Plasma levels of inflammatory and thrombotic/fibrinolytic markers in acute ischemic strokes: Relationship with TOAST subtype, outcome and infarct site

Tuttolomondo, Antonino; Sciacca, Riccardo Di; Raimondo, Domenico Di; Serio, Antonia; D'Aguanno, Gisella; Placa, Simona La; Pecoraro, Rosaria; Arnao, Valentina; Marino, Luciana; Monaco, Serena

doi:10.1016/j.jneuroim.2009.06.019

Cited by 83 publications

(90 citation statements)

References 29 publications

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“…In our previous work [120] we compared only lacunar stroke with non-lacunar strokes (LAAS, CEI and ODE), but in this previous work the small number of subjects enrolled (n=60) did not allow us to analyse immuno-inflammatory profile of the acute phase of ischemic stroke of each diagnostic subtype, due to the fact that when divided into subgroups the numbers become even smaller, enhancing the possibility of chance skewing that could become significant. Nevertheless, in our present study we present data of new enrolled 107 (according sample size calculation) patients with ischemic stroke, so it was feasible to divide our enrolled patients into subgroups in relation to TOAST diagnostic subtype and evaluate cytokine, selectins and adhesion molecules with regard to each diagnostic subtype.…”

Section: Inflammation In Acute Stroke Subtypesmentioning

confidence: 99%

Inflammation in Ischemic Stroke Subtypes

Tuttolomondo

Raimondo²,

Pecoraro³

et al. 2012

CPD

Self Cite

127

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Determining the cause of stroke does influence choices for management. categorization of subtypes of ischemic stroke has had considerable study, but definitions are hard to formulate and their application for diagnosis in an individual patient is often problematic. Cerebral ischemia initiates a complex cascade of events at genomic, molecular, and cellular levels, and inflammation is important in this cascade. In 1993 for For the Trial of Org 10172 in Acute Stroke Treatment (TOAST), Adams et al] conducted a placebo-controlled, randomized, blinded study of the low-molecular-weight heparinoid given to patients within 24 hours after stroke and developed a system for diagnosis of subtype of ischemic stroke that uses components of existing diagnostic schemes. The type of acute ischemic stroke was classified according to the TOAST classification: 1) Large Artery AtheroSclerosis (LAAS); 2) CardioEmbolic Infarct (CEI); 3) LACunar infarct (LAC); 4) stroke of Other Determined Etiology (ODE); 5) stroke of UnDetermined Etiology (UDE) (see Fig. (1)). On the basis of pathophysiologic differences of each stroke subtype it's possible to hypothesize a different pattern of immuno-inflammatory activation in relation of ischemic stroke subtype. A nonspecific systemic inflammatory response occurs after both ischemic and hemorrhagic stroke, either as part of the process of brain damage or in response to complications such as deep venous thrombosis. Several studies have reported that higher levels of inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) are associated with worse outcome after ischemic stroke.Our group reported that patients with cardioembolic subtype showed significantly higher median plasma levels of TNF-, IL-6, IL-1 whereas the lacunar subtype showed significantly lower median plasma levels of TNF-, IL-6 and IL-1 . Our findings underlined the significant association was noted between the severity of neurological deficit at admission, the diagnostic subtype and some inflammatory variables.

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Section: Inflammation In Acute Stroke Subtypesmentioning

confidence: 99%

Inflammation in Ischemic Stroke Subtypes

Tuttolomondo

Raimondo²,

Pecoraro³

et al. 2012

CPD

Self Cite

127

View full text Add to dashboard Cite

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“…antiplatelets 25%-38%) (Winbeck et al 2002;Emsley et al 2003;Ladenvall et al 2006;Rallidis et al 2009;Tuttolomondo et al 2009;Whiteley et al 2009). Cytokines expressed locally at sites of tissue inflammation, such as IL-1 and TNF- are not consistently detected in plasma of patients with acute ischaemic stroke compared to controls (Tarkowski et al 1995;Emsley et al 2007), but plasma concentrations of other cytokines (e.g.…”

Section: Inflammation and Outcome Following Ischemic Strokementioning

confidence: 99%

“…(ICAM-1, E/P-selectin) and chemokines (e.g. CXCL16) are elevated early after ischemic stroke and relate to clinical outcome (Rallidis et al 2009;Tuttolomondo et al 2009;Emsley et al 2007;Vila et al 1999;Ueland et al 2012). …”

Section: Inflammation and Outcome Following Ischemic Strokementioning

confidence: 99%

The Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research

Smith

Lawrence

Rodriguez‐Grande

et al. 2013

J Neuroimmune Pharmacol

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Stroke represents an unresolved challenge for both developed and developing countries and has a huge socio-economic impact. Although considerable effort has been made to limit stroke incidence and improve outcome, strategies aimed at protecting injured neurons in the brain have all failed. This failure is likely to be due to both the incompleteness of modelling the disease and its causes in experimental research, and also the lack of understanding of how systemic mechanisms lead to an acute cerebrovascular event or contribute to outcome.Inflammation has been implicated in all forms of brain injury and it is now clear that immune mechanisms profoundly influence (and are responsible for the development of) risk and causation of stroke, and the outcome following the onset of cerebral ischemia. Until very recently, systemic inflammatory mechanisms, with respect to common comorbidities in stroke, have largely been ignored in experimental studies. The main aim is therefore to understand interactions between the immune system and brain injury in order to develop novel therapeutic approaches. Recent data from clinical and experimental research clearly show that systemic inflammatory diseases -such as atherosclerosis, obesity, diabetes or infectionsimilar to stress and advanced age, are associated with dysregulated immune responses which can profoundly contribute to cerebrovascular inflammation and injury in the central nervous system. In this review, we summarize recent advances in the field of inflammation and stroke, focusing on the challenges of translation between pre-clinical and clinical studies, and potential anti-inflammatory/immunomodulatory therapeutic approaches.

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“…34 Similar to adiponectin, the secretion of proinflammatory cytokines was known to be affected by diabetes 35,36 and cardiovascular diseases. [37][38][39] In addition, their levels rose on infection, inflammation or acute stress. 40 To determine the independent effect of obesity on their levels, our analysis was again restricted to data from studies that enrolled clinically evaluated non-intervened healthy subjects.…”

Section: Introductionmentioning

confidence: 99%

Lack of association between body mass index and plasma adiponectin levels in healthy adults

Kuo

2011

Int J Obes

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Objectives: To test the hypothesis that obesity (increase in fat mass) independently affects the level of adipokines: adiponectin, tumor necrosis factor-a (TNFa) and interleukin (IL)-6. Methods: Publications in the past decade reporting adult plasma adiponectin, leptin, TNFa and/or IL-6 levels were compiled. Mean gender-specific values were extracted from studies that included medical screening to confirm physical health (43 groups, total 4852 subjects). Correlation analysis was conducted between adipokine levels and body mass index (BMI), a widely used estimate of adiposity. Results: For healthy lean to obese adults of both genders, no significant correlation between plasma adiponectin and BMI was detected. There was also no gender difference in plasma adiponectin level. In contrast, leptin levels showed a positive correlation with BMI in both genders, and women had significantly higher levels of plasma leptin consistent with a higher percentage of body fat. The proinflammatory cytokine TNFa failed to show correlation with BMI. Although IL-6 showed a positive correlation with BMI in women, the obesity-related increase was very limited. Conclusions: Data analysis based on studies performed on healthy adults did not support the hypothesis that obesity independently affects the plasma level of adiponectin and TNFa. Reported obesity-related changes in plasma adipokine levels may be a consequence of obesity-related metabolic disorders. Future studies are especially needed to understand the homeostasis of adiponectin.

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Plasma levels of inflammatory and thrombotic/fibrinolytic markers in acute ischemic strokes: Relationship with TOAST subtype, outcome and infarct site

Cited by 83 publications

References 29 publications

Inflammation in Ischemic Stroke Subtypes

Inflammation in Ischemic Stroke Subtypes

The Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research

Lack of association between body mass index and plasma adiponectin levels in healthy adults

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