|Goans, Ronald - NICHD, NIH|
|Weiss, George - DCRT, NIH|
|Abrams, Steven - BAYLOR COLL OF MEDICINE|
|Perez, Maria - BAYLOR COLL OF MEDICINE|
|Yergey, Alfred - NICHD, NIH|
Submitted to: Calcified Tissues International
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 1, 1994
Publication Date: N/A
Interpretive Summary: We have created a new mathematical model to describe the activity of calcium flow in people who chronically use steroids. We used calcium isotopes to do this in 14 people with an illness called juvenile dermatomyositis, about half of whom took a steroid medication to relieve their symptoms, and the other half of whom did not. Our model predicts a reduction in bone buildup for steroid-treated patients that reflects the results we have seen in the clinic. It also predicts that calcium flow into reversible bone is the main flow and that is not changed between the two patient groups. However, calcium flow into the irreversible, stable bone component is decreased in steroid-treated patients, results which are consistent with a direct effect of the steroid drug, prednisone, on bone-forming cell function.
Technical Abstract: Osteopenia resulting from pharmacologic doses of glucocorticoids is well know. Previously, there has been no satisfactory quantitative model describing the kinetics of calcium flow in subjects on chronic steroid use. A mathematical model of calcium isotope interaction with bone is described and applied to determine an estimate of kinetic parameters characterizing these changes. Calcium tracer dilution kinetics after a bolus injection of 42Ca were measured in 14 subjects with juvenile dermatomyositis, six on prednisone regimens and eight on treatment regimens without prednisone. Irreversible tracer loss from plasma to bone is found to be significantly reduced (p=0.043) in the glucocorticoid-treated patients relative to patients on non-steroid regimens. Reversible flow to bone is noted to be similar in the two groups. These results suggest a direct effect of glucocorticoids on osteoblast function.