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We read with interest the paper by Baines and colleagues1 in which the authors reported a strong inverse relationship between total serum calcium concentrations and disease severity in 70 critically ill children with meningococcal disease. Calcitonin concentrations were measured in a subgroup of 23 children on admission, and significantly correlated with disease severity. In particular, however, the authors found no relation between calcitonin concentrations and total or ionised calcium concentrations. In a study of 69 adult patients with acute pancreatitis,2 we have similarly found no correlation between plasma concentrations of calcitonin precursors (CTpr) on admission2 and both the admission and lowest (within 72 hours of admission) adjusted total serum calcium concentrations (unpublished data). The concentrations of CTpr were significantly higher2 and of the lowest calcium were significantly lower (median (IQR): 2.16 (2.0–2.18) mmol/l v 2.23 (2.15–2.30) mmol/l, p=0.017) in patients with severe attacks (n=14, Atlanta criteria) compared with mild attacks. Our data and that of Baines and colleagues1 support the contention that calcitonin and its precursors have a minor effect on calcium metabolism. Indeed, previous investigators found no correlation between the serum concentrations of serum calcitonin and hypocalcaemia in patients with acute pancreatitis3,4 or in experimental models of the disease.5 Whilst CTpr concentrations were reported to rise significantly in critically ill patients, they correlated rather weakly with a concomitant fall in serum ionised calcium.6 A rise in CTpr concentrations did not correlate with the fall in serum calcium concentrations in patients with acute malaria.7 This suggests that factors other than calcitonin and CTpr are involved in the homeostasis of calcium in the critically ill.