Assessment of the Bone Status of Nigerian Children and Adolescents with Sickle Cell Disease Using Calcaneal Ultrasound and Serum Markers of Bone Metabolism

• DOI: 10.1007/s00223-001-1107-x
• Publication Date: 2002-10-14T12:45:16Z
• Authors: D.J. VanderJagt; C. Bonnett; S.N. Okolo; R.H. Glew
• Keywords: Bone remodeling; Bone disease

Growth and skeletal maturation are impaired in sickle cell disease (SCD). SCD is also associated with decreased bone mineral density (BMD) as determined by dual X-ray and photon absorptiometry. Quantitative ultrasound (US), which is as good a predictor of fracture as absorptiometry, provides additional information about bone architecture and elasticity. It is not known if the quantitative US parameters, broadband ultrasound attenuation (BUA) and speed of sound (SOS), are affected in children and adolescents with SCD. We therefore compared the bones of 80 children with SCD in Nigeria to those of age- and gender-matched controls using calcaneal ultrasound and the serum bone markers N-telopeptide of type1 collagen (NTx) and bone-specific alkaline phosphatase (BSAP), which are indicators of bone resorption and formation, respectively. BUA, which is reflective of BMD, was significantly lower for both the male and female SCD subjects compared with controls (86 vs 113 dB/MHz, P < 0.001 and 87 vs 100 dB/MHz, P < 0.001, respectively). However, SOS, which is more indicative of bone elasticity, was significantly different only for the male SCD subjects. Both NTx and BSAP were significantly reduced in the serum of the male and female SCD subjects. Correlations between BUA and serum NTx were found for both female controls and SCD subjects (r = 0.58, P < 0.001 and r = 0.32, P = 0.05, respectively), but not for the male subjects or controls. Significant correlations between BUA and BSAP were observed only for the female controls. In summary, we have shown that US analysis, in combination with serum markers of bone metabolism, can be used to distinguish bone development in children with SCD from that of nonaffected controls.