6 research outputs found

    The clinical utility of shock index to predict the need for blood transfusion and outcomes in trauma

    No full text
    BACKGROUND: We aimed to evaluate the clinical utility of shock index (SI) to assess the need for blood transfusion and predict the outcomes in trauma. MATERIALS AND METHODS: We conducted a retrospective analysis for trauma patients between 2012 and 2016 in a level-1 trauma center. Data included patient demographics, vital signs, mechanism of injury, Injury Severity Score (ISS), New Injury Severity Score (NISS), Trauma and Injury Severity Score (TRISS), blood transfusion, hospital length of stay (HLOS), and mortality. Patients were classified into group I (SI /= 0.8). RESULTS: Out of 8710 admitted patients, 1535 (22%) had SI \u3e/= 0.8 and 976 (12.5%) received blood transfusion (89 received massive transfusion, following massive blood transfusion protocol [MTP]). In comparison to lower SI, patients with SI \u3e/= 0.8 were mostly female patients, 8 y younger (43 +/- 22 versus 51 +/- 23), had greater ISS (15 +/- 12 versus 10.5 +/- 8), higher NISS (19 +/- 15 versus 14 +/- 11), lower pulse pressure (43 +/- 14 versus 62 +/- 18), lower TRISS (0.892 +/- 0.20 versus 0.953 +/- 0.11), and received more blood transfusion (28.6% versus 9.0%) or MTP (17.7% versus 3%), P = 0.001. Also, they had mostly exploratory laparotomy (13.3% versus 6.6%, P = 0.001), longer HLOS (11.3 versus 7.0 d, P = 0.001), and higher mortality (7.0% versus 3.1%, P = 0.001). SI was correlated with age (r = -0.188), pulse pressure (r = -0.51), HLOS (r = 0.168), ISS (r = 0.251), NISS (r = 0.211), amount of blood transfused (r = 0.27), Glasgow Coma Scale (r = -0.96), and TRISS (r = -0.230). After adjusting for age and sex, ISS, and Glasgow Coma Scale in two multivariable analyses, high SI was found to be an independent predictor for mortality (odd ratio, 2.553; 95% confidence intervals: 1.604-4.062) and blood transfusion (odd ratio, 3.57; 95% confidence intervals: 3.012-4.239). The cutoff point of SI for predicting MTP is 0.81 (sensitivity, 85%; specificity, 64%; positive predictive value, 16%; and negative predictive value, 98%). CONCLUSIONS: The SI after injury can be used early to predict the need for MTP and laparotomy and mortality. It correlates with other physiological and anatomical variables. However, its cutoff values for risk stratification and prognostication need further evaluation

    AML1 is overexpressed in patients with myeloproliferative neoplasms and mediates JAK2V617F-independent overexpression of NF-E2

    No full text
    The transcription factor NF-E2 is overexpressed in the majority of patients with polycythemia vera (PV). Concomitantly, 95% of these patients carry the JAK2V617F mutation. Although NF-E2 levels correlate with JAK2V671F allele burden in some PV cohorts, the molecular mechanism causing aberrant NF-E2 expression has not been described. Here we show that NF-E2 expression is also increased in patients with essential thrombocythemia and primary myelofibrosis independent of the presence of the JAK2V617F mutation. Characterization of the NF-E2 promoter revealed multiple functional binding sites for AML1/RUNX-1. Chromatin immunoprecipitation demonstrated AML1 binding to the NF-E2 promoter in vivo. Moreover, AML1 binding to the NF-E2 promoter was significantly increased in granulocytes from PV patients compared with healthy controls. AML1 mRNA expression was elevated in patients with PV, essential thrombocythemia, and primary myelofibrosis both in the presence and absence of JAK2V617F. In addition, AML1 and NF-E2 expression were highly correlated. RNAi-mediated suppression of either AML1 or of its binding partner CBF-β significantly decreased NF-E2 expression. Moreover, expression of the leukemic fusion protein AML/ETO drastically decreased NF-E2 protein levels. Our data identify NF-E2 as a novel AML1 target gene and delineate a role for aberrant AML1 expression in mediating elevated NF-E2 expression in MPN patients
    corecore