Isosexual pseudoprecocity in a 6-year-old boy with a testicular interstitial cell adenoma

Root, Allen W.; Steinberger, Emil; Smith, Keith D.; Steinberger, Anna; Russ, David W.; Somers, Laurence A.; Rosenfield, Robert L.

doi:10.1016/s0022-3476(72)80588-2

Cited by 32 publications

(8 citation statements)

References 17 publications

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“…However, testicular size was more closely related to sleep LH than to FSH. These findings suggest that after a critical level of FSH is achieved in the late prepubertal years, LH stimulation of testicular androgen production may be important in stimulating pubertal seminiferous tubule development, analogous to the well-established role of intratesticular androgenization in initiating spermatogenesis (33,34). The concept of a role for LH in testicular tubule development is supported by the rise in inhibin B that begins before the onset of clinical puberty and that is consistent with early intratesticular androgenization of Sertoli cells (32).…”

Section: Discussionsupporting

confidence: 52%

Comparison of Detection of Normal Puberty in Boys by a Hormonal Sleep Test and a Gonadotropin-Releasing Hormone Agonist Test

Rosenfield

Bordini

2012

The Journal of Clinical Endocrinology &Amp; Metabolism

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Section: Discussionsupporting

confidence: 52%

Comparison of Detection of Normal Puberty in Boys by a Hormonal Sleep Test and a Gonadotropin-Releasing Hormone Agonist Test

Rosenfield

Bordini

2012

The Journal of Clinical Endocrinology &Amp; Metabolism

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“…The raised urinary 17-oxosteroids, pregnanetriol, plasma androstenedione and testosterone reported in this case have been found in patients with interstitial cell tumours (14,15). Exploration in this case, however, revealed bilateral Leydig cell hyperplasia.…”

Section: Age (Years)mentioning

confidence: 42%

Pseudo‐precocious Puberty Caused by Bilateral Idiopathic Testicular Hyperplasia

et al. 1985

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A boy aged two years presenting with advanced development of the genitalia, but with prepubertal testes, and accelerated growth is described. Investigation indicated pseudo-precocious puberty, due to idiopathic interstitial cell hyperplasia. Difficulties in interpretation of the hormonal studies were encountered due to an aberrant left testicular vein. This rare condition which has been called Testotoxicosis is probably due to an inborn error of metabolism not yet identified.

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“…One-year’s treatment of a patient with partial GnD, altering the interval of GnRHag administration and varying the dosage by ten-fold, did not lead to sufficiently sustained repetitive LH and FSH responses to normalize testosterone levels or to correct azospermia. Since high intratesticular testosterone levels are important for the initiation of spermatogenesis (20, 21), we attempted supplementing intermittent GnRHag therapy with replacement testosterone; however, this treatment did not improve azoospermia, as has been reported for the combination of FSH and testosterone treatment of GnD men (22). Notably, exogenous testosterone did not alter the LH or FSH response to GnRHag, which is consistent with similar studies with natural GnRH (23–25).…”

Section: Discussionmentioning

confidence: 99%

Potential diagnostic utility of intermittent administration of short-acting gonadotropin-releasing hormone agonist in gonadotropin deficiency

Zimmer

Ehrmann

Rosenfield

2010

Fertility and Sterility

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Objective-The objective was to determine if intermittent, low-dose, short-acting GnRH agonist (GnRHag) administration up-regulates pituitary-gonadal function in gonadotropin deficiency (GnD) sufficiently to be of diagnostic or therapeutic value.Design/Intervention-Low-dose leuprolide acetate was administered SC at 4-5 d intervals up to one year.Patients-Adult volunteers and GnD patients were studied.Setting-The studies were performed in a General Clinical Research Center. Main Outcome Measures-LH, FSH, and sex steroid responses were determined.Results-In normal men and women, low-dose GnRHag repetitively transiently stimulated gonadotropins in a gender-dimorphic manner. In congenitally GnD deficient men (n=6) and women (n=1), none of whom had a normal LH response to an initial GnRHag test dose, this regimen consistently stimulated LH to the normal baseline range within two weeks. Long-term GnRHag administration to a partially GnD man did not alleviate hypogonadism, however. Women with hypothalamic amenorrhea (n=2) responded normally to a single GnRHag injection; however, repeated dosing did not seem to induce the normal priming effect.Conclusions-The subnormal LH response to GnRHag of congenital GnD normalized in response to repetitive intermittent GnRHag, but not sufficiently to improve hypogonadism. Hypothalamic amenorrhea patients lacked the priming response to repeated GnRHag, but otherwise had normal hormonal responses to GnRHag. We conclude that intermittent administration of a short-acting GnRHag is of potential diagnostic value in distinguishing hypothalamic from pituitary causes of GnD.

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Isosexual pseudoprecocity in a 6-year-old boy with a testicular interstitial cell adenoma

Cited by 32 publications

References 17 publications

Comparison of Detection of Normal Puberty in Boys by a Hormonal Sleep Test and a Gonadotropin-Releasing Hormone Agonist Test

Comparison of Detection of Normal Puberty in Boys by a Hormonal Sleep Test and a Gonadotropin-Releasing Hormone Agonist Test

Pseudo‐precocious Puberty Caused by Bilateral Idiopathic Testicular Hyperplasia

Potential diagnostic utility of intermittent administration of short-acting gonadotropin-releasing hormone agonist in gonadotropin deficiency

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