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      Crescimento em meninos e meninas com puberdade precoce Translated title: Growth in boys and girls with precocious puberty

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          Abstract

          O desenvolvimento puberal acompanha-se de aceleração da velocidade de crescimento, secundária à elevação dos esteróides sexuais, do hormônio de crescimento e do IGF-1. O número de centímetros ganhos nesse período representa 16% da estatura adulta. A puberdade precoce (PP) pode levar à fusão prematura da cartilagem de crescimento, reduzindo a duração do crescimento e a estatura final. Assim, o principal objetivo do tratamento frenador da PP é evitar o comprometimento estatural. É importante ressaltar que a PP não evolui uniformemente, podendo ter curso lento (slow evolutive form) e não requerer tratamento. Os autores abordam aspectos do crescimento puberal normal, da puberdade precoce e suas variantes, destacando os efeitos do tratamento com GnRHa (análogos de GnRH) na estatura adulta. Situações especiais, como as puberdades avançada e acelerada, são também discutidas.

          Translated abstract

          Pubertal development is associated with increased growth velocity secondary to the interaction of three hormones: sex steroids, growth hormone and IGF-1. The pubertal spurt represents 16% of adult height. Precocious puberty (PP) may induce early fusion of growth plates, reducing growth duration and, consequently, adult height. Thus, the main objective of the treatment with GnRH analogues is to avoid the height commitment. It is important to emphasize that PP does not evolve uniformly, sometimes having a slow course (slow evolutive form), which does not require treatment. The authors discuss aspects of normal pubertal growth, precocious puberty and its variants, and the effects of treatment on final height. Special situations as early and fast puberty are also mentioned.

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          Earlier onset of puberty in girls: relation to increased body mass index and race.

          A recent study conducted by the Pediatric Research in Office Settings network provided evidence that girls in the United States, especially black girls, are starting puberty at a younger age than earlier studies had found, but the reasons for this are not known. Because nutritional status is known to affect timing of puberty and there is a clear trend for increasing obesity in US children during the past 25 years, it was hypothesized that the earlier onset of puberty could be attributable to the increasing prevalence of obesity in young girls. Therefore, the objective of this study was to reexamine the Pediatric Research in Office Settings puberty data by comparing the age-normalized body mass index (BMI-ZS; a crude estimate of fatness) of girls who had breast or pubic hair development versus those who were still prepubertal, looking at the effects of age and race. For white girls, the BMI-ZS were markedly higher in pubertal versus prepubertal 6- to 9-year-olds; for black girls, a smaller difference was seen, which was significant only for 9-year-olds. Higher BMI-ZS also were found in girls who had pubic hair but no breast development versus girls who had neither pubic hair nor breast development. A multivariate analysis confirms that obesity (as measured by BMI) is significantly associated with early puberty in white girls and is associated with early puberty in black girls as well, but to a lesser extent. The results are consistent with obesity's being an important contributing factor to the earlier onset of puberty in girls. Factors other than obesity, however, perhaps genetic and/or environmental ones, are needed to explain the higher prevalence of early puberty in black versus white girls.
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            The Neuroendocrinology of Human Puberty Revisited

            The fundamental aspects of the hypothalamic luteinizing hormone-releasing hormone (LHRH) 1 [ 1 ]pulse generator-pituitary gonadotrophin-gonadal apparatus in mammals have striking commonalities. There are, however, critical, substantive differences in the neuroendocrinology of puberty among species. The onset of puberty in the human is marked by an increase in the amplitude of LH pulses, an indirect indicator of the increase in amplitude of LHRH pulses. The hypothalamic LHRH-pituitary gonadotrophin complex is functional by at least 0.3 gestation in the human foetus; the sex difference in the fetal and neonatal pattern of LH and FSH secretion is an apparent consequence of imprinting of the fetal hypothalamus-pituitary-gonadotropin apparatus by fetal testosterone. Until about 6 months of age in boys and 12–24 months in girls, the testes and ovaries respond to the increased LH in boys and follicle-stimulating hormone (FSH) in girls by secreting testosterone and oestradiol, respectively, reaching levels that are not again achieved before the onset of puberty. Striking features of the ontogeny of the human hypothalamic pulse generator are: (1) its development and function in the foetus; (2) the continued function of the hypothalamic LHRH pulse generator-pituitary gonadotrophin-gonadal axis in infancy; (3) the gradual damping of hypothalamic LHRH oscillator activity during late infancy; (4) its quiescence during childhood – the so-called juvenile pause; (5) during late childhood the gradual disinhibition and reactivation of the LHRH pulse generator, mainly at night; (6) the increasing amplitude of the LHRH pulses, which are reflected in the progressively increased and changing pattern of circulating LH pulses, with the approach of and during puberty. The intrinsic central nervous system (CNS) mechanisms responsible for the inhibition of the LHRH pulse generator during childhood (the juvenile phase) involve the major role of an inhibitory neuronal system – the CNS inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and GABAergic neurons, as revealed by studies in the rhesus monkey by Terasawa and her associates. With the onset of puberty, the disinhibition and reactivation of the LHRH pulse generator is associated with a fall in GABAergic neurotransmission and a concomitant increase in the input of excitatory amino acid neurotransmitters (including glutamate) and possibly astroglial-derived growth factors. Despite remarkable progress over the past three decades, large gaps remain in our understanding of the neurobiological, genetic and environmental mechanisms involved in the control of the onset of puberty. The role of leptin in the control of the onset of puberty is reviewed. Severe leptin deficiency is associated with hypogonadotrophic hypogonadism; it appears that a critical level of leptin and a leptin signal is required to achieve puberty. The weight of evidence supports the hypothesis that leptin acts as one of several permissive factors and not a trigger in the onset of human puberty. The application of these advances provides a framework for the described classification of sexual precocity and delayed puberty. 1 GnRH is synonymous with LHRH.
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              Increased final height in precocious puberty after long-term treatment with LHRH agonists: the National Institutes of Health experience.

              We report 98 children who have reached final adult height in a long-term trial of LHRH agonist treatment. These children were 5.3 +/- 2.1 yr old at the start of treatment and were treated with either deslorelin (4 microg/kg.d sc) or histrelin (4-10 microg/kg.d) for an average of 6.1 +/- 2.5 yr. Final height averaged 159.8 +/- 7.6 cm in the 80 girls, which was significantly greater than pretreatment predicted height (149.3 +/- 9.6 cm) but still significantly less than midparental height (MPH) (163.7 +/- 5.6). Final height averaged 171.1 +/- 8.7 cm in the 18 boys, which was significantly greater than pretreatment predicted height (156.1 +/- 14.2 cm) but still significantly less than MPH (178.3 +/- 5.2 cm). However, the average adult height of the 54 children who had less than a 2-yr delay in the onset of treatment was not significantly different from their MPH, and 21 children exceeded MPH. Final height SD score correlated positively with duration of treatment (P < 0.01), midparental height (P < 0.001), predicted height at the start of treatment (P < 0.001), and growth velocity during the last year of treatment (P < 0.001) and correlated inversely with delay in the onset of treatment (P < 0.001), age at the start of treatment (P < 0.001), bone age at the start of treatment (P < 0.001), bone age at the end of treatment (P < 0.001), breast stage at the start of treatment (P = 0.02), and bone age minus chronological age at the start of treatment (P = 0.001). We conclude that LHRH agonist treatment improves the final height for children with rapidly progressing precocious puberty treated before the age of 8 yr for girls or 9 yr for boys. Less delay in the onset of treatment, longer duration of treatment, and lower chronological and bone age at the onset of treatment all lead to greater final height. All children with onset of pubertal symptoms before age 8 in girls and age 9 in boys should be evaluated for possible treatment. Treatment is appropriate in children with rapidly progressing puberty, accelerated bone maturation, and compromise of adult height prediction, regardless of bone age or chronological age at time of evaluation. However, once treatment is considered appropriate, it should be initiated quickly, because longer delays lead to shorter final height. In addition, the longer the treatment is continued, the greater is the final height outcome.
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                Author and article information

                Journal
                abem
                Arquivos Brasileiros de Endocrinologia & Metabologia
                Arq Bras Endocrinol Metab
                Sociedade Brasileira de Endocrinologia e Metabologia (São Paulo, SP, Brazil )
                1677-9487
                August 2003
                : 47
                : 4
                : 422-431
                Affiliations
                [02] Salvador BA orgnameUniversidade Federal da Bahia orgdiv1Departamento de Pediatria
                [01] orgnameCentro de Diabetes e Endocrinologia do Estado da Bahia orgdiv1Serviço de Endocrinologia Pediátrica
                Article
                S0004-27302003000400014 S0004-2730(03)04700414
                87424706-29b4-42ac-9c9e-3bc4699c39c5

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 18 June 2003
                : 23 April 2003
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 73, Pages: 10
                Product

                SciELO Brazil

                Self URI: Texto completo somente em PDF (PT)
                Categories
                Artigos Originais, Revisões e Atualizações

                Análogos de GnRH,Precocious puberty,Early puberty,Fast puberty,Growth,GnRH analogues,Puberdade precoce,Puberdade avançada,Puberdade acelerada,Crescimento

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