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Journal of Clinical Endocrinology & Metabolism, Vol 79, 1082-1085, Copyright © 1994 by Endocrine Society
ARTICLES |
MA Magiakou, G Mastorakos and GP Chrousos
Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892.
Growth retardation to complete growth arrest is the hallmark of Cushing's syndrome in children and growing adolescents; however, the effect of endogenous hypercortisolism on the final adult stature of these patients is not known. We examined this in 10 children and adolescents with endogenous Cushing's syndrome who were evaluated and successfully treated at the NIH Clinical Center before having completed their growth. The bone age was consistent with the chronological age or accelerated in four of six (67%) and delayed in two of six patients (33%). The pretreatment height of patients with Cushing's syndrome in SD units was -1.7 +/- 1.3 (mean +/- SD), the final adult height -1.3 +/- 0.9, and the midparental height was 0 +/- 0.8. All patients had a compromised final adult stature compared to their midparental height (162.8 +/- 9.0 vs. 171.7 +/- 6.3 cm; P < 0.05). The mean (midparental height - final adult height) +/- SD was 8.9 +/- 7.3 cm. The final adult height in both centimeters and SD units was significantly lower than the midparental height (P < 0.05), whereas it did not differ significantly from the predicted heights by the Bayley-Pinneau and Roche-Wainer-Thissen methods. We conclude that the growth retardation caused during the hypercortisolemic state of Cushing's syndrome is associated with a compromised final adult height, possibly as a result of inadequate postcure catch-up growth.
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