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The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 5 2505
Copyright © 2004 by The Endocrine Society


Letter to the Editor

Authors’ Response: Cortical Bone Density Is Normal in Prepubertal Children with Growth Hormone (GH) Deficiency, but Initially Decreases during GH Replacement due to Early Bone Remodeling

R. Schweizer, D. D. Martin, C. P. Schwarze, G. Binder, A. Georgiadou, J. Roth and M. B. Ranke

Pediatric Endocrinology Section, University Children’s Hospital, Tuebingen, D-72076 Germany

Address correspondence to: Roland Schweizer, M.D., University Children’s Hospital, Pediatric Endocrinology Section, Hoppe-Syler Strasse 1, Tuebingen, D-72076, Germany.

To the editor:

Baroncelli et al. (1) suggest in their letter that cortical area (CA) and cortical thickness (CT) should increase during GH treatment because DXA measurements have shown that there is an increase in area density. Our findings, however, provided no evidence of an increase in CA and CT in our patients; instead, there was a decrease in cortical density and no change in CA and CT. Our findings are, in fact, supported by the literature. In this context, there is only one published paper describing DXA in GHD children; in this study Boot et al. (2) found a slight decrease in total body bone mineral density and bone mineral content. Values higher than the starting level were only reached after 2 yr, and not during the first year on GH. There are various papers about GH-deficient adults that describe similar results, namely, a slight decrease in the first 6 to 12 months on GH therapy and, thereafter, an increase (3, 4).

Concerning the second point of criticism: the answer is provided in our paper and indeed by Baroncelli himself in his letter. Thus, bone metabolism parameters do not correlate with changes in bone structure because they reflect a multitude of processes, such as an increase in modeling and remodeling as well as the process of linear growth; in addition, the time range of changes in bone metabolism and bone structure is also very different.

To transform the bone structure parameters of five patients who were under 6 yr of age, we applied extrapolated values according to the published data. The ability of children to sit still for 5 min differs greatly, irrespective of age, and, in our experience, it was sometimes a challenge to do a good pQCT measurement even with pubertal, 15-yr-old patients.

Concerning the question raised about puberty, we would like to point out that, in the paper, we mentioned that all patients were in the prepubertal stage during the observation period. We also calculated the SD values of bone structure parameters by taking bone age into account but refrained from publishing these data because the results were similar for height age, which is a superior and more precise parameter.

We thank Giampiero Igli Baroncelli for raising important questions and are grateful for the opportunity to clarify them in this reply.

Received January 23, 2004.

References

  1. Baroncelli GI, Bertelloni S, Galli L, Sodini F, Saggese G 2004 Cortical bone density is normal in prepubertal children with growth hormone (GH) deficiency, but initially decreases during GH replacement due to early bone remodeling. J Clin Endocrinol Metab 89:2505 (Letter)[Free Full Text]
  2. Boot AM, Engels MA, Boerma GJ, Krenning EP, De Muinck-Kaizer S 1997 Changes in bone mineral density, body composition, and lipid metabolism during growth hormone (GH) treatment in children with GH deficiency. J Clin Endocrinol Metab 82:2423–2428[Abstract/Free Full Text]
  3. Kann P, Piepkorn B, Schehler B, Andreas J, Lotz J, Prellwitz W, Beyer J 1998 Effect of long-term treatment with GH on bone metabolism, bone mineral density and bone elasticity in GH-deficient adults. Clin Endocrinol (Oxf) 48:561–568[CrossRef][Medline]
  4. Amato G, Carella C, Fazio S, La Montagna G, Citadini A, Sabatini D, Marciano-Mone C, Saccá L, Bellastella A 1993 Body composition, bone metabolism, and heart structure and function in growth hormone (GH)-deficient adults before and after GH replacement therapy at low doses. J Clin Endocrinol Metab 77:1671–1676[Abstract]




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