Parathormone, Calcitonin, and Vitamin D Metabolites During Normal Fracture Healing in Geriatric Patients

In order to study the role of calcium-regulating hormones during callus formation in elderly patients, serum levels of parathormone (PTH), calcitonin (a), 25-hydroxyvitamin D [25-OH-D], 1,25-dihydroxyvitamin D [1,25(OH)2 D], 24,25-di-hydroxyvitamin D [24,25(OH)2 D], and calcium (Ca) were determined in 41 patients with fractures of long bones, primarily hip fractures. The parameters were measured on admission and after eight weeks. There were almost no changes in hormone serum levels during bone repair, except for a decrease in serum levels of 1,25(OH),D from 25.3 ± 2.3 pg/ml on admission to 21.0 ± 2.0 pg/ml eight weeks later (p < .001). Patients with fractures compared to normal elderly humans have lower serum levels of FTH (0.99 ± 0.06 ng/ml versus 1.88 ± 0.34 ng/ml; p < .001), 25-OH-D (10.7 ± 1.0 ng/ml versus 17.1 ± 1.8 ng/ml; p < .001), and Ca (9.1 ± 0.1 mg% versus 9.7 ± 0.1 mg%; p .001) and higher serum levels of 1,25(OH)2D (25.3 ± 2.3 ng/ml versus 17.1 ± 2.3 pg/ml; p < .001). Female patients have lower serum levels of 24,25(OH),D compared to males (1.65 ± 0.15 ng/ml versus 2.06 ± 0.29 ng/ml; p < .05). A similar trend was noted in serum CT levels during callus formation (0.12 k 0.02 ng/ml versus 0.16 ± 0.02 ng/ml; p < .05). Patients with subcapital fractures of the femur have significantly lower serum levels of all vitamin D metabolites on admission, compared with patients suffering from extracapsular fractures. The former were treated by primary prosthetic replacement of the femoral head; their serum levels of 24,25(OH)2D dropped during the healing period (1.50 ± 0.22 ng/ml to 1.14 ± 0.16 ng/ml; p < .01). In a previous report, significant increases in serum levels of CIT and 24.25(OH)2D were observed during fracture healing in young adults. These changes were not found in elderly patients with fractures in the present study. It seems that, in geriatric patients, the hormonal system regulating calcium metabolism is deficient from the beginning and responds poorly to the challenge of a calcium-incorporating process such as callus formation.