Glucocorticoid excess during adolescence leads to a major persistent deficit in bone mass and an increase in central body fat

Endogenous Cushing's syndrome (CS) in children causes growth retardation, d ecreased bone mass, and increased total body fat. No prospective controlled studies have been performed in children to determine the long-term sequela e of CS on peak bone mass and body composition. A 15-year-old girl with Cus hing disease (CD), and her healthy identical co-twin, were followed for 6 y ears after the CD was cured. At the 6-year follow-up both twins had areal b one mineral density (BMD) and body composition determined by dual-energy X- ray absorptiometry (DXA) and three-dimensional quantitative computed tomogr aphy (3DQCT). Z scores for height, weight, and body mass index (BMI) were - 2.3, -0.8 and 0.2, and 1.2, 0.2, and -0.6, in the twin with CD and her co-t win, respectively. In the twin with CD, areal BMD and bone mineral apparent density (BMAD) at different sites varied from 0.7 to 3 SD below her co-twi n. Volumetric lumbar spine bone density Z score was -0.75 and 1.0, and tota l body, abdominal visceral, and subcutaneous fat (%) was 42, 10, and 41 ver sus 26, 4, and 17 in the twin with CD and her co-twin, respectively. The re lationship between total body fat and L2-L4 BMAD was inverse in the twin wi th CD (p < 0.05), which by contrast in her co-twin was opposite and direct (p < 0.001). In the twin with CD, despite cure, there was a persistent defi cit in bone mass and increase in total and visceral body fat. These observa tions suggest that hypercortisolism (exogenous or endogenous) during adoles cence may have persistent adverse effects on bone and fat mass.