Evaluation of Bone Mineral Density in a Cohort of Children with Growth Hormone Deficiency

Background: Growth Hormone (GH) plays an important role in linear growth and in bone turnover during childhood. GH deficiency (GHD) may cause secondary osteoporosis associated to low bone mineral density (BMD), impairment of bone turnover and increased fracture rate. The effects of treatment with recombinant human Growth Hormone (rhGH) on bone metabolism are controversial. We aimed to assess BMD using dual energy x-ray absorptiometry (DEXA) among a cohort of children with GHD before rhGH therapy. Furthermore, we aimed to evaluate the association between BMD and auxological, biochemical and therapeutic data at baseline and during rhGH therapy. Methods: We enrolled 193 patients (9.68 ± 3.27 years, 58% males, 75% in a pre-pubertal age) with diagnosed GHD. DEXA was performed before treatment. Anamnestic, anthropometric, biochemical and radiological data were evaluated at baseline and during rhGH treatment (6, 12 and 24 months). Results: The median value of BMD Z-score before rhGH therapy was -1.15 ± 0.97. Analyzing BMD values at baseline, we found differences between pubertal and pre-pubertal patients (BMD SDS -1.54± 0.95 vs. -0.97±0.93; p < 0.001) and between patients with a normal brain magnetic resonance imaging (MRI) and subjects with a pathologic MRI (BMD SDS -1.09±0.99 vs.-1.48±0.82 p 0.03, respectively). The absolute value of BMD (g/cm²) was positively correlated with height SDS (r 0.20, p <0.05), BMI SDS (r 0.24, p <0.05) and IGF-1 values (r 0.33, p <0.05); BMD SDS value was positively correlated with target height SDS (r 0.28, p <0.05) and BMI SDS (r 0.36, p <0.05) whereas there was a negative correlation between BMD SDS and the age at GHD diagnosis (r² 0.40, p <0.05). There was no association between BMD values and biochemical and therapeutic data. Conclusions: Our study shows that pubertal patients have a lower BMD than pre-pubertal ones as a consequence of the mild bone demineralization (BMD Z-score -1.15±0.97) secondary to GHD. Therefore, our data suggest starting rhGH therapy early as to promote an optimal growth. DEXA might represent a valid mean to complete the diagnosis in GHD patients and to optimally orient the therapeutic decisions; it should be repeated at the end of treatment in order to evaluate its effect on bone metabolism.