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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 8 2735-2741
Copyright © 1998 by The Endocrine Society


Original Studies

Short-Term Changes in Serum Leptin Levels Provide a Strong Metabolic Marker for the Growth Response to Growth Hormone Treatment in Children1

B. Kriström, B. Carlsson, S. Rosberg, L. M. S. Carlsson, K. Albertsson-Wikland and on behalf of the Swedish Study Group for Growth Hormone Treatment2

International Pediatric Growth Research Center, Department of Pediatrics, University of Umea (B.K.) and University of Goteborg (B.K., S.R., K.A.-W.), and Research Center for Endocrinology and Metabolism, Department of Medicine, University of Goteborg (B.C., L.M.S.C.), Goteborg, Sweden

Address all correspondence and requests for reprints to: Dr. Berit Kriström, University of Goteborg, Department of Pediatrics, International Pediatric Growth Research Center, Sahlgrenska University Hospital East, S-416 85 Gothenburg, Sweden. E-mail: berit.kristrom{at}pediatri.umu.se

The growth response to GH treatment varies between children. Besides regulating longitudinal growth, GH exerts important metabolic effects, including lipolysis. In this study we examined whether GH-induced changes in serum levels of the adipose tissue-derived hormone leptin can be used as a marker for the long term growth response to GH treatment in short prepubertal children. The study group consisted of 150 children (21 girls and 129 boys), who were 3–15 yr of age at the start of GH treatment and had a maximum GH secretory capacity ranging from very low to high. They were treated with GH (0.1 IU/kg·day) and followed for at least 1 yr.

The first year mean increase in height SD score was 0.79 (SD, 0.34), with a broad range (0.08–2.27). Serum leptin concentrations were significantly reduced after 1, 3, and 12 months of GH treatment compared with levels at the start of treatment. The growth response correlated with the serum leptin concentration at the start of treatment (r = 0.49; P < 0.0001) and with the change in serum leptin concentration after both 1 month (r = -0.41; P < 0.01) and 3 months (r = -0.60; P < 0.0001) of treatment. When multiple stepwise regression analysis was applied to the auxological and biochemical variables that correlated (P < 0.10) with the first year growth response to GH treatment, the 3-month change in serum leptin concentration was the single most important variable for explaining the variance in individual growth responses. We conclude that leptin levels at the start of GH treatment as well as short term changes in leptin levels in response to GH treatment are valuable markers of the long term growth response.




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