Transient Partial hGH Deficiency in Prepubertal Children with Delay of Growth

Gourmelen, M; Pham-Huu-Trung, M T; Girard, François

doi:10.1203/00006450-197904000-00002

Cited by 123 publications

(45 citation statements)

References 2 publications

(2 reference statements)

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“…The parents of children with CDG frequently reported a later growth spurt or a late age at menarche in concordance with the literature [8,9,26]. In CDG, a transient reduction in the secretion of GH [27,28] and GH-releasing hormone [29] has been reported. However, in our study, IGF-1 levels were in the lower normal range at the time of presentation at our clinic.…”

Section: Discussionsupporting

confidence: 71%

Progressive Decline in Height Standard Deviation Scores in the First 5 Years of Life Distinguished Idiopathic Growth Hormone Deficiency from Familial Short Stature and Constitutional Delay of Growth

Rothermel

Lass²,

Toschke³

et al. 2016

Horm Res Paediatr

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Background: Familial short stature (FSS) and constitutional delay of growth (CDG) are the most frequent norm variants in children presenting with short stature. Knowing the growth patterns of these entities in the first years of life might be helpful to distinguish them from growth hormone deficiency (GHD) or other chronic diseases. Methods: We studied the height in the first 5 years of life in 26 children with FSS, in 38 children with CDG and in 14 children with idiopathic GHD. Results: Height standard deviation scores (SDS) did not change between birth and 6 months of life, while height SDS decreased significantly afterwards in GHD, FSS, and CDG. The loss of height SDS was higher in the first 2 years of life than between 2 and 5 years of life in children with CDG (-0.92 vs. -0.11; p = 0.003) or FSS (-0.79 vs. -0.01; p = 0.002). In idiopathic GHD, the loss of height SDS did not differ between the first 2 years of life and the next 3 years (-0.78 vs. -0.77; p = 0.821). Conclusion: Children with FSS and CDG showed a decline in height SDS mainly in the first 2 years of life, whereas the height SDS of children with idiopathic GHD decreased almost continuously over the first 5 years of life.

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Section: Discussionsupporting

confidence: 71%

Progressive Decline in Height Standard Deviation Scores in the First 5 Years of Life Distinguished Idiopathic Growth Hormone Deficiency from Familial Short Stature and Constitutional Delay of Growth

Rothermel

Lass²,

Toschke³

et al. 2016

Horm Res Paediatr

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“…The negative correlation of basal fasting G H with age may be related to the previously reported prepubertal decrease in G H secretion in short children (21,22,45,46); although the peak G H responses did not show this correlation. The negative correlation of second-test peak G H levels with the degree of bone age delay may also be related to this factor.…”

Section: Discussionmentioning

confidence: 58%

Efficacy of Insulin-Like Growth Factor I Levels in Predicting the Response to Provocative Growth Hormone Testing

et al. 1990

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ABSTRACT. Clinical testing of growth hormone (GH) sufficiency is a controversial area in endocrinology. Due to the episodic nature of endogenous GH secretion, diagnosis of GH deficiency has been defined as a failure to achieve normal GH levels in response to at least two stimuli. This testing is associated with significant patient morbidity and cost. We analyzed our experience over a 4-y period to determine whether clinical or biochemical variables could be used to predict the results of a specific GH testing procedure. Of 180 cases analyzed (67% male, mean age 8.89 f 4.39 y, range neonate-16 y), eight cases had incomplete GH testing results. Of the remaining 172, 19 were GH deficient (GH level <7 ng/mL). Younger age, higher body mass index and a greater degree of bone age delay were characteristic of the GH-deficient population; however, none of these variables alone was of diagnostic utility. Serum IGF-I level was below the normal range for 81% of the GH deficient and 47% of the GH-sufficient children; and was the only single variable that provided a reasonable between-group distinction. Discriminant analysis resulted in development of a new variable, based on IGF-I z scores, chronologic age, degree of bone age delay, and body mass index, which would have allowed exclusion of GH deficiency without provocative testing for 58% of the GH sufficient population, whereas permitting the diagnosis of GH deficiency for all GH-deficient subjects. Our data are dependent on the IGF-I assay method and the clinical definition for GH deficiency; therefore, the calculated predictive values are not applicable to all clinical populations. However, our data provide a new perspective on the integration of IGF-I levels and clinical information in predicting GH sufficiency. (Pediatu Res 27: [45][46][47][48][49][50][51]1990)

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“…Although GH testing performed in peripubertal children with growth retardation may give subnormal results, a number of studies conducted in previous decades showed that approximately half of the children who exhibited low GH secretion and were eventually treated by GH had a normal GH response to stimulation tests at reassessment following cessation of treatment. Moreover, untreated children showed an acceleration of growth, with an increase in both spontaneous and stimulated GH secretion as they progressed through puberty [4,5,6,7]. These findings indicated that subnormal GH secretion in the peripubertal period most likely stemmed from a lack of sex hormones rather than GH deficiency.…”

Section: Introductionmentioning

confidence: 81%

Is Sex Hormone Priming in Peripubertal Children prior to Growth Hormone Stimulation Tests Still Appropriate?

Lazar

Phillip

2010

Horm Res Paediatr

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Low growth hormone (GH) secretion during puberty may stem from either a permanent GH axis abnormality or from transient GH deficiency secondary to lack of sex hormones. Although well known to enhance stimulated GH secretion in pre- or early puberty, sex hormone priming for the evaluation of the function of the GH-IGF-I axis remains controversial. Many pediatric endocrinologists consider that omission of such priming during the preadolescent period decreases the specificity of GH stimulation tests and increases the percentage of false-positive diagnosis results. Others believe that it leads only to a temporary augmentation of GH secretion followed by a decrease in spontaneous secretion to levels which may be insufficient for normal pubertal growth; thus priming with sex hormones may lead to underdiagnosis of peripubertal children that could have benefited from GH treatment. The increased availability of biosynthetic GH has enabled expanding the indications for GH therapy and judging and renewing the criteria for the diagnosis of GH deficiency, including the practice of sex hormone priming which was and still is executed in clinical use in many centers in the world. We would like to recommend that priming should not be routinely performed in every peripubertal child undergoing GH evaluation but may be considered in adolescents with pubertal delay – girls aged >11.5–12 years and boys aged >13–13.5 years exhibiting no evidence of puberty or only initial signs.

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Transient Partial hGH Deficiency in Prepubertal Children with Delay of Growth

Cited by 123 publications

References 2 publications

Progressive Decline in Height Standard Deviation Scores in the First 5 Years of Life Distinguished Idiopathic Growth Hormone Deficiency from Familial Short Stature and Constitutional Delay of Growth

Progressive Decline in Height Standard Deviation Scores in the First 5 Years of Life Distinguished Idiopathic Growth Hormone Deficiency from Familial Short Stature and Constitutional Delay of Growth

Efficacy of Insulin-Like Growth Factor I Levels in Predicting the Response to Provocative Growth Hormone Testing

Is Sex Hormone Priming in Peripubertal Children prior to Growth Hormone Stimulation Tests Still Appropriate?

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