Early antithrombin depletion after trauma is associated with biomarkers of endotheliopathy and systemic protein loss: a retrospective observational study.
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引用次数: 0
Abstract
Background: Early antithrombin (AT) depletion after trauma may result from thrombin-related consumption, vascular leakage, and systemic protein loss. We examined the biomarker profile associated with early AT depletion and whether reduced AT activity identifies an adverse early injury phenotype.
Methods: In this single-center retrospective observational study, 100 adult trauma patients were analyzed on admission. AT activity, albumin (Alb), syndecan-1 (SDC-1), and thrombin-antithrombin complex (TAT) were measured in residual blood samples obtained at hospital arrival. Associations among biomarkers were assessed using locally estimated scatterplot smoothing and generalized additive models. LASSO and elastic-net regression identified variables associated with AT activity, and exploratory Bayesian regression assessed directional associations. Clinical outcomes were compared between patients with reduced (<80%) and preserved (≥80%) AT activity.
Results: Reduced AT activity was present in 32% of patients and remained associated with shock (adjusted OR 9.42, 95% CI 1.32-109.00, p=0.037) and disseminated intravascular coagulation (DIC) (adjusted OR 12.20, 95% CI 2.17-113.00, p=0.010) after adjustment for age, sex, ISS, and lactate. AT activity was positively associated with Alb and negatively associated with SDC-1 and TAT. In regularized regression, Alb and SDC-1 were more consistently associated with AT activity, whereas TAT was not selected. Bayesian analyses showed stronger directional evidence for Alb and SDC-1 than for TAT.
Conclusion: Early AT depletion after trauma was associated with adverse clinical features and biomarker patterns consistent with endothelial injury and circulating protein depletion, beyond thrombin-related consumption alone.
期刊介绍:
SHOCK®: Injury, Inflammation, and Sepsis: Laboratory and Clinical Approaches includes studies of novel therapeutic approaches, such as immunomodulation, gene therapy, nutrition, and others. The mission of the Journal is to foster and promote multidisciplinary studies, both experimental and clinical in nature, that critically examine the etiology, mechanisms and novel therapeutics of shock-related pathophysiological conditions. Its purpose is to excel as a vehicle for timely publication in the areas of basic and clinical studies of shock, trauma, sepsis, inflammation, ischemia, and related pathobiological states, with particular emphasis on the biologic mechanisms that determine the response to such injury. Making such information available will ultimately facilitate improved care of the traumatized or septic individual.