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PubMed2001

Total urogenital sinus mobilization: a modified perineal approach for feminizing genitoplasty and urogenital sinus repair.

PURPOSE: We report a modification of the total urogenital sinus mobilization technique adapted to the repair of isolated persistent urogenital sinus and masculinized external female genitalia. MATERIALS AND METHODS: The records of 6 girls undergoing total urogenital sinus mobilization were reviewed. Diagnosis was the adrenogenital syndrome in 4 girls, and persistent urogenital sinus and true hermaphroditism in 1 girl each. Mean patient age at the time of surgery was 5.9 years (range 4.5 months to 19.5 years). The surgical technique was modified by using the perineal approach since all patients had normal anorectal anatomy. A posterior perineal skin flap was used to widen the vaginal introitus. The wall of the mobilized urogenital sinus was opened and used to create a mucous lined vestibule. In those cases of the adrenogenital syndrome reduction clitoroplasty was performed at the same time. Postoperative results were assessed subjectively by observation of the vulvar appearance and objectively by determining the location of the urethral meatus and caliber of the vagina. RESULTS: Mean followup was 3.7 months (range 1 to 9). There were no postoperative complications. Most patients were discharged home within 3 days of surgery. All patients have a satisfactory cosmetic appearance. The urethral meatus was situated in the vestibule and easily accessible. There were no changes in voiding habits postoperatively in those patients who were toilet trained before surgery. Vaginal calibration was performed in 4 patients and mean vaginal caliber was 10.5 Hegar (range 6 to 14). CONCLUSIONS: The repair of persistent urogenital sinus less than 3 cm. long can be accomplished with total urogenital sinus mobilization through the perineal approach. The technique can be combined with reduction clitoroplasty for the surgical management of girls with masculinized external genitalia.

Adolescent↗
PubMed1994

Lack of feminization of the cremaster nucleus in cryptorchid androgen insensitive rats.

Androgens may control rat testicular descent via effects on the genitofemoral nerve or cranial gonadal ligaments. Androgen-mediated release of calcitonin gene-related peptide from the genito-femoral nerve (whose motoneuron cell bodies reside in the sexually dimorphic cremaster nucleus) may stimulate cremaster sac formation and testicular descent. Alternatively, androgens may cause regression of cranial gonadal ligaments and thereby allow the testes to descend. To evaluate these theories testicular position, and the cremaster sac and nucleus were studied in Tfm (androgen insensitive) rats. Testes were abdominal, inguinal and scrotal in 20%, 67% and 13% of Tfm male rats, respectively, and cranial ligaments were present in all cases. Mean cremaster nucleus motoneuron number was lower in female rats (70 +/- 14) but not significantly different between normal male (256 +/- 44) and Tfm male (231 +/- 42) rats, and it correlated poorly with testicular position. Calcitonin gene-related peptide immunoreactivity was rarely observed in cremaster motoneurons. These data suggest that the cremaster nucleus is not androgen-dependent, calcitonin gene-related peptide release from cremaster motoneurons is not the likely mechanism of testicular descent and persistent cranial ligaments may cause cryptorchidism in the Tfm rat.

Androgen-Insensitivity Syndrome↗
PubMed1994

Molecular feminization of mouse seminal vesicle by prenatal exposure to diethylstilbestrol: altered expression of messenger RNA.

Exposure to estrogens during critical stages of development has been reported to cause irreversible changes in estrogen target tissues such as the reproductive tract. In fact, recent studies using mice describe prenatal estrogen exposure resulting in the expression of the major estrogen-inducible uterine secretory protein, lactoferrin (LF), by the seminal vesicles of the male offspring. Thus, we have studied the role of estrogens in abnormal and normal gene expression in the developing male reproductive tract using LF and seminal vesicle secretory protein IV (SVS IV), an androgen-regulated murine seminal vesicle secretory protein, as markers. Lactoferrin and SVS IV protein and mRNA expression were studied in histological samples by using the techniques of in situ hybridization (ISH) and immunohistochemistry (IHC). Seminal vesicle secretory protein IV was expressed in all (100%) epithelial cells of the control seminal vesicle, but this protein was decreased by castration. However, LF expression was undetectable by ISH or IHC in control seminal vesicle epithelium. Lactoferrin was inducible in 2% of the seminal vesicle epithelial cells from adult castrated mice treated with estradiol 17 beta (E2; 20 micrograms/kg/day for 3 days), indicating that a small percentage of the seminal vesicle cells could be induced to secrete LF after modification of the endocrine environment. Prenatal DES treatment (100 micrograms./kg. maternal body weight on days 9 through 16 of gestation) resulted in the male offspring exhibiting constitutive expression of LF in 5% of the seminal vesicle epithelial cells, while expression of the androgen-regulated protein SVS IV was slightly decreased. The maximal contrast between LF and SVS IV expression was observed in prenatally DES-treated mice that were subsequently castrated as adults and further treated with E2; LF was detected in 40% of the epithelial cells in these mice. Double immunostaining techniques revealed that epithelial cells which were making LF had ceased production of SVS IV. Since a large percentage of the epithelial cells in the intact prenatal DES exposed male was capable of expressing the normal gene product, SVS IV, it was concluded that DES treatment during prenatal development appears to imprint or induce estrogenic sensitivity in the adult seminal vesicle, causing increased production of LF. The results suggest that this altered protein response may be an example of atypical gene expression in male reproductive tract tissues following hormonal manipulation early in development.

Animals↗
PubMed1983

Feminizing genitoplasty: a synthesis.

The female child with the adrenogenital syndrome is subject to a variable degree of masculinization. Surgery should be directed to 3 goals: 1) removing the corpora and preserving the glans with its innervation to create a clitoris with normal sensation, 2) creating a normal-appearing introitus by fashioning labia minora from phallic skin and foreskin, and 3) vaginoplasty to provide an adequate opening for the vagina onto the perineum. The entire repair may be completed before the age of 6 months unless the vagina enters the urogenital sinus at a high level in which case vaginoplasty should be delayed until the child is older. The evolution of this operative approach is described and the details of the operative technique are presented.

Adrenal Hyperplasia, Congenital↗
PubMed1988

Anorexia, psychoanalysis, and feminism: fantasy and reality.

Two distinct trends inform current psychoanalytic and feminist approaches to anorexia: one focuses on its roots in the fantasy, the other in the reality of childhood and adolescent deprivation and abuse. In outlining these two approaches, this article shows how both increasingly attend to the place of the mother to the neglect of the father in the genesis of anorexia--a shift of perspective somewhat redressed by systemic family therapy.

Adult↗
PubMedDate not supplied

Gonadal feminization and halogenated environmental contaminants in common terns (Sterna hirundo): evidence that ovotestes in male embryos do not persist to the prefledgling stage.

Common terns (Sterna hirundo) and roseate terns (Sterna dougallii) breed on Bird Island, Massachusetts, USA, near a Superfund site highly contaminated with polychlorinated biphenyls (PCBs). Observations of skewed sex ratios and female-female pairings among endangered roseate terns (Nisbet and Hatch (1999) Ibis 141, 307) suggested the possibility of contaminant-related endocrine disruption in these birds and prompted investigation of common terns as a surrogate species. In 1993 and 1994, 60-90% of pipping male common tern embryos sampled exhibited ovarian cortical tissue in their testes (ovotestes) (Nisbet et al. (1996) Bull. Environ. Contam. Toxicol. 57, 895; Hart et al. (1998) Mar. Environ. Res. 46, 174). To examine the possible impact of ovotestes on the reproductive capabilities of common terns, we examined gonadal histology in common tern prefledglings (approximately 21 days old) collected from Bird Island in 1995. As a measure of embryonic contaminant exposure, contaminants were measured in a subset of eggs collected from the same nests as the prefledglings. Concentrations of total PCBs in these eggs ranged from 14.4 to 546 microg/g lipid. No evidence of ovotesticular development was observed in any of the 19 male prefledglings examined. Some gonadal irregularities were observed, including small nodules of testicular tissue within the epithelial capsule of the testes, but these were judged not likely to affect testicular function. There was no relationship between any observed irregularities and levels of contaminants present in the matched eggs. The results suggest that the ovotestes that occur in 60-90% of pipping common tern embryos from this site become fully regressed by approximately 21 days posthatch. Our data from this and previous studies are consistent with the idea that ovotestes occur naturally in some individual common terns at hatching, although the frequency of occurrence may be enhanced by exposure to chlorinated organic contaminants such as PCBs. In either case, we suggest that the presence of ovotestes in common tern embryos from PCB-contaminated sites such as Bird Island does not lead to permanent alterations in gonadal histology that would be expected to impair reproductive function.

Animals↗