BIOCHEMICAL PREDICTION OF CHANGES IN SPINAL BONE MASS IN JUVENILE CHRONIC (OR RHEUMATOID) ARTHRITIS TREATED WITH GLUCOCORTICOIDS

Citation
J. Reeve et al., BIOCHEMICAL PREDICTION OF CHANGES IN SPINAL BONE MASS IN JUVENILE CHRONIC (OR RHEUMATOID) ARTHRITIS TREATED WITH GLUCOCORTICOIDS, Journal of rheumatology, 20(7), 1993, pp. 1189-1195
Citations number
24
Categorie Soggetti
Rheumatology
Journal title
ISSN journal
0315162X
Volume
20
Issue
7
Year of publication
1993
Pages
1189 - 1195
Database
ISI
SICI code
0315-162X(1993)20:7<1189:BPOCIS>2.0.ZU;2-Q
Abstract
Objective. To identify biochemical predictors of spinal bone mineral g rowth and the development of spinal osteoporosis in children with juve nile chronic arthritis (JCA) treated with glucocorticoids. Methods. Bo ne mass measurements were made at 3 monthly intervals for one year in 31 children. At each visit, blood and urine were obtained for assessme nt of laboratory indices related to the acute phase response and bone remodelling rates. Assessments were also made of joint inflammation (s imple joint count). Results. Plasma albumin and C-reactive protein (CR P) concentrations contributed independently of height velocity to the prediction of lumbar spinal bone mineral growth, but only when average d over the year of observation. The simple joint count did not usefull y predict spinal bone mineral changes in the individual patient, nor d id any measured index normally related to bone turnover (plasma osteoc alcin, 25 (OH) vitamin D, urinary hydroxyproline). Mean values of the simple joint count were predicted by mean CRP and CRP trends. Joint co unt trends were predicted by hemoglobin trends. None of these relation ships, although statistically significant, was strong enough to predic t individual outcomes precisely. Conclusions. Failure of spinal bone m ineral growth is related to failure of growth in height and weight but also to biochemical markers for the activation of the acute phase res ponse. Failure of bone growth to correlate with increased hydroxyproli nuria or plasma osteocalcin concentrations may be attributed to the co nfounding effect of glucocorticoid treatment on plasma osteocalcin lev els in children whose bone resorption is little changed from normal le vels despite their reduced growth. Biochemical measurements are weak s ubstitutes for bone densitometry in monitoring spinal growth in these children.