Burns: where has all the calcium (and vitamin D) gone?

A considerable part of the difficulty of determining nutrient requirements in pathologic states is the failure to understand the physiology unique to the specific condition. Here we take the specific example of burns in childhood and discuss the roles of the inflammatory and stress responses to the burn and the consequent transient increased bone resorption followed by osteoblast apoptosis and adynamic bone. This condition leads to a failure of the bone to take up and thus conserve the increased calcium liberated by the acutely increased bone resorption. On top of this mechanism, there is a cytokine-mediated upregulation in the parathyroid gland calcium-sensing receptor that results in hypocalcemic hypoparathyroidism and consequent urinary calcium wasting. As if that were not sufficient, the skin of the burned patient, both scarred area and normal-appearing adjacent skin, convert 7 dehydrocholesterol to pre-vitamin D(3) at a rate that is 20-25% of normal skin and circulating levels of 25-hydroxyvitamin D are chronically low. Thus, burn injury gives rise to calcium wasting, failure of bone to take up excessive calcium, and vitamin D insufficiency to frank deficiency. These and other areas must be addressed before it can be determined how much vitamin D and calcium should be given to a patient with severe burn injury.