Use of a Potent, Long Acting Agonist of Gonadotropin-Releasing Hormone in the Treatment of Precocious Puberty*

Pa, Boepple; Mansfield, M. Joan; Me, Wierman; Cr, Rudlin; Hh, Bode; Jf, Crigler; Crawford, J. Douglas; Wf, Crowley

doi:10.1210/edrv-7-1-24

Cited by 160 publications

(56 citation statements)

References 83 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In CAH, transition from precocious pseudo-puberty to secondary central precocious puberty has been observed and is thought to be due to the induction of the GNRH pulse generator by persistently increased sex steroids (66). Pubertal progression in central precocious puberty is efficiently halted by GNRH analogues blocking GNRH action (67,68).…”

Section: Pa: Definitions and Differential Diagnosismentioning

confidence: 99%

Premature adrenarche: novel lessons from early onset androgen excess

Idkowiak

Lavery

Dhir

et al. 2011

European Journal of Endocrinology

110

View full text Add to dashboard Cite

Adrenarche reflects the maturation of the adrenal zona reticularis resulting in increased secretion of the adrenal androgen precursor DHEA and its sulphate ester DHEAS. Premature adrenarche (PA) is defined by increased levels of DHEA and DHEAS before the age of 8 years in girls and 9 years in boys and the concurrent presence of signs of androgen action including adult-type body odour, oily skin and hair and pubic hair growth. PA is distinct from precocious puberty, which manifests with the development of secondary sexual characteristics including testicular growth and breast development. Idiopathic PA (IPA) has long been considered an extreme of normal variation, but emerging evidence links IPA to an increased risk of developing the metabolic syndrome (MS) and thus ultimately cardiovascular morbidity. Areas of controversy include the question whether IPA in girls is associated with a higher rate of progression to the polycystic ovary syndrome (PCOS) and whether low birth weight increases the risk of developing IPA. The recent discoveries of two novel monogenic causes of early onset androgen excess, apparent cortisone reductase deficiency and apparent DHEA sulphotransferase deficiency, support the notion that PA may represent a forerunner condition for PCOS. Future research including carefully designed longitudinal studies is required to address the apparent link between early onset androgen excess and the development of insulin resistance and the MS.

show abstract

Section: Pa: Definitions and Differential Diagnosismentioning

confidence: 99%

Premature adrenarche: novel lessons from early onset androgen excess

Idkowiak

Lavery

Dhir

et al. 2011

European Journal of Endocrinology

110

View full text Add to dashboard Cite

show abstract

“…Therapy using a GnRH agonist is the accepted form of treatment for idiopathic central precocious puberty and has been shown to be effective both in the short term [3] and in the long term. [15] Treatment with the newer sustained-release preparations, Lupron-Depot [6,16] and decapeptyl, [18,20] has resulted in normalization of GV, regression of secondary sexual characteristics, a slowed rate of skeletal maturation, and the attainment of adult height appropriate to genetic potential.…”

Section: Medical Therapymentioning

confidence: 99%

Role of surgical resection in the treatment of hypothalamic hamartomas causing precocious puberty

Stewart¹,

Steinbok²,

Daaboul³

1997

FOC

View full text Add to dashboard Cite

Hypothalamic hamartomas (HHs) are benign tumors that are often associated with central precocious puberty. Resection of HHs has been recommended as a treatment option for selected cases of pedunculated lesions, especially in young children. The role of surgery has to be evaluated in the light of the availability of effective medical treatment with gonadotropin-releasing hormone analogs (GnRHas). The authors report the long-term results of total resection of HHs in two children with central precocious puberty and compare it with medical management in four children. The two surgically treated patients underwent total resection of pedunculated HHs at 1.75 (Case 1) and 3.25 years (Case 2) and have received follow-up care for 9 and 8 years, respectively. There were no postoperative complications and computerized tomography scanning confirmed complete tumor removal in both patients. Both patients subsequently experienced some regression of secondary sexual characteristics. The response of luteinizing hormone to GnRH became prepubertal in one patient and was diminished in the other. However, the growth velocity remained elevated (gt 7 cm/year), bone age remained advanced (gt +2 standard deviations) 5 years after surgery, decreasing adult height prediction. In one child, GnRHa therapy was initiated 7 years postsurgery. Four children were treated solely with GnRH agonists and have received follow-up care for 2.3, 6, 9, and 9 years, respectively. These patients have had a complete regression of endocrinological abnormalities, including a normalization of growth velocity and reduction in the rate of skeletal maturation. No side effects were noted with decapeptyl treatment, and one child developed sterile abscesses while receiving Lupron-Depot. The proven efficacy of GnRHa in suppressing puberty and reducing bone age advancement leads the authors to advise against surgery as the initial management of central precocious puberty caused by HHs.

show abstract

“…O uso do LHRHa retarda a maturação esquelética mais do que diminui a velocidade de crescimento, sugerindo que uma estatura final maior poderia ser alcançada. 8,9,10 A puberdade precoce central pode ser eficazmente suprimida pela administração de um análogo de LHRH (LHRHa). Apesar de o tratamento com LHRHa ser frequentemente acompanhado de uma concomitante desaceleração da velocidade do crescimento, é improvável que tenha um impacto significante na altura final por si só.…”

Section: Resultsunclassified

Novas perspectivas no tratamento da hiperplasia adrenal congênita

Faria¹,

Sampaio²,

Oliveira³

et al. 2010

cmbio

View full text Add to dashboard Cite

A HAC é um distúrbio congênito, caracterizado pela deficiência na biossíntese do cortisol, associado ou não à deficiência de aldosterona e, consequentemente, à superprodução de andrógeno. Essa condição afeta igualmente homens e mulheres. No sexo feminino, acarreta virilização da genitália externa em graus variados. No sexo masculino, nenhuma anormalidade se apresenta fenotipicamente ao nascimento. Tradicionalmente, o tratamento dessa síndrome consiste na reposição diária de glicocorticoides e mineralocorticoides. Novas terapias têm sido propostas com intuito de se obterem resultados mais satisfatórios; dentre elas, existem: análogos do LHRH, GH, inibidores da aromatase, antiandrógenos e a adrenalectomia. Resultados preliminares apontam para uma melhora da altura final e do manejo clínico dos pacientes submetidos aos novos tratamentos. O objetivo deste estudo foi revisar a literatura acerca dessas novas modalidades terapêuticas, com o intuito de explorar o que há de mais novo na abordagem dessa síndrome.

show abstract

Use of a Potent, Long Acting Agonist of Gonadotropin-Releasing Hormone in the Treatment of Precocious Puberty*

Cited by 160 publications

References 83 publications

Premature adrenarche: novel lessons from early onset androgen excess

Premature adrenarche: novel lessons from early onset androgen excess

Role of surgical resection in the treatment of hypothalamic hamartomas causing precocious puberty

Novas perspectivas no tratamento da hiperplasia adrenal congênita

Contact Info

Product

Resources

About