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Disorders of childhood growth and development: precocious puberty.

Alia Chauhan, Maureen Grissom

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Abstract

Precocious puberty is defined as pubertal development that begins at an earlier age than expected; most US pediatric endocrinology subspecialists use cutoff ages of 8 years for girls and 9 years for boys. Early activation and maturation of the hypothalamic-pituitary-gonadal axis leads to hormonal changes, physical signs of puberty, and acceleration of linear growth. Factors affecting puberty include race/ethnicity, obesity, and endocrine disruptors. The 2 forms of precocious puberty are central (gonadotropin-dependent precocious puberty) and peripheral (gonadotropin-independent precocious puberty). Most cases of the former have no identifiable etiology, whereas the latter is caused by increased secretion of sex hormones by the gonads or adrenal glands. It is important to differentiate progressive from nonprogressive precocious puberty to avoid unnecessary treatment for the latter; if diagnosis is uncertain, the child should be reassessed within several months. Evaluation begins with a detailed history and physical examination followed by an x-ray for bone age; in precocious puberty, bone age is greater than chronologic age. If indicated, additional serum testing (basal luteinizing hormone) and imaging studies should be obtained. Patients should be referred to a pediatric endocrinology subspecialist for treatment. It is essential to manage underlying etiologies. Gonadotropin-releasing hormone agonists should be considered only for children with progressive central precocious puberty to prevent short stature. For children with apparent nonprogressive precocious puberty, follow-up every 3 to 6 months between ages 6 and 7 years is recommended to assess for progression.

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What this paper is about

Precocious puberty is defined as pubertal development that begins at an earlier age than expected; most US pediatric endocrinology subspecialists use cutoff ages of 8 years for girls and 9 years for boys. Early activation and maturation of the hypothalamic-pituitary-gonadal axis leads to hormonal changes, physical signs of puberty, and acceleration of linear growth. Factors affecting puberty include race/ethnicity, obesity, and endocrine disruptors. The 2 forms of precocious puberty are central (gonadotropin-dependent precocious puberty) and peripheral (gonadotropin-independent precocious puberty). Most cases of the former have no identifiable etiology, whereas the latter is caused by increased secretion of sex hormones by the gonads or adrenal glands. It is important to differentiate progressive from nonprogressive precocious puberty to avoid unnecessary treatment for the latter; if diagnosis is uncertain, the child should be reassessed within several months. Evaluation begins with a detailed history and physical examination followed by an x-ray for bone age; in precocious puberty, bone age is greater than chronologic age. If indicated, additional serum testing (basal luteinizing hormone) and imaging studies should be obtained. Patients should be referred to a pediatric endocrinology subspecialist for treatment. It is essential to manage underlying etiologies. Gonadotropin-releasing hormone agonists should be considered only for children with progressive central precocious puberty to prevent short stature. For children with apparent nonprogressive precocious puberty, follow-up every 3 to 6 months between ages 6 and 7 years is recommended to assess for progression.

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Available abstract

Precocious puberty is defined as pubertal development that begins at an earlier age than expected; most US pediatric endocrinology subspecialists use cutoff ages of 8 years for girls and 9 years for boys. Early activation and maturation of the hypothalamic-pituitary-gonadal axis leads to hormonal changes, physical signs of puberty, and acceleration of linear growth. Factors affecting puberty include race/ethnicity, obesity, and endocrine disruptors. The 2 forms of precocious puberty are central (gonadotropin-dependent precocious puberty) and peripheral (gonadotropin-independent precocious puberty). Most cases of the former have no identifiable etiology, whereas the latter is caused by increased secretion of sex hormones by the gonads or adrenal glands. It is important to differentiate progressive from nonprogressive precocious puberty to avoid unnecessary treatment for the latter; if diagnosis is uncertain, the child should be reassessed within several months. Evaluation begins with a detailed history and physical examination followed by an x-ray for bone age; in precocious puberty, bone age is greater than chronologic age. If indicated, additional serum testing (basal luteinizing hormone) and imaging studies should be obtained. Patients should be referred to a pediatric endocrinology subspecialist for treatment. It is essential to manage underlying etiologies. Gonadotropin-releasing hormone agonists should be considered only for children with progressive central precocious puberty to prevent short stature. For children with apparent nonprogressive precocious puberty, follow-up every 3 to 6 months between ages 6 and 7 years is recommended to assess for progression.

Key concepts: Precocious puberty, Bone age, Medicine, Internal medicine, Bone maturation, Endocrinology, Luteinizing hormone, Etiology

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