243. Plasma Glypican-4 Levels are Associated with Disease Severity in ED Patients with Severe Sepsis and Septic Shock
Session: Poster Abstract Session: Diagnostics: Miscellaneous
Thursday, October 8, 2015
Room: Poster Hall
Background: Increased vascular permeability is a key feature in the pathophysiology of severe sepsis. The glycocalyx, consisting of cell-bound proteoglycans (syndecans and glypicans) and glycosaminoglycan (GAG) side chains, plays an integral role in maintaining endothelial stability. Plasma levels of glypicans have never been studied in patients with sepsis. We hypothesized that plasma levels of glypicans are elevated in severe sepsis.  

Methods: Commercial ELISAs for Glypicans 1,2,3, and 4 was used for analyzing plasma from 10 patients with severe sepsis and 10 healthy controls as an initial screening. Further on plasma Glypican-4 was analysed in a cohort of 202 emergency department patients with a suspected infection. We classified the patients into severe sepsis/septic shock, sepsis and infection without SIRS and analysed the Glypican-4 levels in these patient groups. Correlations between Glypican-4 and other commonly used markers were investigated.

Results: In the pilot study only Glypican-1 (P=0.015) and Glypican-4 (P=0.031) were significantly increased in the severe sepsis/septic shock groups. Glypican-4 levels were also significantly higher (P<0.001) in the severe sepsis/septic shock group (n=64) compared to the sepsis group (n=83). The patients with sepsis (n=83) had significantly higher Glypican-4 levels than patients with infection without SIRS (n=37), (P=0.016). The concentrations of Glypican-4 correlated positively (P<0.001) to Heparin-binding protein, CRP, lactate, Procalcitonin and negatively (P<0.001) to Apolipoprotein M and Sphingosine-1-phosphate.

Conclusion: We show that Glypican-4 is elevated in plasma of patients with severe sepsis/septic shock and correlate with disease severity and other markers of endothelial dysfunction and systemic inflammation.

Adam Linder, MD, PhD, Infection Medicine, Division of Clinical Sciences Lund University, Lund, Sweden and Jane Fisher, Bsc, Division of Clinical Sciences Lund University, Lund, Sweden

Disclosures:

A. Linder, None

J. Fisher, None

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