In a small cohort of adults intubated for respiratory failure, plasma HS concentrations (particularly highly sulfated HS disaccharides) were higher among patients with nonpulmonary sepsis (compared to healthy controls).38 Preclinical data has demonstrated heparanase inhibitors attenuate lipopolysaccharide-induced HS fragmentation, endothelial hyperpermeability, and neutrophil extravasation.18 These data as well as the concordance between endothelial-derived syndecan-1 and HS in our study, supports plasma HS as a potent index of EGCX degradation. The gene discussed is HPSE; the disease is respiratory failure.