Context
Fluid restriction (FR) is the recommended first-line treatment for syndrome of inappropriate antidiuresis (SIAD), despite the lack of prospective data to support its efficacy.
Design
A prospective non-blinded randomised controlled trial of FR versus no treatment in chronic SIAD.
Interventions and Outcome
46 patients with chronic asymptomatic SIAD were randomised to either FR (1 liter/day) or no specific hyponatremia treatment (NoTx) for one month. The primary endpoints were change in plasma sodium concentration (pNa) at days 4 and 30.
Results
Median baseline pNa was similar in the two groups [127 mmol/L (IQR 126-129) FR and 128 mmol/L (IQR 126-129) NoTx, p=0.36]. pNa rose by 3 mmol/L (IQR 2-4) after three days FR, compared with 1 mmol/L (IQR 0-3) NoTx, p=0.005. There was minimal additional rise in pNa by day 30; median pNa increased from baseline by 4 mmol/L (IQR 2-6) in FR, compared with 1 mmol/L (IQR 0-1) NoTx, p=0.04. 17% of FR had a rise in pNa of ≥5 mmol/L after three days, compared with 4% NoTx, RR 4.0 (95% CI 0.66-25.69), p=0.35. 61% of FR corrected pNa to ≥130 mmol/L after three days, compared with 39% of NoTx, RR 1.56 (95% CI 0.87-2.94), p=0.24.
Conclusion
FR induces a modest early rise in pNa in patients with chronic SIAD, with minimal additional rise thereafter, and is well-tolerated. More than one third of patients fail to reach a pNa ≥130 mmol/L after three days of FR, emphasising the clinical need for additional therapies for SIAD, in some patients.
Context
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.
Design
A prospective observational pilot study.
Methods
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.
Results
Eight patients developed acute hyponatraemia, median nadir plasma sodium concentration 131 mmol/L (IQR 128–132), and 14 remained eunatraemic, nadir plasma sodium concentration 136 mmol/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, 545 nmol/L (IQR 373–778) versus 444 nmol/L (IQR 379–542) p = .03.
Conclusion
These data suggest that acute mild hyponatraemia is associated with a reduction in bone formation activity.
Chronic hypophosphataemia impairs bone mineralisation and can result in significant proximal myopathy, however, patients are often asymptomatic and phosphate depletion is identified incidentally. Consequently, FGF23 is a useful biomarker in the diagnosis of tumour-induced osteomalacia, which if resected can be curative.
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