The Changes of the Bone Mineral Density in the Girls with Turner Syndrome, using Recombinant Human Growth Hormone

ABSTRACT

PURPOSE: Estrogen deficiency causes sexual infantilism in Turner syndrome, which could decrease the bone mineral density(BMD) since birth. This decreased BMD might be contributed by the decreased growth hormone(GH) secretion. To improve the decreased BMD, estrogen therapy is recommended, especially after the pubertal age, but estrogen therpay during childhood can accelerate the epiphyseal fusion, resulting in shorter final height. There is a possibility that GH therapy not only ameliorates the final height, but also improve the decreased BMD, because GH is known to be involved in the normal bone metabolism. We observed whether GH therapy, given to improve the growth velocity, can change the BMD in the girls with Turner syndrome. METHODS: Thirteen prepubertal girls with Turner syndrome, who were confirmed by clinical and chromosomal examinations, were given GH(1 U/kg/week, daily, subcutaneous) for one year. During GH therapy, BMDs were mesured by DEXA(dual energy X-ray absorptiometry at trochanter and lumbar spine between the second and fourth vertebra. Growth velocity significantly increased during GH therapy and bone age were significantly advanced during this period. RESULTS: 1) The BMD of femur neck was significantly increased from 0.59+/-0.09 gm/cm2 before therapy to 0.73+/-0.07 gm/cm2 and 0.81+/-0.06 gm/cm2 at 6 and 12 months of therapy, respectively(p<0.01, Fig. 2). 2) The BMD of 2nd lumbar spine did not change during GH therapy. 3) The BMD of 3rd lumbar spine was decreased with marginal significance from 0.73+/-0.09 gm/cm2 before therapy to 0.66+/-0.09 gm/cm2, 0.65+/-0.05 gm/cm2 after 6 and 12 months of therapy, respectively(p=0.05). 4) The BMD of 4th lumbar spine was significantly decreased from 0.75+/-0.06 gm/cm2 before therapy to 0.69+/-0.10 gm/cm2, 0.64+/-0.08 gm/cm2 after 6 and 12 months of therapy, respectively(p<0.01, Fig. 2). 5) There was no significant correlation between the changes of the BMD and Bone or chronological age at initial GH therapy. Conclusion: The positive effect on BMD of GH therapy seems to be dependent on the specific area of skeletal system, where GH might exerts its effect, regardless of the existence of estrogen effect. The BMDs of another areas of skeletal system, where GH does not exert its effect, did not change with GH therapy and rather decreased by probably unknown mechanisms and GH therapy. These unknown mechanisms partially might involve the estrogen defect on BMD, This should be remained to be clarified with more patients and longer duration of study.