Yusuke S Hori1, Satoshi Kodera2, Yasunori Sato3, Toshiaki Shiojiri2. 1. Department of Internal Medicine, Asahi General Hospital, Chiba, Japan. Electronic address: ys-hori@umin.ac.jp. 2. Department of Internal Medicine, Asahi General Hospital, Chiba, Japan. 3. Clinical Research Center, Chiba University Hospital, Chiba, Japan.
Abstract
BACKGROUND: Eosinopenia has been shown to be a prognostic factor in bacteremia, chronic obstructive pulmonary disease, and myocardial infarction, but studies focusing on cerebral infarction are lacking. METHODS: We conducted a retrospective study of 405 patients admitted to the Asahi General Hospital from June 2011 to September 2014 with a diagnosis of cerebral infarction within 24 hours after symptom onset. Differences in mortality, mortality associated with infection, and the prevalence of infection within 2 months of hospital admission were assessed between patients with and without eosinopenia at presentation. RESULTS: Patients with eosinopenia had a significantly higher mortality rate (hazard ratio (HR) 2.54, 95% confidence interval (CI) 1.17-5.21, P = .01), mortality associated with infection (HR 28.7, 95% CI 4.9-542.2, P <.0001), and an increased prevalence of infection (HR 1.83, 95% CI 1.12-2.89, P = .01) than patients without eosinopenia. Patients with neutrophilia and eosinopenia showed a significantly higher mortality rate than patients without neutrophilia (HR 3.15, 95% CI 1.40-6.92, P = .007), whereas patients with neutrophilia without eosinopenia showed no significant difference in mortality compared with patients without neutrophilia (HR 1.57, 95% CI .56-3.93, P = .37). Eosinopenia was a significant risk factor in 2-month mortality rate in multivariate analyses (HR 2.34, 95% CI 1.05-4.95, P = .04). CONCLUSIONS: Eosinopenia is a novel predictive factor for complications after acute cerebral infarction. Stroke patients with eosinopenia should be monitored carefully for infection.
BACKGROUND: Eosinopenia has been shown to be a prognostic factor in bacteremia, chronic obstructive pulmonary disease, and myocardial infarction, but studies focusing on cerebral infarction are lacking. METHODS: We conducted a retrospective study of 405 patients admitted to the Asahi General Hospital from June 2011 to September 2014 with a diagnosis of cerebral infarction within 24 hours after symptom onset. Differences in mortality, mortality associated with infection, and the prevalence of infection within 2 months of hospital admission were assessed between patients with and without eosinopenia at presentation. RESULTS:Patients with eosinopenia had a significantly higher mortality rate (hazard ratio (HR) 2.54, 95% confidence interval (CI) 1.17-5.21, P = .01), mortality associated with infection (HR 28.7, 95% CI 4.9-542.2, P <.0001), and an increased prevalence of infection (HR 1.83, 95% CI 1.12-2.89, P = .01) than patients without eosinopenia. Patients with neutrophilia and eosinopenia showed a significantly higher mortality rate than patients without neutrophilia (HR 3.15, 95% CI 1.40-6.92, P = .007), whereas patients with neutrophilia without eosinopenia showed no significant difference in mortality compared with patients without neutrophilia (HR 1.57, 95% CI .56-3.93, P = .37). Eosinopenia was a significant risk factor in 2-month mortality rate in multivariate analyses (HR 2.34, 95% CI 1.05-4.95, P = .04). CONCLUSIONS: Eosinopenia is a novel predictive factor for complications after acute cerebral infarction. Strokepatients with eosinopenia should be monitored carefully for infection.