Systemic long-term metabolic effects of acute non-severe paediatric burn injury

Sofina Begum1,2,3,4, Blair Z Johnson5, Aude-Claire Morillon4

  • 1Harvard Medical School, Harvard University, 25 Shattuck Street, Boston, MA, 02115, USA.

Scientific Reports
|July 29, 2022
PubMed

Insights

Children with previous non-severe burns show altered metabolism years later. These immunometabolic changes may explain long-term health issues and increased infection risk in pediatric burn survivors.

Area of Science:

  • Immunology
  • Metabolomics
  • Pediatric Medicine

Background:

  • Non-severe thermal trauma can trigger systemic responses, leading to immunosuppression in children.
  • This immunosuppression increases the risk of poor recovery and secondary health problems in pediatric patients.

Purpose of the Study:

  • To investigate the long-term systemic effects of non-severe burns in children.
  • To identify specific metabolic alterations persisting years after burn injury.

Main Methods:

  • Targeted mass spectrometry was used to analyze plasma samples from pediatric burn survivors (at least 3 years post-injury) and healthy controls.
  • Biogenic amines and tryptophan metabolites were quantified.

Main Results:

  • Children with a history of burns had significantly higher concentrations of 12 metabolites, including urea cycle intermediates, aromatic amino acids, and quinolinic acid.
  • Correlation analysis revealed cytokine-metabolite associations in burn survivors, absent in controls, suggesting sustained immune-metabolic interactions.

Conclusions:

  • Non-severe burn trauma leaves a lasting immunometabolic imprint in children.
  • These persistent metabolic changes may underlie long-term immune dysregulation and adverse health outcomes in pediatric burn survivors.

Related Concept Videos

Burn Injuries01:22

Burn Injuries

Burn injuries occur when the skin and underlying tissues are damaged due to exposure to heat, electricity, chemicals, radiation, or friction. They can vary in severity, from minor superficial burns to severe deep burns that can be life-threatening.
The damage results in the death of skin cells, which can lead to a massive loss of fluid. Dehydration, electrolyte imbalance, and renal and circulatory failure follow, which can be fatal. Burn patients are treated with intravenous fluids to offset...
2.8K
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
64
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
66
Toxic Reactions: Overview01:26

Toxic Reactions: Overview

When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
1.1K
Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...
78
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
234