Acute splenic responses in patients with ischemic stroke and intracerebral hemorrhage

Abstract

Animal models provide evidence of spleen mediated post-stroke activation of the peripheral immune system. Translation of these findings to stroke patients requires estimation of pre-stroke spleen volume along with quantification of its dayto-day variation. We enrolled a cohort of 158 healthy volunteers and measured their spleen volume over the course of five consecutive days. We also enrolled a concurrent cohort of 158 stroke patients, measured initial spleen volume within 24 h of stroke symptom onset followed by daily assessments. Blood samples for cytokine analysis were collected from a subset of patients. Using data from healthy volunteers, we fit longitudinal quantile regression models to construct gender and body surface area based normograms of spleen volume. We quantified day-to-day variation and defined splenic contraction. Based on our criteria, approximately 40% of stroke patients experienced substantial post-stroke reduction in splenic volume. African Americans, older patients, and patients with past history of stroke have significantly higher odds of post-stroke splenic contraction. All measured cytokine levels were elevated in patients with splenic contraction, with significant differences for interferon gamma, interleukin 6, 10, 12, and 13. Our work provides reference standards for further work, validation of pre-clinical findings, and characterization of patients with post-stroke splenic contraction.

Neuroprotective Properties of a Macrolide Antibiotic in a Mouse Model of Middle Cerebral Artery Occlusion: Characterization of the Immunomodulatory Effects and Validation of the Efficacy of Intravenous Administration

“…[32][33][34][48][49][50][51] Accordingly, splenic contraction in stroke patients is positively correlated with higher circulating levels of several cytokines. 52 Indeed, our data show a clear correlation between ischemia-induced splenic atrophy or azithromycin-induced splenic preservation and the histological outcome, confirming previous evidence. 18,53,54 Interestingly, although splenic preservation by azithromycin was accompanied by a further elevation of activated microglia/macrophages in the ischemic hemisphere, these cells were characterized by an anti-inflammatory phenotype.…”

Prognostic value of elevated cardiac troponin I in patients with intracerebral hemorrhage

“…Given that catecholamine was capable of producing myocardial necrosis, even in the nonischemic heart, the catecholamine surge theory has been reasonable linked to cardiac injury after ICH . In addition, systemic inflammatory responses are activated after ICH and might contribute to myocyte injury and cell death . Several other putative causes were also responsible for the observed elevated cTnI levels, including cardiopulmmonary disease, renal insufficiency, and ICH patients with neurological deterioration .…”

Brain–Heart Interaction

“…Systemic inflammatory responses are activated after spontaneous intracerebral hemorrhage, and ischemic stroke as well as SAH 115 . Systemic inflammatory responses carry an increased risk of subsequent intracranial complications such as vasospasm and normal pressure hydrocephalus, as well as systemic secondary complications 116 .…”