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Burned skin produces only about 25 percent as much vitamin D – March 2012

Progress in Understanding the Calcium and Vitamin D Endocrinology Following Burn Injury in Children (March 2012)

International journal of Endocrinology and Metabolism; DOI: 10.5812/ijem.2685
Gordon L Klein, gordonklein at ymail.com
Orthopaedic Surgery and Rehabilitation Department, Medical Staff, Shriners Burns Hospital, University of Texas Medical Branch, Galveston, Texas, USA

This review covers the progress made by our group over the past two decades in understanding the effects of severe burn injuries on the endocrine system, especially in relation to calcium and vitamin D metabolism.We examine the phenomena of transient growth hormone deficiency and the dose-dependent effects of recombinant human growth hormone on bone and muscle mass. We move on to discuss the occurrence of post-burn secondary hypoparathyroidism caused by the up-regulation of the parathyroid calcium-sensing receptor, and finally, we discuss vitamin D status, the progressive nature of vitamin D deficiency post-burn, the causes of the progressive deficiency, and what must be done to prevent it.

These conditions taken together, while not primarily responsible for post-burn bone loss, may impair the recovery of normal bone density and leave, especially younger populations of victims, vulnerable to a reduction in peak bone mass with subsequent elevated risk of developing osteoporosis as adults.

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Burned skin produces about 1/4 the vitamin D

Burns: where has all the calcium (and vitamin D) gone?
Adv Nutr 2011 Nov; 2(6):457-62.
Klein GL

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.


See also VitaminDWiki

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