Citation

Porter C, Sousse LE, Irick R, Schryver E, Klein GL. JBMR Plus 2017; 1(2): 59-65.

Affiliation

Department of Orthopaedic Surgery and Rehabilitation University of Texas Medical Branch at Galveston Galveston TX USA.

Copyright

(Copyright © 2017, John Wiley and Sons)

DOI

10.1002/jbm4.10011

PMID

30283881

PMCID

PMC6124193

Abstract

Approximately 85% of the body's phosphate pool resides within the skeleton. The remaining 15% is stored as high-energy phosphates or in its free form, where it acts as a substrate for adenosine triphosphate (ATP) production. Accordingly, phosphate plays a crucial role in energy metabolism. Trauma and critical illness result in a hypermetabolic state in which energy expenditure increases. The impact of trauma and critical illness on the body's phosphate stores and phosphate-dependent metabolic reactions is poorly understood. We had previously observed that after severe burn trauma, increased energy expenditure is temporally related to a marked reduction in serum concentrations of both parathyroid hormone and fibroblast growth factor 23, both of which have phosphaturic effects. The aim of this article is to describe as far as is known the similarities and differences in phosphate metabolism in different types of injury and to infer what these differences tell us about possible signaling pathways that may link increased phosphate utilization and phosphate retention. © 2017 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.

Language: en

Keywords

BURNS; PARATHYROID HORMONE; PHOSPHORUS; SPINAL CORD INJURY; TRAUMATIC BRAIN INJURY