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The child with tall stature and/or abnormally rapid growth

Erick J Richmond, MD
Alan D Rogol, MD, PhD
Section Editor
Mitchell E Geffner, MD
Deputy Editor
Alison G Hoppin, MD


Statural growth, a fundamental characteristic of childhood, is a complex process that is determined by the interaction of genetics, nutrition, and socioeconomic factors [1]. Regular assessment of growth is an essential part of pediatric practice and includes comparison of a child's growth pattern to established norms. When determining the normality of a child's growth pattern, serial measurements of height and calculation of height velocity (HV) is more useful than a single height-for-age percentile [2]. In interpreting a child's HV, allowance must be made for age, pubertal development, and other factors.

The causes, diagnosis, and treatment of children with abnormally rapid growth and tall stature will be reviewed here. The evaluation of children with short stature is discussed elsewhere. (See "Causes of short stature" and "Diagnostic approach to children and adolescents with short stature".)


Emerging evidence reveals that normal and pathologic variations in linear growth depend on the balance between proliferation and senescence of chondrocytes at the growth plate. This process is regulated by many systems, including:

Endocrine mechanisms – Growth hormone (GH), insulin-like growth factor I (IGF-I), androgens, and thyroid hormone all stimulate chondrogenesis, while glucocorticoids inhibit chondrogenesis. Estrogens promote linear growth by stimulating GH and IGF-I secretion, but also accelerate chondrocyte senescence, leading to fusion of the growth plates and cessation of linear growth [3]. As a result, estrogen deficiency or insensitivity (eg, caused by mutations in the estrogen receptor and aromatase genes), inhibits closure of the epiphyses, thus causing continued linear growth and tall stature. (See 'Sex hormone deficiency or insensitivity' below.)

Proinflammatory cytokines – Some cytokines negatively regulate growth plate function. These are elevated in chronic inflammatory diseases, in which they slow linear growth and also growth plate senescence, which permits catch-up growth after the cytokine effect resolves [4,5].

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Literature review current through: Nov 2017. | This topic last updated: Oct 24, 2016.
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