Abstract

Introduction: Preclinical models suggest an inflammatory response mediated by monocytes may contribute to secondary injury after intracerebral hemorrhage (ICH). We recently found an association of absolute monocyte count (AMC) with 30-day case fatality following ICH. We sought to validate this finding in an independent cohort of ICH patients. Hypothesis: AMC is independently associated with 30-day case-fatality following ICH. Methods: The Ethnic/Racial Variations of ICH (ERICH) study is a prospective, multi-center, case-control study of ICH among Caucasian, Black, and Hispanic patients. In 241 adult patients with nontraumatic ICH within 24 hours of symptom onset, demographic information, Glasgow Coma Scale (GCS), ICH volume, 30-day case-fatality, total white blood cell (WBC) count, absolute neutrophil count (ANC), AMC, and hemoglobin concentration were determined. Participating centers were requested to obtain WBC differentials on the 30 most recently enrolled cases. After receiving data on 411 subjects, we excluded 170 subjects whose initial WBC was >24 hours from onset and in those where monocytes and neutrophils were not available, resulting in 241 cases for the analysis. Linear regression was used to evaluate factors associated with ICH volume (log transformed), and logistic regression for factors associated with 30-day case-fatality. Results: Mean age was 62.8 years (SD ± 14 years), 61.8% were men and 33.6% were Black. Median ICH volume was 9.7ml (IQR 4.3-26.7). After adjusting for patient age and initial hemoglobin, higher ANC (p= 0.001) and total WBC count (p=0.0005) were associated with larger ICH volume, whereas AMC was not (p=0.14). After adjusting for age, GCS, and ICH volume, baseline AMC was independently associated with higher 30-day case-fatality (OR 5.24, 95% CI 1.62-16.89, p=0.0056) whereas ANC (OR 0.85, CI 0.15-4.68, p=0.85) and WBC count (OR 0.58, CI 0.04-7.67, p=0.68) were not. Conclusions: In this independent cohort an association between higher admission monocytes and case fatality was corroborated independent of known clinical variables. This suggests a specific role of monocytes in secondary injury following ICH. Inflammatory and neuronal apoptotic pathways mediated by monocytes may be a target for neuroprotection in ICH.

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