Biochemical markers of bone metabolism and calciuria with inhaled budesonide therapy
- PMID: 15007718
- DOI: 10.1007/s00467-004-1418-z
Biochemical markers of bone metabolism and calciuria with inhaled budesonide therapy
Abstract
We investigated the changes in renal excretion of calcium, sodium, and potassium in asthmatic children treated with inhaled budesonide, an inhaled glucocorticoid. Twenty-two asthmatic patients (7 female, 15 male, mean age 10.1+/-4.3 years) treated with 400-600 microg/day inhaled budesonide and 23 healthy children (6 female, 17 male, mean age 10.2+/-2.8 years) were enrolled in the study. The parameters recorded were serum sodium, potassium, calcium, phosphorus, alkaline phosphatase (ALP), type I collagen carboxyterminal telopeptide (ICTP), osteocalcin, intact parathyroid hormone (PTH) levels, first spot morning urine calcium/creatinine ratio, sodium/potassium ratio, and daily renal calcium excretion rate (UCa-ER). These parameters were measured in the control group and pre- and post-budesonide treatment in asthmatic children. Serum electrolytes, ALP, PTH, ICTP, and UCa-ER were in the normal ranges and were not significantly different between controls and asthmatic children. Serum levels of ICTP increased, while levels of osteocalcin decreased after budesonide therapy in the asthmatic group ( P=0.001, P=0.005). UCa-ER was decreased after budesonide therapy in asthmatics ( P=0.000). In conclusion, moderate doses of inhaled budesonide cause hypocalciuria and decreased bone turnover. These results may be attributed to a mechanism compensating for decreased absorption of calcium in the gut due to the topical effect of swallowed budesonide rather than the systemic effects of the drug. Increased bone metabolism and decreased turnover may have an important role in this compensatory mechanism.
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