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Bone Status Evaluation with Calcaneal Ultrasound
in Children with Chronic Rheumatic Diseases.
A One Year Followup Study
FERNANDA FALCINI, GIUSEPPE BINDI, GABRIELE SIMONINI, STEFANO STAGI, FIORELLA GALLUZZI, LAURA MASI, and ROLANDO CIMAZ
ABSTRACT.
Methods. We evaluated bone status in 67 children, 52 female, 15 male, age range 2.80 to 18.10 years; 46 juvenile idiopathic arthritis, 11 juvenile dermatomyositis, and 10 systemic lupus erythematosus. Twenty-seven of 67 patients were taking only nonsteroidal antiinflammatory drugs (NSAID), 11 were given NSAID and methotrexate (MTX), 15 were also receiving steroids (prednisone), and 14 patients were given steroids and alendronate. Broadband ultrasound attenuation (BUA) by bone was determined at the left calcaneus using two 12.5 mm diameter, 1 MHz transducers mounted in hand-held calipers linked to a pediatric contact ultrasound bone analyzer. Results. At baseline in the whole patient group mean BUA values and Z scores were significantly lower than in controls: 41.84 ± 21.64 vs 61.69 ± 17.42 dB/MHz (p < 0.001); Z score -0.91 ± 1.07 vs 0.09 ± 0.62 in controls (p < 0.001). At one year followup in the patient group BUA values were significantly increased compared to baseline (BUA 46.43 ± 21.51 dB/MHz; p = 0.002); no significant difference was found in Z score. The 15 children receiving steroids in addition to NSAID and MTX showed a decrease in BUA value at one year (NS), while Z scores were significantly reduced compared to baseline (-1.45 ± 1.40 vs -1.08 ± 1.11; p < 0.05). The 14 patients in the group receiving NSAID and MTX who also received alendronate showed significant increases in BUA (56.93 ± 19.32 vs 44.21 ± 15.67; p < 0.001) and Z score (-0.87 ± 1.19 vs -1.56 ± 0.82; p < 0.002). Conclusion. Contact ultrasound bone analysis at the calcaneus is a useful tool in the assessment and monitoring of bone status in children with CRD. (J Rheumatol 2003;30:179-84) Key Indexing Terms:
CHRONIC RHEUMATIC DISEASES
From the Department of Pediatrics, Rheumatology Unit; the Department of Clinical Physiology, Endocrine Unit, University of Florence, Florence; and the Department of Pediatrics, Istituti Clinici di Perfezionamento, Milan, Italy. F. Falcini, MD, Associate Professor of Pediatrics; G. Bindi, MD, Assistant Professor; G. Simonini, MD, Fellow in Pediatric Rheumatology, Department of Pediatrics, Rheumatology Unit; S. Stagi, MD, Fellow in Pediatrics; F. Galluzzi, MD, Associate Professor of Pediatrics, Department of Pediatrics, Endocrine Unit; L. Masi, MD, Assistant Professor, Department of Clinical Physiopathology, Endocrine Unit, University of Florence; R. Cimaz, MD, Assistant Professor, Pediatrics, Istituti Clinici di Perfezionamento, Milan. Address reprint requests to Dr. F. Falcini, Dipartimento di Pediatria, Via Luca Giordano 13, 50132 Firenze, Italy. E-mail: falcini@unifi.it Submitted July 10, 2001; revision accepted July 25, 2002. |