records · Page 4Linked to original sources
PubMed1987

Detection of late-onset adrenal hyperplasia in girls with peripubertal virilization.

We investigated the value of serum levels of adrenal steroids (dehydroepiandrosterone sulphate, testosterone, 17-hydroxyprogesterone, cortisol) in the identification in peripubertal females with late-onset congenital adrenal hyperplasia owing to 21-hydroxylase deficiency. Among 68 females (age 3-18 years) with virilization in childhood, peripubertally or postpubertally, we selected 21 girls for an ACTH test by measurement of basal blood-spot or serum 17-hydroxyprogesterone (17-OHP) levels. Eight of 21 patients had supranormal post-ACTH serum 17-OHP concentration (57-153 nmol/l) with low normal cortisol concentration. All of them had supranormal basal and post-ACTH 17-OHP to cortisol ratios. These data show a relatively high incidence (about 12%) of mild 21-hydroxylase deficiency among prepubertal and adolescent girls with virilization. It is concluded that the first step in the investigation of peripubertally virilized girls should be the determination of serum 17-OHP and cortisol. Patients with basal morning 17-OHP concentration and 17-OHP to cortisol ratio above reference range should be given an ACTH test.

17-alpha-Hydroxyprogesterone↗
PubMed1967

Hirsutism and virilization.

In normal females, androstenedione from both the adrenal cortex and ovary, as a result of peripheral conversion, is the source of the majority of biologically active testosterone in the circulation. The control of the secretion of precursor steroid and androgenic hormone (testosterone) in females is not clear at this time. There are a number of possibilities to explain various types of hirsutism and virilization. The presence of true virilization indicates a significant disorder and requires complete investigation. The presence of increased amounts of 17-ketosteroids in the urine implicates the adrenal cortex as a source of the pathologic manifestations. The suppressibility of elevated 17-ketosteroids with cortisol analogues aids in distinguishing between adrenal hyperplasia and autonomous neoplasm of the adrenal cortex. By far the most common entity in this area is simple hirsutism without virilization. Although our knowledge of this disorder is quite incomplete, conservative management is indicated. Further progress in this field is rapidly occurring. An informed clinician can do an adequate job of diagnosis and treatment with the clinical and laboratory tools generally available.

Androgens↗
PubMed1984

Hirsutism and virilism in women.

Hirsutism in women may be defined as excessive thick (terminal) hair growth in facial and body regions. It is one of the early manifestations of virilization that correlate closely with elevated testosterone production. Testosterone production rates in normal women average 0.2 mg/day, with 25% secreted by the ovaries, 25% by the adrenals, and 50% arising from the peripheral metabolism of prehormones, notably androstenedione. Increased testosterone from adrenal and/or ovarian sources induces 5 alpha-reductase activity within the susceptible hair follicle. This results in the local production of dihydrotestosterone, the potent androgen that is likely responsible for the growth and stimulation of the hair follicle that leads to hirsutism. Activation of the hair follicle by androgens provides a secondary pathway for testosterone metabolism, unfortunately at the expense of undesirable hair growth. Although virilization in women may be caused by exogenous androgens, it occurs primarily from diseases of the adrenals or ovaries. Androgen-producing tumors of the adrenals cause virilization in association with excessive production of a wide variety of C19 androgens. In contrast, ovarian tumors tend to secrete a narrower range of androgens and their presence may be more occult. The most common causes of hirsutism in women arise from nontumorous states, chiefly ovarian in origin. The androgenized ovary syndrome represents a spectrum of abnormalities ranging from idiopathic hirsutism to the polycystic ovary syndrome to ovarian hyperthecosis. These states are associated with mild to severe abnormalities of androgen production and concomitant mild to severe abnormalities of ovarian histology. The pathogenesis of these abnormalities is still speculative, but appears to be related to increased pulsatile and tonic secretion of LH with ovarian hyperstimulation. Of the various laboratory tests to evaluate hirsutism, simple measurements of plasma testosterone, free testosterone, and most recently androstanediol glucuronide seem to provide the best chemical evidence of androgen abnormalities. Treatment of hirsutism/virilism in women is difficult and frequently unsatisfactory. At present, treatment schemes include local methods, suppression of androgens via glucocorticoids or oral contraceptives, and antiandrogens.

Adrenal Cortex Neoplasms↗
PubMed1978

[Biological parameters of virilism in women].

Comparative results of the suppression-stimulation test by dexamethasone and chorionic gonadotropin, chromatographic separation of 17-ketosteroids, and plasma testosterone levels in the ovarian and adrenal veins, in cases of virilism in women. Thirteen patients with hirsutism and virilization were investigated as follows: 1. measurement of plasma testosterone (T) levels by radioimmunoassay (RIA) during suppression-stimulation tests by the administration of Dexamethasone (DXM) and chorionic Gonadotropin (HCG). 2. chromatographic determination of urinary 17-ketosteroids, pregnanediol (P2), and pregnanetriol (P3). An attempt was made to classify virilism as "ovarian" or "adrenal" based on the results of 1. and 2. 3. bilateral ovarian and adrenal venous catheterization through the femoral vein to measure T (RIA) levels. 4. laparotomy with bilateral wedge resections of the ovaries for therapeutic and biopsy purposes. Surgical catheterization of the ovarian veins was carried out during the operation. The results of these tests show that: a) the dynamic DXM-HCG test can be used to separate those cases in which the ovary is not involved in T formation from those in which, apparently, it is involved. b) chromatographic determination of urinary steroids has no aetiological value, as the variations in the different fractions are not significant. c) in all patients, the principal source of T is the adrenals and not the ovaries, even when there is an increase in T in the ovarian efferent blood vessels.

Adrenal Glands↗
PubMed1998

Postmenopausal virilization in a woman with gonadotropin dependent ovarian hyperthecosis.

We report a case of a 66-yr-old woman with progressive hair balding, hirsutism and virilization. Gonadotropins and estradiol levels were in the postmenopausal range; total testosterone (TT), free testosterone (FT) and 17-hydroxyprogesterone (17-OHP) were elevated with dehydroepiandrosterone sulphate, androstendione and cortisol serum levels in the normal range, as 24-hr free urinary cortisol. TT, FT and 17-OHP were normalized, and FSH and LH fell to premenopausal levels on 18th day after a single i.m. injection of the GnRH analogue (GnRHa), triptorelin. Then, a diagnosis of hyperandrogenism of ovarian origin was made and bilateral ovariectomy was performed. Histological study of gonadal tissue revealed diffuse stromal hyperplasia of both ovaries with occasional nests of luteinized cells. With immunoperoxidase techniques these cells stained positively for testosterone and progesterone. One month after surgery, androgen levels were normalized together with regression of most of the clinical signs of virilization. In conclusion, our patient showed a severe virilization developed after menopause; hormonal investigations suggested a gonadotropin dependent ovarian hyperandrogenism, confirmed by histological examination; the presence of luteinized cells in the ovarian stroma was responsible for hyperandrogenism, as confirmed by the immunoperoxidase technique.

17-alpha-Hydroxyprogesterone↗
PubMed1984

17,20-desmolase deficiency in a female newborn, paradoxically virilized in utero.

The patient was born with ambiguous genitalia (stade III of Prader). The karyotype revealed a normal female genotype. A defect in 21-hydroxylase, at first suspected, was denied by the hormonal studies. Indeed, extremely high levels of pregnenolone, pregnenolone sulfate, progesterone were found in association with low plasma levels of delta 4-androstenedione, testosterone, dehydroepiandrosterone and its sulfate, while cortisol 17OH-progesterone and ACTH levels and plasma renin activity were normal. The hormonal pattern was thus consistent with 17,20-desmolase deficiency. The dynamic studies further supported this contention: all the progestagens rose further after ACTH stimulation and were suppressed by dexamethasone. Meanwhile, all androgens failed to rise after ACTH: the responses of cortisol were normal. The in utero virilization of the female fetus was not understood until an history of virilization was allegedly found in the mother (luteoma of pregnancy). This is the first case of 17-20 desmolase defect recognized in a female newborn. This child, born with ambiguous genitalia had presented the concurrence of two very rare conditions. The in utero virilization of maternal origin enabled us to make the diagnosis of the 17-20 desmolase defect, which otherwise would have been ignored in a XX subject in the neonatal period because it would obviously be unsymptomatic at this age.

Adrenocorticotropic Hormone↗
PubMed2001

Virilization of the urogenital sinus of the tammar wallaby is not unique to 5alpha-androstane-3alpha,17beta-diol.

The androgen 5alpha-androstane-3alpha,17beta-diol (5alpha-adiol) is synthesized in testes and secreted into plasma of male tammar wallaby pouch young and appears to virilize the urogenital sinus. To provide insight into its mechanism of action, a dose response study showed that administration of 1 microg 5alpha-adiol monoenanthate per g body wt. per week for 3 weeks to 24-day-old female pouch young induced prostate bud formation equivalent to that of males of the same age. Administration of this same dose of the enanthates of testosterone, dihydrotestosterone, and 5alpha-adiol to female pouch young caused equivalent virilization of the urogenital sinus. The fact that 5alpha-adiol does not exert a unique effect, together with our earlier findings in this species that 5alpha-adiol and testosterone are converted to dihydrotestosterone in the urogenital sinus and that virilization of the urogenital sinus is prevented by the androgen receptor antagonist flutamide, suggest that 5alpha-adiol is a circulating precursor for dihydrotestosterone formation in this tissue.

Androgens↗
PubMed1999

Virilization of the male pouch young of the tammar wallaby does not appear to be mediated by plasma testosterone or dihydrotestosterone.

Virilization of the male urogenital tract of all mammals, including marsupials, is mediated by androgenic hormones secreted by the testes. We have previously demonstrated profound sexual dimorphism in the concentrations of gonadal androgens in pouch young of the tammar wallaby Macropus eugenii during the interval when the urogenital sinus virilizes. To provide insight into the mechanisms by which androgens are transported from the testes to the target tissues, we measured testosterone and dihydrotestosterone in plasma pools from tammar pouch young from the day of birth to Day 150. Plasma testosterone levels were measurable (0.5-2 ng/ml) at all times studied, but there were no differences between males and females. These low concentrations of plasma testosterone appear to be derived from the adrenal glands and not the testes. Plasma dihydrotestosterone levels in plasma pools from these animals were also low and not sexually dimorphic. We conclude that virilization of the male urogenital tract cannot be explained by the usual transport of testosterone or dihydrotestosterone in plasma but may be mediated by the direct delivery of androgens to the urogenital tract via the Wolffian ducts. Alternatively, circulating prohormones may be converted to androgens in target tissues.

Adrenal Glands↗
PubMed1998

[Virilizing and feminizing adrenal syndrome].

OBJECTIVE: To inquire into diagnosis, differential diagnosis and treatment of virilizing and feminizing adrenal syndrome especially differential diagnosis between benign and malignant of sex hormone producing adrenal neoplasma and treatment principles of congenital adrenal hyperplasia (CAH). METHOD: Eight cases of CAH and five cases of sex hormone producing adrenal neoplasma were presented during 1986-1996. The former included 3 rare cases of 17 alpha hydroxylase deficiency and others. The latter included 3 cases of feminizing adrenal tumors and 2 cases of virilizing adrenal tumors. RESULT: Weight and diameter of tumor, DHEA, 17-ks and sex hormone levels, appearance of CT imaging, infiltration and metastasis, were closely related to differentiation of benign and malignant tumors. CONCLUSION: Some standards are not absolute because of limited practice, follow-up is very important. Adrenal virilizing and feminizing neoplasms were surgically resected by different incision. Modified subcostal incision is recommended as a best choice for huge adrenal mass. Corticoadrenal hormone treatment of CAH should select different kind of corticoadrenal medicine for different kind of CAH. Treatment of sex hormones is not suitable for children suffered from 17 hydroxylase deficiency until prepuberty.

Adrenal Gland Neoplasms↗
PubMed2005

[Experiment on the sexual virility of immature mice immunized with LHRH fusion protein vaccine].

OBJECTIVE: To observe the sexual virility of immature immature male mice were divided into a pre-ablactation group (n 10). The first two groups were immunized with the LHRH fusion proportion of pregnant female mice, the morphological and histological examined to conform the emasculating effect of the vaccine. When ted with testosterone (1.0 ml each) , the post-ablactation ones were rameters. RESULTS: The sexual virility of the immature mice immunized in 3 -4 months. CONCLUSION: The LHRH fusion protein vaccine mice after ablactation, and the sexual virility can recover in the pre-ablactation decrease.

Animals↗
PubMed2026

Unexpected Virilization in a Patient with Turner Syndrome with Unbalanced Y/7 Translocation in the Gonadal Tissue: Gonadoblastoma Diagnosis.

Turner syndrome (TS) may involve tissue-restricted mosaicism, undetectable in standard peripheral blood karyotyping. This poses a diagnostic challenge, particularly when occult Y-chromosome material increases gonadoblastoma risk. We report an 18-year-old girl with TS (45,X), short stature on recombinant human growth hormone and severe intellectual disability, who developed virilization at age 12. Laboratory testing showed hypergonadotropic hypogonadism with elevated testosterone. Imaging failed to detect gonads. Bilateral gonadectomy revealed streak gonad tissue and testicular tissue with intratubular germ cell neoplasia and focal gonadoblastoma. High-resolution cytogenetics confirmed gonadal mosaicism with unbalanced Y/7 translocation, absent in lymphocytes. This case highlights that unexplained virilization in TS warrants immediate evaluation and that high-resolution genomic methods and timely gonadectomy are essential for cancer risk reduction.

Humans↗
PubMed1982

Fetal and maternal virilization associated with pregnancy. A case report and review of the literature.

A masculinized female infant was born to a mother who had virilizing signs dating from the fourth month of pregnancy. Serum 17 alpha-hydroxyprogesterone, dehydroepiandrosterone, and testosterone levels were all normal in the infant. Maternal testosterone level was markedly elevated one week post partum. Dexamethasone phosphate suppression was normal. Human chorionic gonadotropin stimulation five weeks post partum revealed further elevation of high baseline free and total testosterone levels. Free and total testosterone levels 30 weeks post partum were normal, and all maternal virilizing signs had regressed with the exception of her deepened voice. The child has had no progression of masculinization. The mother is believed to have had a luteoma of pregnancy.

Adult↗
PubMed2000

Isodicentric Y chromosome in an Ullrich-Turner patient without virilization.

We report on a 17-year-old young woman with Ullrich-Turner syndrome (UTS), who was found to have a karyotype 45,X/46,X,idic(Y)(q11). She had age-appropriate genitalia without virilization in spite of the presence of the Y-derived marker chromosome and SRY locus in 70% of her lymphocytes. Having reviewed the literature, we conclude that a possible explanation for the lack of virilization in these mosaic patients is most likely an uneven distribution of tissue mosaicism (gonadal mosaicism).

Adolescent↗
PubMed1990

Mammary ovarian metastases with stroma cell hyperplasia and postmenopausal virilization.

The case of a 57-year-old woman with a history of breast cancer is reported. She presented 10 years later with virilization. Stroma cell hyperplasia was present in the metastatic ovaries. The authors describe hormonal data and discuss the pathogenesis of the stromal activity. Mammary ovarian metastases associated with stroma cell hyperplasia, in the absence of pregnancy, that cause virilization are rare.

17-alpha-Hydroxyprogesterone↗
PubMed1980

Virilism as a late manifestation in the Bardet-Biedl syndrome.

The second case of virilism as a late manifestation of Bardet-Biedl syndrome (BBS) is described, with endocrine and histological evaluation. Both cases manifested ovulatory cycles and developed virilism in adulthood. Elevated plasma testosterone and 17-OH-progesterone were not suppressed by dexamethasone but were suppressed by medroxyprogesterone acetate. Peripheral and ovarian venous blood obtained at the time of surgery demonstrated a marked gradient for testosterone in both ovaries and for progesterone in the ovary bearing the corpus luteum. Histological evaluation of the ovaries demonstrated bilateral ovarian stromal hyperplasia with focal hyperthecosis. Bilateral ovariectomy resulted in complete correction of the endocrine abnormality, although the established hirsutism remains a mark of previous androgen excess.

Adult↗
PubMed1989

Occurrence of male phenotype in genotypic females with congenital virilizing adrenal hyperplasia.

We report on two genotypic females with complete masculinization of the external genitalia secondary to congenital adrenal hyperplasia resulting from 21-hydroxylase deficiency. One patient had the salt-losing variant, and the other had the simple virilizing or nonsalt-losing variant. One was evaluated neonatally during an adrenal crisis and misidentified as male; the second was unrecognized. Both were being reared as males when the true genotype was recognized during evaluation for cryptorchidism. The female internal genitalia were subsequently removed and testicular implants placed. These cases demonstrate the need to exclude congenital virilizing adrenal hyperplasia in any phenotypic male infant with bilateral cryptorchidism. When this condition is diagnosed, early and genotypically appropriate sex assignment is important if reproductive function is to be preserved and subsequent emotional and social complications avoided.

Adrenal Hyperplasia, Congenital↗
PubMed1995

Postmenopausal virilization due to ovarian hyperthecosis.

A case of a 66-year-old obese woman with type II diabetes mellitus and a 4 year history of virilism is presented. After removal of the ovaries the raised testosterone levels returned to normal and signs of virilism gradually receded. The histological finding of nodular hyperthecosis of the ovaries is discussed in relation to hyperinsulinaemia.

Aged↗
PubMed1985

A case of mucinous cystadenocarcinoma of the ovary associated with virilization: pre and post-operative steroid plasma levels.

A premenopausal woman with a mucinous carcinoma of one ovary, and a mucinous adenoma of the other, together with secondary virilization, is reported. Preoperative levels of androstenedione, testosterone and dehydroepiandrosterone sulphate were high, suggesting the presence of a virilizing tumor. Preoperative plasma estrone (E1), but not estradiol (E2), was elevated along with inversion of the E2/E1 ratio, suggesting a peripheral origin of the estrogens. FSH and LH plasma concentrations were low. After bilateral ovariectomy, levels of all steroids measured significantly decreased and gonadotropins rose to the postmenopausal range.

Adenoma↗