PubMed · 5548049
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H S Thorpe. 1971-04-08. Fondue rendue.. https://doi.org/10.1056/nejm197104082841427
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BACKGROUND: Burn injuries trigger complex immune responses and gene expression changes, impacting wound healing and systemic inflammation. Understanding these changes is crucial for identifying biomarkers and therapeutic targets. METHODS: We analyzed two gene expression omnibus datasets (wound tissue [GSE8056] and blood [GSE37069]) to identify differentially expressed genes (DEGs) in burn injury samples versus controls. Immune cell proportions were assessed using CIBERSORT. Functional enrichment analyses (Gene Ontology and Kyoto Encyclopedia of Genes and Genomes) and protein-protein interaction networks were constructed to identify key genes and pathways. RESULTS: We identified 1170 upregulated and 1227 downregulated DEGs. Gene Ontology analysis revealed enrichment in neutrophil activation, inflammatory response, and extracellular matrix organization. Kyoto Encyclopedia of Genes and Genomes analysis highlighted cytokine-cytokine receptor interaction, TNF, and IL-17 signaling pathways. Immune infiltration analysis showed significant changes in neutrophils, macrophages (M1/M2), and T-cell subsets. Protein-protein interaction network analysis identified five hub genes: JUN, STAT1, Bcl2, MMP9, and TLR2. CONCLUSIONS: This study provides a comprehensive bioinformatic analysis of gene expression and immune responses in burn injuries. The identified DEGs, hub genes, and pathways offer insights into the immune response mechanisms and suggest potential targets for diagnostic and therapeutic interventions in burn injury management.
OBJECTIVE: The authors provide an update on a multidisciplinary approach to the treatment of severely burned patients. A review of studies and clinical trials from the past to the present include fluid resuscitation, sepsis, immune function, hypermetabolism, early excision, wound healing, scar formation, and inhalation injury. SUMMARY BACKGROUND DATA: Advances in treating initial burn shock, infection control, early wound closure, and modulation of the hypermetabolic response have decreased morbidity and mortality in the last two decades. Specialized burn care centers, using a multidisciplinary approach, not only successfully treat large burns and their complications, but provide the necessary rehabilitation and psychological support required for readjustment back into society. CONCLUSIONS: Thermal injury results in a number of physiologic alterations that can be minimized by adequate fluid resuscitation to maintain tissue perfusion, early excision of burn wounds, and rapid wound coverage. These measures, in combination with antibiotic coverage and nutritional support in the form of early enteral tube feedings, will decrease the hypermetabolic response and the incidence of sepsis that can lead to hemodynamic instability and organ failure. Ongoing clinical trials using anabolic agents (e.g., recombinant human growth hormone) and pharmacologic agents that modulate inflammatory and endocrine mediators (e.g., ibuprofen and propranolol) show promise in the treatment of severe burn injuries.
A new method of surgical treatment of postburn boutonniere deformity was used in 124 fingers of 66 patients. This method includes reconstruction of the lateral band's position of an extensor apparatus and anatomic continuity of a central band. Before tendon plasty, passive movements in a proximal interphalangeal joint are restored and contracture of others joints is released. If the soft tissue of the digital back is affected, tendon grafts are covered with a groin pedicled flap. With this method we could restore active movements in the proximal interphalangeal joint in 89.2 percent of the patients and avoid fusion or amputation. The failures were connected with serious intrajoint changes.