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Table 1 Molecular mechanisms targeted by additive therapeutic plasma exchange (TPE) in septic shock

From: Letter to the Editor: Innovative future concepts of extracorporeal strategies in sepsis and septic shock

Molecular mechanism targeted by TPE

REPLACE (replenished by substitution with healthy donor plasma)

REMOVE (removed by taking out patient plasma)

Immune system

Immune restauration: IgG, IgM, IgA

Pro-inflammatory cytokines, DAMPs, PAMPs

Endothelial permeability

Anti-permeability: Angpt-1, Hpa-2

Pro-permeability: Angpt-2, VEGF, sTie2, Hpa-1

Coagulation

Anti-coagulation: Protein C/S, AT-III

Pro-coagulation: vWF:Ag, D-Dimer

Microcirculation

Restoring microcirculatory function: ADAMTS-13

Causing microcirculatory dysfunction: vWF-M

  1. Demonstrated are molecular mechanisms involved in the pathological host response of sepsis that are influenced by use of TPE. Protective, but consumed factors are replenished by TPE (REPLACE). Excessive injurious mediators are removed by TPE (REMOVE)
  2. Angpt-1 Angiopoietin-1, Angpt-2 Angiopoietin-2, ADAMTS13 A disintegrin and metalloprotease with thrombospondin-1-like domains 13, AT-III Antithrombin-III, DAMPs Damage-associated molecular patterns, Hpa-1 Heparanase-1, Hpa-2 Heparanase-2, PAMPs Pathogen-associated molecular patterns, sTie2 A soluble receptor of tyrosine kinase with immunoglobulin-like and EGF-like domains 2, VEGF Vascular endothelial growth factor, vWF:Ag von Willebrand factor antigen, vWF-M (Ultra) large von Willebrand factor multimers
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Critical Care

ISSN: 1364-8535