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Efficacy of Serum Antithrombin III Test in Patients With Severe Traumatic Brain Injury

OBJECTIVE: Immune reactions following traumatic brain injury (TBI) cause many complications, including intravascular dissemination. Antithrombin III (AT-III) plays an important role in suppressing abnormal clot formation and ensuring hemostasis. Therefore, we investigated the efficacy of serum AT-II...

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Detalles Bibliográficos
Autores principales: Noh, HeeSeung, Yoon, Sun Geon, Choi, Kyunghak, Kyung, Kyu-Hyouck, Kim, Min Soo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Neurotraumatology Society 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10329882/
https://www.ncbi.nlm.nih.gov/pubmed/37431370
http://dx.doi.org/10.13004/kjnt.2023.19.e29
Descripción
Sumario:OBJECTIVE: Immune reactions following traumatic brain injury (TBI) cause many complications, including intravascular dissemination. Antithrombin III (AT-III) plays an important role in suppressing abnormal clot formation and ensuring hemostasis. Therefore, we investigated the efficacy of serum AT-III in patients with severe TBI. METHODS: This retrospective study included 224 patients with severe TBI who visited a single regional trauma center between 2018 and 2020. AT-III levels were measured immediately after the TBI diagnosis. AT-III deficiency was defined as an AT-III serum level <70%. Patient characteristics, injury severity, and procedures were also investigated. Patient outcomes included Glasgow Outcome Scale scores at discharge and mortality. RESULTS: AT-III levels were significantly lower in the AT-III deficient group (n=89; 48.27% ± 1.91%) than in the AT-III sufficient group (n = 135, 78.90% ± 1.52%) (p < 0.001). Mortality occurred in 72 of the 224 patients (33.04%), indicating that there were significantly more patients in the AT-III-deficient group (45/89, 50.6%) than in the AT-III-sufficient group (27/135, 20%). Significant risk factors for mortality included the Glasgow Coma Scale score (P = 0.003), pupil dilatation (P = 0.031), disseminated intravascular coagulopathy (P = 0.012), serum AT-III level (P = 0.033), and procedures including barbiturate coma therapy (P = 0.010). Serum AT-III levels were significantly correlated with Glasgow Outcome Scale scores at discharge (correlation coefficient = 0.455, p < 0.001). CONCLUSION: Patients with AT-III deficiency after severe TBI may require more intensive care during treatment, because AT-III levels reflect injury severity and correlate with mortality.