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José F. Cara, MD; Robert L. Rosenfield, MD; Richard W. Furlanetto, MD, PhD

Am J Dis Child. 1987;141(5):562-564.

Abstract
• Cross-sectional studies from our institutions (Wyler Children's Hospital, Chicago, and Children's Hospital of Philadelphia) and others have shown that plasma somatomedin-C (Sm-C) concentrations rise during puberty. To determine the relationship between rising plasma Sm-C levels and the growth spurt at puberty, we undertook a longitudinal study of 11- to 18-year-old children. Twelve male and eight female subjects were followed up on a yearly basis for two to seven years (mean, 4.4 years). Height velocity, plasma Sm-C concentrations, and stage of sexual development were determined during each visit. All patients progressed normally in puberty during the study. The plasma Sm-C level rose during early puberty in each child and reached a maximal level of at least 2 U/mL in midpuberty, approximately one year after the attainment of peak height velocity. Maximal plasma concentrations of Sm-C were similar in male (3.5±0.71, mean±SEM) and female (3.5±1.46) subjects. Plasma Sm-C levels subsequently decreased slowly but remained above normal adult values for as long as four years after peak height velocity was reached. Plasma Sm-C concentrations increased steadily with increasing height velocity until peak height velocity was attained with a mean rise of approximately 0.5 U for each centimeter per year increase in height velocity. Since Sm-C levels remained elevated while height velocity decreased, there was no significant correlation between Sm-C levels and height velocity throughout puberty. These results suggest that caution is required in interpreting Sm-C concentrations during puberty; while normal pubertal levels may be in the acromegalic range for adults, a plasma Sm-C level of less than 1 U/mL in early puberty or less than 1.5 U/mL during middle to late puberty must be considered subnormal.

(AJDC 1987;141:562-564)

Author Affiliations
From the Section of Pediatric Endocrinology, Wyler Children's Hospital, University of Chicago Pritzker School of Medicine (Drs Cara and Rosenfield); and the Department of Endocrinology and Metabolism, Children's Hospital of Philadelphia, University of Pennsylvania (Dr Furlanetto).

Footnotes
Accepted for publication Jan 27, 1987.

Presented in part at the Annual Meeting of the Society for Pediatric Research and the American Pediatric Society, Washington, DC, May 6, 1986.

Reprint requests to Wyler Children's Hospital, Box 118, University of Chicago Medical Center, 5841 S Maryland Ave, Chicago, IL 60637 (Dr Cara).

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