Elevated syndecan-1 indicates endothelial glycocalyx disruption in sepsis, and is closely linked to worse prognosis, septic shock and organ dysfunction. As a complementary biomarker to lactate, procalcitonin and C-reactive protein, it improves multi-domain sepsis risk stratification and supports individualized resuscitation and endothelial-protective intervention research. Key messages What is already known on this topic? Syndecan-1 is a marker of endothelial glycocalyx degradation and has been linked to sepsis severity. However, its precise association with prognosis and complications remains unclear, and its clinical value relative to traditional sepsis biomarkers (lactate/PCT/CRP) has not been systematically clarified, necessitating a meta-analysis to quantify its clinical relevance and complementary role. What this study adds This study confirms that syndecan-1 levels are significantly elevated in sepsis, especially in severe cases, non-survivors, and patients with AKI or DIC, validating its role as a specific biomarker of sepsis-associated endothelial glycocalyx injury. Importantly, it clarifies that syndecan-1 is not a replacement for traditional biomarkers but a complementary indicator that captures the endotheliopathy domain unmeasured by lactate/PCT/CRP. Its lack of specificity for sepsis limits its utility as a standalone diagnostic biomarker, but it provides incremental prognostic value for risk stratification. How this study might affect research, practice, or policy Syndecan-1 may serve as a prognostic marker for endothelial dysfunction in sepsis and a stratification tool for identifying patients at high risk of capillary leak and fluid resuscitation-related adverse outcomes. It should be used alongside other biomarkers to inform personalized resuscitation strategies. This meta-analysis provides the most comprehensive quantitative evidence to date for the integration of "glycocalyx-friendly" management into future sepsis research and clinical guidelines, and guides the design of forthcoming trials targeting endothelial barrier protection.
Xu et al. (Wed,) studied this question.