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Increased globulin and its association with hemorrhagic transformation in patients receiving intra-arterial thrombolysis therapy.

Authors
  • 1
Type
Published Article
Journal
Neuroscience bulletin
1995-8218
Publication Date
Volume
30
Issue
3
Pages
469–476
Identifiers
DOI: 10.1007/s12264-013-1440-x
PMID: 24871645
Source
Medline

Abstract

Previous studies have identified a diverse set of predisposing factors for the occurrence of hemorrhagic transformation (HT), but the independent clinical predictors of HT after intraarterial thrombolysis have not been determined. In this retrospective study, we investigated the characteristics of patients with or without HT who had received intra-arterial thrombolysis therapy, using biochemical analysis, renal function test, routine blood test, blood lipid test, coagulation blood test, liver function test, random blood glucose test, time-window for intra-arterial thrombolysis, recanalization, National Institutes of Health Stroke Scale (NIHSS) score and systolic blood pressure before intra-arterial thrombolysis. The mortality rates were similar in the HT and non-HT groups (P = 0.944). In the single-factor analysis, patients with a higher globulin level (P <0.002), prothrombin time activity percentage (PTA; P = 0.026), and NIHSS score (P = 0.002), had a significantly increased risk of developing HT. In the multifactor logistic regression model involving globulin level, PTA, white blood cell count, and NIHSS score, the globulin level (P <0.001; OR, 1.185; 95% confidence interval [CI], 1.090-1.288), PTA (P = 0.018; OR, 1.016; 95% CI, 1.003-1.029), white blood cell count (P = 0.025; OR, 1.097; 95% CI, 1.012-1.190) and NIHSS score (P = 0.003; OR, 1.097; 95% CI, 1.031-1.166) were significantly increased in the HT group. The increase in globulin level is an independent risk factor for HT in patients receiving intra-arterial thrombolysis. The possible mechanisms may involve inflammatory cytokines, matrix metalloproteinase 9, and positive acute-phase reactants synthesized by the liver.

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