Prognostic assessment of acute ischemic stroke by systemic immune-inflammatory index: a comprehensive meta-analysis of multidimensional outcomes

Predicting failure to recover IS ABSOLUTELY FUCKING USELESS! Does no one in stroke have any brains at all?

 Prognostic assessment of acute ischemic stroke by systemic immune-inflammatory index: a comprehensive meta-analysis of multidimensional outcomes

Yanhong Jiang¹Yifan Cui¹Xiaojie Hu²Jiaying Lian³Xueying Qin⁴Xingchen Wang^1,2*Xuran Ma^1*

• ¹The Second Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, China
• ²Department of Neurology, The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China
• ³Department of Neurology, Quzhou Traditional Chinese Medicine Hospital, Quzhou, China
• ⁴The First Clinical Medical College, Beijing University of Traditional Chinese Medicine, Beijing, China

Introduction: Our study aimed to quantify the predictive ability of the Systemic Immune-inflammatory Index (SII) for predicting the prognosis and multidimensional complications in acute ischemic stroke (AIS) patients. The primary outcome was poor prognosis, and secondary outcomes included mortality, severity, hemorrhagic transformation/symptomatic intracerebral hemorrhage, stroke-associated pneumonia/poststroke pneumonia, early neurological deterioration, post-stroke depression, progression or recurrence, and other adverse outcomes.

Methods: We searched 15 databases from their establishment to 13 October 2024 and selected cohort or case-control analyses that analyzed the association of continuous or categorized SII as exposures with the above adverse outcomes of AIS populations.

Results: The results showed that 78 studies with 40,682 participants were included in meta-analyses. Continuous SII values were significantly higher in poor prognosis groups than in controls (SMD = 248.13, 95% CI: 198.77 to 297.50; p = 0.000). Poor prognosis incidences rose with higher continuous SII values (OR = 1.004, 95% CI: 1.002 to 1.005; p = 0.000). More patients in High SII groups had poor prognosis (RR = 1.95, 95% CI: 1.66 to 2.28; p = 0.000). The risk of poor prognosis was higher in the high SII groups, though this was not statistically significant (OR = 1.007, 95% CI: 0.998 to 1.015; p = 0.120).

Discussion: In conclusion, our study found that continuous SII and high SII were associated with poor prognosis of AIS and various complications. Given the accessibility and low cost of SII, integrating it into prognostic scores merits further research for better clinical choices.

Systematic review registration: PROSPERO (CRD42024586414), https://www.crd.york.ac.uk/PROSPERO/view/CRD42024586414.

Antigen-specific immune reactions to ischemic stroke

I'm not sure how this will help us so ask your doctors what they will do with this information. Hopefully not scoff at you. Mine pretty much did when I asked about specific research articles. I doubt he had read anything new since medical school. That lack of acquiring knowledge needs to be brought up to the hospital president because that means the stroke department head is not setting proper goals and expectations. 

Antigen-specific immune reactions to ischemic stroke

http://journal.frontiersin.org/Journal/10.3389/fncel.2014.00278/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w41-2014
Xabier Urra^1,2, Francesc Miró², Angel Chamorro^1,2 and Anna M. Planas^2,3*

• ¹Functional Unit of Cerebrovascular Diseases, Hospital Clínic, Barcelona, Spain
• ²August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain
• ³Department of Brain Ischemia and Neurodegeneration, Instituto de Investigaciones Biomédicas de Barcelona (IIBB), Consejo Superior de Investigaciones Científicas (CSIC), Barcelona, Spain

Brain proteins are detected in the cerebrospinal fluid (CSF) and blood of stroke patients and their concentration is related to the extent of brain damage. Antibodies against brain antigens develop after stroke, suggesting a humoral immune response to the brain injury. Furthermore, induced immune tolerance is beneficial in animal models of cerebral ischemia. The presence of circulating T cells sensitized against brain antigens, and antigen presenting cells (APCs) carrying brain antigens in draining lymphoid tissue of stroke patients support the notion that stroke might induce antigen-specific immune responses. After stroke, brain proteins that are normally hidden from the periphery, inflammatory mediators, and danger signals can exit the brain through several efflux routes. They can reach the blood after leaking out of the damaged blood-brain barrier (BBB) or following the drainage of interstitial fluid to the dural venous sinus, or reach the cervical lymph nodes through the nasal lymphatics following CSF drainage along the arachnoid sheaths of nerves across the nasal submucosa. The route and mode of access of brain antigens to lymphoid tissue could influence the type of response. Central and peripheral tolerance prevents autoimmunity, but the actual mechanisms of tolerance to brain antigens released into the periphery in the presence of inflammation, danger signals, and APCs, are not fully characterized. Stroke does not systematically trigger autoimmunity, but under certain circumstances, such as pronounced systemic inflammation or infection, autoreactive T cells could escape the tolerance controls. Further investigation is needed to elucidate whether antigen-specific immune events could underlie neurological complications impairing recovery from stroke.