Interactions of Phosphate Metabolism With Serious Injury, Including Burns

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.

A preliminary model of football-related neural stress that integrates metabolomics with transcriptomics and virtual reality

“…Impaired ATP synthesis may be related to depleted energy stores and a subsequent lack of energy sources. Contrary to these observations, serum phosphate levels decreased in patients with severe TBI ( Porter et al., 2017 ), yet football athletes often experience repetitive subconcussive HAEs. More research is required to elucidate the role of phosphate in the full TBI spectrum.…”

Normal-range emergency department serum phosphorus levels and all-cause mortality

“…Patients with severe burn injuries, as well as those with spinal cord compression and traumatic brain injuries, suffer from tissue depletion of phosphate along with increased muscle turnover and thereby ATP utilisation, all of which may result in hypophosphataemia. Consequently, in an attempt to conserve body phosphate and decrease phosphate excretion there is a reciprocal fall in endogenous parathyroid hormone and FGF23 levels 11. Notably, several pharmacological intervention studies aiming at reducing muscle protein breakdown in this clinical context have shown promising results 11.…”

“…Consequently, in an attempt to conserve body phosphate and decrease phosphate excretion there is a reciprocal fall in endogenous parathyroid hormone and FGF23 levels 11. Notably, several pharmacological intervention studies aiming at reducing muscle protein breakdown in this clinical context have shown promising results 11. Overt hypophosphataemia has been previously associated with increased in-hospital mortality in patients with sepsis,12 acute ischaemic stroke13 and community-acquired pneumonia 14.…”

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“…The injuries and death due to white phosphorus may be three ways: Burning deeply into tissue, inhalation of smoke or ingestion of white phosphorous. Phosphorus burns may increase the risk of death or deep due to phosphorous absorption in human body via area of burns causing the damage of heart, liver and kidney some time the reason of failure of various organs 7 . Additionally the smoke of white phosphorous annoys the eyes, membranous area of the respiratory tract and in small amount, while large amount may be the reason of deep burns 8 .…”