BACKGROUND AND OBJECTIVE: Prolonged corticosteroid (CS) use induces osteoporosis; the pathogenesis of this condition is multifactorial and includes CS-induced hypercalciuria. We investigated the course of hypercalciuria and related markers of bone metabolism parameters during and after the CS treatment. MATERIALS AND METHODS: We recruited 42 patients who were taking at least 10 mg/day of methylprednisolone or an equivalent dose of CSs for at least 30 days. The 24-h urinary calcium and sodium, a spot urinary calcium/creatinine ratio, and urinary deoxypyridinoline were measured prior to the treatment, at day 7, at days 30-60, and after the cessation of the treatment. Additionally, the serum levels of phosphorus, calcium, alkaline phosphatase (ALP), albumin, creatinine, osteocalcin, and parathyroid hormone (PTH) were analyzed. RESULTS: The 24-h urinary calcium excretion was significantly increased at day 7 (182.2 ± 158.6 mg/day; p < 0.001) and at days 30-60 (196.9 ± 167.8 mg/day; p < 0.001) compared with baseline (98.7 ± 88.1 mg/day) and returned to basal level after the cessation of the CSs (118.9 ± 90.2 mg/day; p = 0.725). The urinary deoxypyridinoline level was significantly higher at days 30-60 compared with basal level. The serum osteocalcin level was decreased at days 30-60 when compared with day 7. No significant changes were detected in the PTH, phosphorus, creatinine, and ALP levels. CONCLUSIONS: CS treatment induces hypercalciuria just after starting the treatment until the end of it. CS-induced hypercalciuria promptly improved after cessation of the treatment. By days 30-60, the excretion of urinary deoxypyridinoline was accompanied by hypercalciuria. The serum osteocalcin level was decreased at days 30-60 when compared with day 7.
BACKGROUND AND OBJECTIVE: Prolonged corticosteroid (CS) use induces osteoporosis; the pathogenesis of this condition is multifactorial and includes CS-induced hypercalciuria. We investigated the course of hypercalciuria and related markers of bone metabolism parameters during and after the CS treatment. MATERIALS AND METHODS: We recruited 42 patients who were taking at least 10 mg/day of methylprednisolone or an equivalent dose of CSs for at least 30 days. The 24-h urinary calcium and sodium, a spot urinary calcium/creatinine ratio, and urinary deoxypyridinoline were measured prior to the treatment, at day 7, at days 30-60, and after the cessation of the treatment. Additionally, the serum levels of phosphorus, calcium, alkaline phosphatase (ALP), albumin, creatinine, osteocalcin, and parathyroid hormone (PTH) were analyzed. RESULTS: The 24-h urinary calcium excretion was significantly increased at day 7 (182.2 ± 158.6 mg/day; p < 0.001) and at days 30-60 (196.9 ± 167.8 mg/day; p < 0.001) compared with baseline (98.7 ± 88.1 mg/day) and returned to basal level after the cessation of the CSs (118.9 ± 90.2 mg/day; p = 0.725). The urinary deoxypyridinoline level was significantly higher at days 30-60 compared with basal level. The serum osteocalcin level was decreased at days 30-60 when compared with day 7. No significant changes were detected in the PTH, phosphorus, creatinine, and ALP levels. CONCLUSIONS: CS treatment induces hypercalciuria just after starting the treatment until the end of it. CS-induced hypercalciuria promptly improved after cessation of the treatment. By days 30-60, the excretion of urinary deoxypyridinoline was accompanied by hypercalciuria. The serum osteocalcin level was decreased at days 30-60 when compared with day 7.