Vitamin D status, estradiol and bone metabolism in elderly female patients with hip fracture
Abstract
Aim: In postmenopausal women increased bone turnover is associated with hip fracture apart from bone mineral density. The aim of this study was to evaluate bone metabolism in consideration of vitamin D and hormonal status in elderly female hip fracture patients compared to controls.
Material and Methods: Circulating 25-hydroxyvitamin D3 (25(OH)D), sex hormones, BTM [osteocalcin (OC); propeptide of type-I collagen (PINP); C-terminal telopeptide of type I collagen (CTX-1); tartrate resistant acid phosphatase 5b, (TRAP5b)] and osteoclastogenic cytokines [soluble receptor activator of nuclear factor kB ligand (sRANKL); osteoprotegerin (OPG)] were measured in patients with a low-energy hip fracture and controls without an incident hip fracture (each group n= 47 females).
Results: 57.4 % of the patients, but only 10.6. % controls had a severe vitamin D deficiency. T-Score at the lumbar spine was comparable in both groups (-1.8 ± 1.5 vs. -1.6 ± 1.4, p=0.535). In hip fracture patients 25(OH)D (p<0.001), albumin (p<0.001), osteocalcin (OC) (p<0.001) and sRANKL (p<0.001) levels were lower compared to controls, whereas estradiol (p<0.001), cortisol (p<0.001), CTX-1 (p<0.001) and OPG (p<0.001) were higher. Linear regression analysis revealed an independent association between 25(OH)D and CTX-1 in female fracture patients (p=0.023). Higher estradiol levels after hip fracture correlated inversely with OC (p=0.018) and TRAP5b (p=0.004).
Multivariable regression analysis demonstrated that 25(OH)D, OC, estradiol (each p<0.001) and albumin (p=0.002) were independently associated with fracture. Higher estradiol levels correlated inversely with OC in fracture patients (p=0.018).
Conclusion: 25(OH)D was an independent risk factor of hip fracture and demonstrated an independent association with CTX-1. Unchanged or lower levels of bone formation markers were not associated with 25(OH)D and were partly related to higher of levels estradiol presumably induced by trauma.
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