Abstract
BackgroundInflammatory mechanism has been implicated in delayed cerebral ischemia (DCI) and poor functional outcomes after subarachnoid hemorrhage (SAH). Identification of cytokine patterns associated with inflammation in acute SAH will provide insights into underlying biological processes of DCI and poor outcomes that may be amenable to interventions.MethodsSerum samples were collected from a prospective cohort of 60 patients with acute non-traumatic SAH at four time periods (< 24 h, 24–48 h, 3–5 days, and 6–8 days after SAH) and concentration levels of 41 cytokines were measured by multiplex immunoassay. Logistic regression analysis was used to identify cytokines associated with DCI and poor functional outcomes. Correlation networks were constructed to identify cytokine clusters.ResultsOf the 60 patients enrolled in the study, 14 (23.3%) developed DCI and 16 (26.7%) had poor functional outcomes at 3 months. DCI was associated with increased levels of PDGF-ABBB and CCL5 and decreased levels of IP-10 and MIP-1α. Poor functional outcome was associated with increased levels of IL-6 and MCP-1α. Network analysis identified distinct cytokine clusters associated with DCI and functional outcomes.ConclusionsSerum cytokine patterns in early SAH are associated with poor functional outcomes and DCI. The significant cytokines primarily modulate the inflammatory response. This supports earlier SAH studies linking inflammation and poor outcomes. In particular, this study identifies novel cytokine patterns over time that may indicate impending DCI.
Highlights
Aneurysmal subarachnoid hemorrhage (SAH) is a devastating disease caused by the sudden rupture of an intracranial aneurysm which is associated with a high risk of death or severe disability [1]
SAH induces a peripheral immune response and activated peripheral immune cells are recruited to the brain parenchyma [11] where they release cytokines [12] that induce the upregulation of intrinsic receptors leading to widespread inflammation [13]
Study population Patients with acute SAH admitted to the Neuroscience Intensive Care Unit at the Memorial Herman HospitalTexas Medical Center, Houston, TX, between July 2013 and March 2015 were enrolled in a prospective observational study
Summary
Aneurysmal subarachnoid hemorrhage (SAH) is a devastating disease caused by the sudden rupture of an intracranial aneurysm which is associated with a high risk of death or severe disability [1]. In those who survive the initial event, injury expansion after SAH can exacerbate underlying brain injury leading to secondary neurological injuries and poor functional outcomes [2, 3]. Inflammatory mechanism has been implicated in delayed cerebral ischemia (DCI) and poor functional outcomes after subarachnoid hemorrhage (SAH). Identification of cytokine patterns associated with inflammation in acute SAH will provide insights into underlying biological processes of DCI and poor outcomes that may be amenable to interventions
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