title: Short-term effects of glucocorticoid therapy on biochemical markers of bone metabolism in Japanese patients: a prospective study.
abstract: Glucocorticoid (GC) therapy induces rapid bone loss, but the early changes in calcium and bone metabolism in patients treated with GC have not been clarified. To investigate the changes in calcium and bone metabolism during the early stage of GC therapy, we analyzed various biochemical markers of bone metabolism. The serum levels of calcium (Ca), phosphorus, parathyroid hormone (PTH), osteocalcin (OC), bone alkaline phosphatase (BAP), and type I collagen cross-linked N-telopeptide (NTx), as well as the urinary levels of Ca, creatinine, and NTx, were measured on days 0, 3, 7, and 28 of GC therapy. The subjects were divided into the following four groups: 9 patients receiving pulse therapy (P), 18 patients receiving prednisolone (PSL) at doses > or =40 mg/day (H), 9 patients receiving PSL at doses > or =20 mg/day (M), and 11 patients receiving PSL at doses < or =10 mg/day (S). The serum OC level showed a marked decrease on day 3 of GC therapy (-41.2% +/- 6.6%, P < 0.01), while the BAP level decreased gradually. Both serum and urinary NTx levels significantly increased on day 7 of GC therapy (9.9% +/- 4.5%, P < 0.05, and 42.2% +/- 10.6%, P < 0.01, respectively). Urinary Ca excretion was increased on day 3 of GC therapy and continued to increase until 4 weeks, while intact PTH showed an increase on day 3 and then remained constant until 4 weeks. In groups P and H, there were significant early changes in OC, BAP, NTx, and intact PTH levels, as well as urinary Ca excretion. Even a PSL dose of <10 mg/day caused a decrease in the serum OC level. In conclusion, the biochemical markers of Ca and bone metabolism showed different kinetics depending on the dose of GC, and it is important for patients on high-dose GC therapy to receive prophylaxis for bone loss from the start of GC treatment.
authors.affiliation: Internal Medicine, Kobe Century Memorial Hospital, Hyogo-ku, Kobe, 652-0855, Japan. kuroki@kanebou-mh.or.jp
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Kuroki
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kaji
authors.forename: Seiji
authors.initials: S
authors.lastname: Kawano
authors.forename: Fumio
authors.initials: F
authors.lastname: Kanda
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Takai
authors.forename: Michiko
authors.initials: M
authors.lastname: Kajikawa
authors.forename: Toshitsugu
authors.initials: T
authors.lastname: Sugimoto
mesh_terms: D015415:Biomarkers / Q000097:blood* / Q000652:urine; D001842:Bone and Bones / Q000187:drug effects* / Q000378:metabolism*; D002118:Calcium / Q000652:urine; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D007564:Japan; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010281:Parathyroid Hormone / Q000097:blood; D011239:Prednisolone / Q000627:therapeutic use*; D011446:Prospective Studies; D013997:Time Factors
chemical_list: D015415:Biomarkers; D005938:Glucocorticoids; C470125:PTH protein, human; D010281:Parathyroid Hormone; D015675:Osteocalcin; D011239:Prednisolone; D002118:Calcium