Evaluation of plasma angiopoietin-2 and vascular endothelial growth factor in healthy dogs and dogs with systemic inflammatory response syndrome or sepsis.
Publisher DOI
PubMed ID
30575998
Abstract
BACKGROUND:
Angiopoietin-2 (Ang-2) and vascular endothelial growth factor (VEGF) are regulators of endothelial permeability.
OBJECTIVE:
Plasma concentrations of Ang-2 and VEGF are increased in dogs with systemic inflammatory response syndrome (SIRS) and sepsis and are correlated with disease severity and outcome.
ANIMALS:
Healthy dogs (n = 18) and client-owned dogs with SIRS (n = 34) or sepsis (n = 25).
METHODS:
Prospective observational study. Ang-2 and VEGF concentrations in admission plasma samples were compared between healthy dogs and dogs with SIRS or sepsis, and between survivors and non-survivors. Correlations with the acute patient physiologic and laboratory evaluation (APPLEfast ) disease severity score were examined.
RESULTS:
Median Ang-2 was significantly higher in dogs with SIRS (19.3; interquartile range [IQR]: 8.6-25.7 ng/mL) and sepsis (21.2; IQR: 10.3-30.1 ng/mL) compared to healthy dogs (7.6; IQR: 6.7-9.8 ng/mL). Ang-2 was significantly higher in non-survivors (24.1; IQR: 11.9-50.0 ng/mL) than survivors (10.2; IQR: 7.2-21.5 ng/mL) but did not correlate with the APPLEfast score. Admission Ang-2 predicted negative outcome in dogs with SIRS and sepsis with reasonable accuracy (area under the curve [AUC]: 0.75, confidence interval [CI]: 0.59-0.85; sensitivity: 0.5, CI: 0.29-0.71; specificity: 0.87, CI: 0.75-0.95); differentiation between sepsis and SIRS was poor (AUC: 0.58). Plasma VEGF was significantly higher in dogs with sepsis (45; IQR: 14-107.5 pg/mL) than in dogs with SIRS (3.3; IQR: 0-35.6 pg/mL) or healthy dogs (0; IQR: 0 pg/mL; P = 0.008). VEGF was significantly (P = .0004) higher in non-survivors (34.5; IQR: 0-105.7 pg/mL) than in survivors (0; IQR: 0-55.2 pg/mL). The ability of VEGF to predict a negative outcome was poor.
CONCLUSIONS AND CLINICAL IMPORTANCE:
Ang-2 may represent a useful additional prognostic marker in dogs with SIRS.
Angiopoietin-2 (Ang-2) and vascular endothelial growth factor (VEGF) are regulators of endothelial permeability.
OBJECTIVE:
Plasma concentrations of Ang-2 and VEGF are increased in dogs with systemic inflammatory response syndrome (SIRS) and sepsis and are correlated with disease severity and outcome.
ANIMALS:
Healthy dogs (n = 18) and client-owned dogs with SIRS (n = 34) or sepsis (n = 25).
METHODS:
Prospective observational study. Ang-2 and VEGF concentrations in admission plasma samples were compared between healthy dogs and dogs with SIRS or sepsis, and between survivors and non-survivors. Correlations with the acute patient physiologic and laboratory evaluation (APPLEfast ) disease severity score were examined.
RESULTS:
Median Ang-2 was significantly higher in dogs with SIRS (19.3; interquartile range [IQR]: 8.6-25.7 ng/mL) and sepsis (21.2; IQR: 10.3-30.1 ng/mL) compared to healthy dogs (7.6; IQR: 6.7-9.8 ng/mL). Ang-2 was significantly higher in non-survivors (24.1; IQR: 11.9-50.0 ng/mL) than survivors (10.2; IQR: 7.2-21.5 ng/mL) but did not correlate with the APPLEfast score. Admission Ang-2 predicted negative outcome in dogs with SIRS and sepsis with reasonable accuracy (area under the curve [AUC]: 0.75, confidence interval [CI]: 0.59-0.85; sensitivity: 0.5, CI: 0.29-0.71; specificity: 0.87, CI: 0.75-0.95); differentiation between sepsis and SIRS was poor (AUC: 0.58). Plasma VEGF was significantly higher in dogs with sepsis (45; IQR: 14-107.5 pg/mL) than in dogs with SIRS (3.3; IQR: 0-35.6 pg/mL) or healthy dogs (0; IQR: 0 pg/mL; P = 0.008). VEGF was significantly (P = .0004) higher in non-survivors (34.5; IQR: 0-105.7 pg/mL) than in survivors (0; IQR: 0-55.2 pg/mL). The ability of VEGF to predict a negative outcome was poor.
CONCLUSIONS AND CLINICAL IMPORTANCE:
Ang-2 may represent a useful additional prognostic marker in dogs with SIRS.
Date Issued
2019-03
Publication Type
Article
Subject(s)
Language(s)
en
Author(s)
Journal
Journal of veterinary internal medicine
Publisher
Wiley-Blackwell
ISSN
0891-6640
Access(Rights)
open.access