Bone turnover markers, BMD and TBS after short-term, high-dose glucocorticoid therapy in patients with Graves’ orbitopathy: a small prospective pilot study
- 72 Downloads
Chronic GC administration has numerous side effects, but little is known about the side effects of their short-term use (< 3 months)—particularly, when high doses are involved, as in the treatment of Graves’ orbitopathy (GO). We investigated the effects of short-term, high-dose GC on bone turnover markers, bone mineral density (BMD), and trabecular bone scores (TBS).
Eleven patients (10 females and 1 male; median age 56 years) with active GO who were candidates for treatment with intravenous (iv) methylprednisone were consecutively enrolled. All patients were pretreated with a loading dose of 300,000 units of cholecalciferol, then given a median cumulative dose of 4.5 g (range 1.5–5.25 g) iv methylprednisone. Biochemical parameters of bone metabolism (25OHD3, PTH, P1NP, CTX and bALP) were measured at the baseline, and then 1 week and 1, 3, 6 and 12 months. BMD and TBS were obtained by X-ray absorptiometry (DXA) at the baseline and at 6 and 12 months. On DXA image, morphometric vertebral fracture assessment (VFA) was done.
There were no significant changes in PTH, bALP or P1NP. A significant drop in CTX was seen at 1 month (down Δ49.31% from the baseline, p = 0.02), with a return to the baseline at the 3-month measurement. There was a moderate (not significant), but persistent reduction in P1NP. No changes in BMD or TBS came to light. No vertebral fractures were documented.
Short-term, high-dose GC treatment caused a rapid, transient suppression of bone resorption, with no effects on BMD or bone micro-architecture (TBS).
KeywordsGlucocorticoid Bone turnover markers Bone mineral density
Compliance with ethical standards
Conflict of interest
All the authors declare that they have no conflict of interest.
This study was conducted in accordance with the ethical standards of the institutional research committee and with the 1964 Helsinki Declaration and its later amendments.
Written informed consent was obtained from all patients included in this study.
- 14.Bandirali M, Poloni A, Sconfienza LM et al (2015) Short-term precision assessment of trabecular bone score and bone mineral density using dual-energy X-ray absorptiometry with different scan modes: an in vivo study. Eur Radiol 25:2194–2198. https://doi.org/10.1007/s00330-015-3606-6 CrossRefGoogle Scholar
- 16.Harris EK, Yasaka T (1983) On the calculation of a “reference change” for comparing two consecutive measurements. Clin Chem 29:25–30Google Scholar
- 19.Vasikaran S, Cooper C, Eastell R et al (2011) International osteoporosis foundation and international federation of clinical chemistry and laboratory medicine position on bone marker standards in osteoporosis. Clin Chem Lab Med 49:1271–1274. https://doi.org/10.1515/CCLM.2011.602 CrossRefGoogle Scholar
- 24.Paglia F, Dionisi S, De Geronimo S et al (2001) Biomarkers of bone turnover after a short period of steroid therapy in elderly men. Clin Chem 47:1314–1316Google Scholar
- 25.Dovio A, Perazzolo L, Osella G et al (2004) Immediate fall of bone formation and transient increase of bone resorption in the course of high-dose, short-term glucocorticoid therapy in young patients with multiple sclerosis. J Clin Endocrinol Metab 89:4923–4928. https://doi.org/10.1210/jc.2004-0164 CrossRefGoogle Scholar
- 26.Weiss MJ, Ray K, Henthorn PS et al (1988) Structure of the human liver/bone/kidney alkaline phosphatase gene. J Biol Chem 263:12002–12010Google Scholar