Abstract
Animal data and cross-sectional human studies have established that chronic hyponatraemia predisposes to osteoporosis; the effects of acute hyponatraemia on bone turnover have not been determined. Our objective was to test the hypothesis that acute hyponatraemia leads to dynamic effects on bone turnover. A prospective observational pilot study. Bone turnover markers [C-terminal crosslinking telopeptide of type 1 collagen (CTX-1), N-propeptide of type 1 collagen (P1NP) and osteocalcin] were measured prospectively over one week in 22 eunatraemic patients with subarachnoid haemorrhage. Patients treated with glucocorticoids were excluded. Eight patients developed acute hyponatraemia, median nadir plasma sodium concentration 131mmol/L (IQR 128-132), and 14 remained eunatraemic, nadir plasma sodium concentration 136mmol/L (IQR 133-137). Significant main effects of hyponatraemia were found for P1NP (p=.02) and P1NP:CTX-1 ratio (p=.02), both fell in patients with acute hyponatraemia, with significant interaction between hyponatraemia and time from baseline for P1NP (p=.02). Significant main effects of time from baseline (p<.001) but not hyponatraemia (p=.07) were found for osteocalcin. For CTX-1, significant main effects of time from baseline (p=.001) but not hyponatraemia (p=.65) were found. There was a positive correlation between change in P1NP:CTX-1 ratio and nadir plasma sodium concentration, r=+.43, p=.04. Median serum cortisol (measured on days 1, 3 and 7) was higher in the hyponatraemia group than in those who remained eunatraemic, 545nmol/L (IQR 373-778) versus 444nmol/L (IQR 379-542) p=.03. These data suggest that acute mild hyponatraemia is associated with a reduction in bone formation activity.
Published Version
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