A comprehensive approach to the spectrum of abnormal pubertal development. (2012)
“Puberty is the biological transition from childhood to adulthood. The process involves the coordination of hormonal, physical, psychosocial, and cognitive systems to result in physiologic change. Precocious puberty is defined as pubertal development beginning earlier than expected based on normal standards. Gonadotropin dependent precocious puberty is caused by premature activation of the hypothalamus resulting in pulsatile secretion of GnRH. Gonadotropin independent precocious puberty is caused by excess sex hormones from peripheral or external sources. Treatment with GnRH agonists should be offered to prevent early fusion of the epiphyseal plates to avoid unnecessary short stature and should not be based on perceived psychosocial consequences of early puberty. Delayed puberty is the absence of or incomplete development of secondary sexual characteristics. Hypergonadotropic hypogonadism or primary hypogonadism may result from genetic mutation syndromes or can be acquired from antiovarian antibodies, exposure to radiation or chemotherapy, inflammatory insult, or surgical removal of the gonads. Hypogonadotropic hypogonadism or secondary hypogonadism is due to hypothalamic dysfunction resulting in impaired secretion of GnRH. The long-term goal for patients with inadequate estrogen stimulation is to maintain the serum concentration of sex steroids within the normal adult range to promote the development of secondary sexual characteristics, prevent premature bone loss, and ultimately to induce fertility when indicated.”
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“The decline in age at puberty in the general population has been paralleled by an increase in the number of girls referred for evaluation of precocious puberty (PP). In 1999, The Lawson Wilkins Pediatric Endocrine Society recommended a lowering of the age limit for evaluation of PP in girls. However, the limited evidence on which these recommendations were based led many experts to question these new suggestions. The emergence of new European pubertal timing data evaluated by robust clinical as well as biochemical markers has broadened our insight on how to interpret the recent pubertal changes. The recent pubertal trends have resulted in a concomitant lowering of the lower limit of normality of the pubertal onset. However, evidence suggests that age at the gonadotropin and sex steroid surges have not changed. Thus, it looks as if an increasing proportion of contemporary early pubertal girls may experience isolated gonadotropin-independent thelarche rather than central PP, which may not be discernible on pubertal examination alone. Thus, the population-based limits of normality should not be directly translated into revision of age limits for evaluation of PP due to the risk of misdiagnosing rapid progressive PP as well as intracranial and other underlying pathology.”
“This review describes several aspects of the management of precocious puberty (PP) and variants in girls and boys. PP is characterized by early pubertal changes, acceleration of growth velocity and rapid bone maturation that often result in reduced adult height. Onset of pubertal signs before the age of 8 years in girls and 9 years in boys should always be evaluated carefully. The main principles of therapy are to stop the progression of secondary sex characteristics and menses (in girls), to increase final adult height, to promote psychosocial well-being, and to treat the underlying cause if known.”
Clinical practice. Precocious puberty. (2008)
“In the case described in the vignette, advanced breast development (Tanner stage 3), pubic hair development, higher-than-expected height given parental height, and increased growth velocity at 6 years of age suggest progressive precocious puberty. Evidence of possible causes of precocious puberty should be sought by means of a thorough history taking and careful examination, but this search is often unrevealing. Further evaluation should include measurements of bone age (which would probably be advanced) and levels of estradiol and luteinizing hormone.”
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