Growth Hormone in the Treatment of Short Stature in Young Children with Intrauterine Growth Retardation

Abstract

Growth acceleration and bone maturation were studied in children with severe short stature and a history of intrauterine growth retardation (IUGR) to determine the effect of growth hormone (GH)-treatment. Patients were enrolled in an open randomized, multicenter trial and allocated to either the treated group (group 1, n = 38) or the control group (group 2, n = 31). Both groups were treated daily with 0.2 IU/kg/body weight during 3 years. The children in group 2 started the study with a 1-year observation period followed by a 3-year treatment period. At baseline, the mean age was 4.5 years, bone age was 3.3 years, height standard deviation score (SDS) was –3.4, height velocity (HV) SDS was –1.6. Auxologic data were measured every 3 months and bone age was assessed at the start of the study (baseline) and then every 12 months thereafter. After 1 year of treatment, linear HV in group 1 increased significantly in comparison with the pretreatment period (from 5.7 ± 2.0 to 10.1 ± 1.7 cm/year; p < 0.001). Increased HV was sustained during the 2nd and 3rd year of treatment and was significantly higher than at baseline. A similar growth pattern was seen during the 3 years of growth hormone (GH) treatment in group 2. The mean height SDS for chronological age increased by 2.0 ± 0.7 in the 2 groups after 3 years of treatment. Bone age remained retarded but increased with a mean of almost 4 years after 3 years of treatment in both groups. Even at a dose that is three times the replacement dose, treatment with recombinant human GH was well tolerated. From these results, we conclude that recombinant human GH treatment over 3 years can induce sustained catch-up growth in young children with severe short stature and a history of IUGR.

Critical Ages and Stages of Puberty in the Accumulation of Spinal and Femoral Bone Mass: The Validity of Bone Mass Measurements

“…These data support Frost’s theory that muscle strength is a major determinant of bone metabolism [44]. In contrast, radial spongiosa and cortical bone densities do not correlate with muscular strength [39]. These data indicate that the main change in bone morphology during childhood is an increase in cortical thickness, throughout appositional growth, and the changes in bone geometry.…”

“…Augat et al [43]showed that the CSMI at the human radius correlated with fracture load at the femoral neck (r = 0.85). BSI increases with age and correlates with handgrip strength (measured by hand dynamometry), bone cross-sectional area and cortical area [39]. These data support Frost’s theory that muscle strength is a major determinant of bone metabolism [44].…”

“…During childhood there is no age- or sex-dependent increase in radial spongiosa and cortical bone densities, measured at 4% and 20% of the ulnar length proximal to the growth plate, respectively [38, 39]. The values of spongiosa bone density do not differ between children and adults; by contrast, total bone density is lower in children than in adults [39].…”

“…The values of spongiosa bone density do not differ between children and adults; by contrast, total bone density is lower in children than in adults [39]. In both sexes, cortical thickness shows a progressive increase during childhood and adolescence, and in girls (but not in boys) this increase is limited after the age of 14 years [40].…”

First Two Years’ Response to Growth Hormone Treatment in Very Young Preterm Small for Gestational Age Children

“…Altogether, the data suggest that preterm infants present a growth restraint pattern characterized by an extrauterine growth retardation that attenuates the catch-up growth and is responsible for the persistent short stature of these patients. Recombinant human GH (rhGH) therapy is a well-established treatment for SGA patients who fail to achieve spontaneous catch-up [12,13,14,15,16,17,18]. In SGA patients, GH treatment is able to increase IGF-I and IGFBP-3 concentrations [19].…”