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A Review of GM-CSF Therapy in Sepsis

Determine what clinical role, if any, GM-CSF may have in the clinical treatment of sepsis in the adult patient. Advancements in the management of sepsis have led to significant decreases in early mortality; however, sepsis remains a significant source of long-term mortality and disability which plac...

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Autores principales: Mathias, Brittany, Szpila, Benjamin E., Moore, Frederick A., Efron, Philip A., Moldawer, Lyle L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5058885/
https://www.ncbi.nlm.nih.gov/pubmed/26683913
http://dx.doi.org/10.1097/MD.0000000000002044
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author Mathias, Brittany
Szpila, Benjamin E.
Moore, Frederick A.
Efron, Philip A.
Moldawer, Lyle L.
author_facet Mathias, Brittany
Szpila, Benjamin E.
Moore, Frederick A.
Efron, Philip A.
Moldawer, Lyle L.
author_sort Mathias, Brittany
collection PubMed
description Determine what clinical role, if any, GM-CSF may have in the clinical treatment of sepsis in the adult patient. Advancements in the management of sepsis have led to significant decreases in early mortality; however, sepsis remains a significant source of long-term mortality and disability which places strain on healthcare resources with a substantial growing economic impact. Historically, early multiple organ failure (MOF) and death in patients with severe sepsis was thought to result from an exaggerated proinflammatory response called the systemic inflammatory response syndrome (SIRS). Numerous prospective randomized controlled trials (PRCTs) tested therapies aimed at decreasing the organ injury associated with an exaggerated inflammatory response. With few exceptions, the results from these PRCTs have been disappointing, and currently no specific therapeutic agent is approved to counteract the early SIRS response in patients with severe sepsis. It has long been recognized that there is a delayed immunosuppressive state that contributes to long-term morbidity. However, recent findings now support a concurrent proinflammatory and anti-inflammatory response present throughout sepsis. Multiple immunomodulating agents have been studied to combat the immunosuppressive phase of sepsis with the goal of decreasing secondary infection, reducing organ dysfunction, decreasing ICU stays, and improving survival. Granulocyte-macrophage colony stimulating factor (GM-CSF), a myelopoietic growth factor currently used in patients with neutropenia secondary to chemotherapy-induced myelosuppression, has been studied as a potential immune-activating agent. The applicability of GM-CSF as a standard therapy for generalized sepsis is still largely understudied; however, small-scale studies available have demonstrated some improved recovery from infection, decreased hospital length of stay, decreased days requiring mechanical ventilation, and decreased medical costs.
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spelling pubmed-50588852016-11-01 A Review of GM-CSF Therapy in Sepsis Mathias, Brittany Szpila, Benjamin E. Moore, Frederick A. Efron, Philip A. Moldawer, Lyle L. Medicine (Baltimore) 3600 Determine what clinical role, if any, GM-CSF may have in the clinical treatment of sepsis in the adult patient. Advancements in the management of sepsis have led to significant decreases in early mortality; however, sepsis remains a significant source of long-term mortality and disability which places strain on healthcare resources with a substantial growing economic impact. Historically, early multiple organ failure (MOF) and death in patients with severe sepsis was thought to result from an exaggerated proinflammatory response called the systemic inflammatory response syndrome (SIRS). Numerous prospective randomized controlled trials (PRCTs) tested therapies aimed at decreasing the organ injury associated with an exaggerated inflammatory response. With few exceptions, the results from these PRCTs have been disappointing, and currently no specific therapeutic agent is approved to counteract the early SIRS response in patients with severe sepsis. It has long been recognized that there is a delayed immunosuppressive state that contributes to long-term morbidity. However, recent findings now support a concurrent proinflammatory and anti-inflammatory response present throughout sepsis. Multiple immunomodulating agents have been studied to combat the immunosuppressive phase of sepsis with the goal of decreasing secondary infection, reducing organ dysfunction, decreasing ICU stays, and improving survival. Granulocyte-macrophage colony stimulating factor (GM-CSF), a myelopoietic growth factor currently used in patients with neutropenia secondary to chemotherapy-induced myelosuppression, has been studied as a potential immune-activating agent. The applicability of GM-CSF as a standard therapy for generalized sepsis is still largely understudied; however, small-scale studies available have demonstrated some improved recovery from infection, decreased hospital length of stay, decreased days requiring mechanical ventilation, and decreased medical costs. Wolters Kluwer Health 2015-12-18 /pmc/articles/PMC5058885/ /pubmed/26683913 http://dx.doi.org/10.1097/MD.0000000000002044 Text en Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. http://creativecommons.org/licenses/by/4.0 This is an open access article distributed under the Creative Commons Attribution License 4.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0
spellingShingle 3600
Mathias, Brittany
Szpila, Benjamin E.
Moore, Frederick A.
Efron, Philip A.
Moldawer, Lyle L.
A Review of GM-CSF Therapy in Sepsis
title A Review of GM-CSF Therapy in Sepsis
title_full A Review of GM-CSF Therapy in Sepsis
title_fullStr A Review of GM-CSF Therapy in Sepsis
title_full_unstemmed A Review of GM-CSF Therapy in Sepsis
title_short A Review of GM-CSF Therapy in Sepsis
title_sort review of gm-csf therapy in sepsis
topic 3600
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5058885/
https://www.ncbi.nlm.nih.gov/pubmed/26683913
http://dx.doi.org/10.1097/MD.0000000000002044
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