J Korean Med Assoc.  2018 Oct;61(10):591-598. 10.5124/jkma.2018.61.10.591.

Etiology and treatment of central precocious puberty

Affiliations
  • 1Division of Endocrinology and Metabolism, Department of Pediatrics, Bundang Jesaeng General Hospital, Daejin Medical Center, Seongnam, Korea. odajulia@dmc.or.kr

Abstract

The timing of pubertal onset is occurring at younger ages. This phenomenon is associated with many environmental factors such as sufficient nutrition, stress, many kinds of endocrine-disrupting chemicals, and genetic background. The loss of transcriptional repression induces kisspeptin release, resulting in pulsatile gonadotropin-releasing hormone secretion, which trigger pubertal onset. According to many reports, gonadotropin-releasing hormone agonists therapy for patients with rapidly progressive central precocious puberty is effective for improving final adult height. However, those results were obtained from the treatment of relatively young patients at earlier stages of puberty. A large cohort study investigating the environmental causes of precocious puberty as well as genetic factors is needed.

Keyword

Precocity; Puberty; Endocrine disruptors; Gonadotropin releasing hormone agonists; Final height

MeSH Terms

Adolescent
Adult
Cohort Studies
Endocrine Disruptors
Genetic Background
Gonadotropin-Releasing Hormone
Humans
Puberty
Puberty, Precocious*
Repression, Psychology
Endocrine Disruptors
Gonadotropin-Releasing Hormone

Figure

  • Figure 1 Classification of puberty-related disorders and normal puberty according to onset-timing.

  • Figure 2 Average (mean or median) ages at onset of breast development (B2) or menarche in different well-off populations around the world (Reproduced from Parent AS, et al. Endocr Rev 2003;24:668–693, according to the Creative Common license) [2].

  • Figure 3 Integration of timing of puberty within a spectrum of processes that are influenced by both genetic and environmental factors (Reproduced from Parent AS, et al. Endocr Rev 2003;24:668–693, according to the Creative Common license) [2].

  • Figure 4 Overview of the hypothalamic-pituitary-gonadal axis. Kisspeptin released by neurons in the anteroventral periventricular nucleus (AVPN) and arcuate nucleus (ARC) stimulates Gonadotropin releasing hormone (GnRH) release, which induces the release of lutenizing hormone (LH) and follicular stimulating hormone (FSH). The gonads respond to gonadotropins by secreting sex steroids, and sex steroids differentially regulate the expression of Kiss1 mRNA in different nuclei within the forebrain by inhibiting Kiss1 expression in the ARC and inducing its expression in the AVPN. Mutations in several genes involved in each site have been shown to cause isolated GnRH deficiency in humans (Reproduced from Choi JH, et al. Curr Opin Endocrinol Diabetes Obes 2013;20:62–68, according to the Creative Common license) [11].


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