Neutrophil-to-Lymphocyte Ratio in Acute Cerebral Hemorrhage: a System Review
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Spontaneous intracerebral hemorrhage (ICH) accounts for approximately 10 to 30% of all acute cerebrovascular events, and it is the type of stroke associated with the highest rates of mortality and residual disability. The inflammatory response is early triggered by hematoma components and can enhance the damage within the hemorrhagic brain. Assessment of peripheral biomarkers of inflammation could contribute to increase knowledge about some of the mechanisms involved in the ICH-induced injury and yield information on the disease course. The neutrophil-to-lymphocyte ratio (NLR) integrates information on both the innate and adaptive compartments of the immunity and represents a reliable measure of the inflammatory burden. The aim of the current review is to highlight the available evidence about the relationships between the NLR and clinical outcome in patients with acute ICH and provide critical insights into the underlying pathophysiology. Since no therapy targeting ICH-induced primary injury has yielded conclusive benefits and ICH treatment remains mainly supportive within a framework of general critical care management, these findings could also contribute to identify new potential targets for neuroprotection and develop novel therapeutic strategies.
KeywordsCerebral hemorrhage Stroke Cerebrovascular disease Inflammation Neutrophil-to-lymphocyte ratio
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Conflict of Interest
SL, CC, MDN, and MS declare no conflict of interest. FB has received speakers’ honoraria from Eisai and PeerVoice; payment for consultancy from Eisai; and travel support from Eisai, ITALFARMACO, and UCB Pharma. ET received speaker’s honoraria from UCB, Biogen, Gerot-Lannach, Bial, Eisai, Takeda, Newbridge, Sunovion Pharmaceuticals Inc., and Novartis; consultancy funds from UCB, Biogen, Gerot-Lannach, Bial, Eisai, Takeda, Newbridge, Sunovion Pharmaceuticals Inc., and Novartis; directorship funds from Neuroconsult GmbH; and commercial funds from Biogen, Novartis, and Bayer. E. Trinka’s Institution received grants from Biogen, Red Bull, Merck, UCB, European Union, FWF Österreichischer Fond zur Wissenschaftsförderung, and Bundesministerium für Wissenschaft und Forschung.
This article does not contain any study with human participants performed by any of the authors.
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