Response

Response

We thank the correspondents for their interest in our case and comments. Our patient had been transferred to our care following a period in a rehabilitation ward which she had been admitted to following an unrelated inpatient hospital stay. It was during this time, when she was mobile (albeit not fully), that the ulcer originally developed. During this period she persistently had normal adjusted calcium and albumin levels (adjusted Ca²⁺ range, 2.14–2.40 mmol/L; albumin 36–39 g/L). When the ulcer failed to heal, progressed and became increasingly painful despite prolonged antibiotic courses, she then became immobile and was referred back to the acute hospital for further assessment. Importantly there was no prior history of primary hyperparathyroidism and at the time of admission, parathyroid hormone concentration was normal.

Serum ionized (free) calcium is maintained within a narrow range through parathyroid hormone secretion, which in turn is regulated by serum ionized calcium acting via calcium-sensing receptors on the surface of the parathyroid cells. Therefore normal parathyroid hormone levels would indicate that our patient was normocalcaemic even in her hypoalbuminaemic state. Although both immobility and hypoalbuminaemia can lead to an increase in ionized calcium, this would consequently lead to a reduction in parathyroid hormone secretion which was not the case. Thus, although her immobility may potentially have contributed to her overall condition, we did not feel that it was the trigger to the calciphylaxis.