Physiological Growth Hormone Secretion in Children with Short Stature and Intra-Uterine Growth Retardation

Abstract

31 prepubertal children with short stature [mean height standard deviation score (SDS) -2.84] and low birth weight (mean -2.82 SDS) were studied. Mean age was 6.0 years and mean height velocity SDS was -0.76. Patients were classified as having either the clinical characteristics of Russell-Silver syndrome (RSS) (4 F, 13 M) or not (4 F, 10 M). All children had an overnight profile of spontaneous growth hormone (GH) secretion. 4 children achieved a maximum GH concentration of less than 20 mU/1. 9 children with RSS secreted only one large GH peak during the night. Most of the non-RSS group had normal GH pulse frequency but 3 boys had a fast-frequency pattern. Abnormal GH secretion may contribute towards growth failure in children with low birth weight/RSS.

The Somatotropic Axis in Short Children Born Small for Gestational Age: Relation to Insulin Resistance

“…Despite their severe short stature, all parameters of overnight GH secretion (maximum, mean, minimum, AUCb, and pulse frequency) were higher in short SGA children compared with normal-stature prepubertal controls, and also higher compared with published normative data in prepubertal populations (17,19,39). Previous studies in short SGA children have reported reduced spontaneous GH secretion compared with controls, although most are not GH deficient (17)(18)(19).…”

Diagnosis and management of Silver–Russell syndrome: first international consensus statement

“…Classic GH deficiency is neither a common nor a relevant cause of short stature in SRS, nor is it predictive of the response to GH treatment in children born SGA 103,105,110 . Furthermore, given the risk of hypoglycaemia associated with fasting required for GH testing, testing children with SRS might carry added risks.…”

Effects of Intrauterine and Early Postnatal Growth Restriction on Hypothalamic Somatostatin Gene Expression in the Rat

“…The secretion of GH by the pituitary is controlled by the reciprocal and coordinated discharge of SS and GHRH from hypothalamic neurons located in the PeN and arcuate nucleus, respectively (8). The extent to which the central mechanisms governing the activity of the GH axis are involved in mediating postnatal growth failure as a conse-quence of either prenatal or early postnatal malnutrition is unknown; however, approximately half the children who are born small for gestational age and continue to undergo growth retardation appear to have abnormal GH secretory patterns (9). We postulated that nutrient restriction during the perinatal period causes permanent alterations in the function of hypothalamic SS neurons, contributing to abnormal growth and development later in life.…”