Calciotropic hormones in elderly people with and without hip fracture

The effects of age on calciotropic hormones are not completely understood. The presence of secondary hyperparathyroidism has previously been demonstrated, particularly in patients with hip fracture. The role of a disturbance of vitamin D metabolism, especially a defect in lα-hydroxylation, is debated. The aim of this study was to compare serum parathyroid hormone (PTH), osteocalcin and vitamin D metabolites (25(OH)D and 1,25(OH)2D) in osteoporotic elderly patients with hip fracture (HF) and in elderly controls. We studied 57 HF patients aged 83.9±5.9 years (mean±SD) and 68 controls aged 82.5±5 years recruited during two periods: 1 January and 30 April 1988 and 1989. Patients with chronic renal failure (serum creatinine above 150, µmol/l), cancer, or other metabolic bone disease were excluded. Thirty healthy young adults were studied in 1989 only for measurement of 1,25(OH)2D. (1,25(OH)2D was measured by different laboratories in 1988 and 1989 for technical reasons.) We also measured serum PTH, osteocalcin, total calcium and ionized calcium. 1,25(OH)2D levels were not statistically different between HF patients and controls for the two years, nor between HF patients and young healthy adults in 1989. 25(OH)D was decreased in HF patients (p<0.003), as was ionized calcium. Serum PTH levels were higher in HF patients than in controls (p<0.01). A positive correlation has been found between PTH and age in HF patients (r=0.29;p<0.03) and in the whole group of HF patients and controls. There was a significant decrease in osteocalcin in HF patients versus elderly controls (p<0.04). Our results confirm the high levels of intact PTH in elderly HF patients, this elevation of PTH being known to increase bone resporption. Low serum osteocalcin in HF patients seems to reflect decreased bone formation. Thus, this association contributes to the accelerated bone loss in hip fracture. This study also suggests that 1,25(OH)2D is not significantly lowered in case of hip fracture, and lα-hydroxylase is not deficient, in spite of a lack of the substrate of this enzyme (25(OH)D). Therefore, a defect of 1,25(OH)2D does not appear to be a pathogenetic factor in bone aging.