Background Although corticosteroid resistant (CR) bronchial asthma is associated with impaired in vitro and in vivo glucocorticoid (GC) responsiveness in mononuclear cell function, it is not known whether this is a cell specific phenomenon or whether these patients are yt similar risk of glucocorticoid side-effects as corticosteroid-sensitive (CS) subjects. In order to address this question we have examined the effects of GCs on biochemical indices of bone turnover in vivo.
Methods Six CS and six CR subjects received prednisolone 40 mg orally at 09.00 daily for 5 days. At 08.30 on day 1 and day 6 a fasting blood was taken for estimation of serum osteocalcin, tartrate resistant acid phosphatase (TRAP) and alkaline phosphatase (ALP: total and bone isoenzyme), and a urine sample taken for estimation of free deoxy-pyridinoline crosslinks. TRAP and ALP were measured by a colorimetric method and osteocalcin and deoxy-pyridinoline crosslinks by ELISA.
Results Serum osteocalcin (nmol/L) decreased from 1.39 ± 0.O9 (mean ± SEM) to 1.14 ± 0.07 (P= 0.023) and from 1.19 ± 0.05 to 0.96 ± 0.1 (P= 0.037) in the CS and CR groups, respectively. There was no difference between baseline and post-treatment levels in either group. Serum total ALP (units/L) decreased from 178 ± 7 to 168 ± 4 (P= 0.02) and from 195 ± 22 to 175 ± 16 (p=0.04) in ihe CS and CR groups, respectively. There was no difference between baseline and post-treatment levels in either group. There was no significant elevation of deoxy-pyridinoline crosslinks or TRAP and no suppression of bone ALP in either group.
Conclusion We suggest that CR asthmatics may be equally at risk from the metabolic side-effects of glucoeortieoids.
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