Deans' stroke musings: Plasma Calprotectin Is Predictive for Short-Term Functional Outcomes of Acute Ischemic Stroke

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, March 29, 2022

Plasma Calprotectin Is Predictive for Short-Term Functional Outcomes of Acute Ischemic Stroke

And you really think predicting failure to recover is of ANY FUCKING USE AT ALL TO SURVIVORS?

Plasma Calprotectin Is Predictive for Short-Term Functional Outcomes of Acute Ischemic Stroke

Zicheng Hu¹,

Haihua Li¹,

Yongping Zhu¹,

Jun Zhang¹,

Xiao Yang²,

Rongzhong Huang³,

Yongyong Li³,

Haitao Ran⁴^* and

Tingting Shang⁴^*

¹Department of Neurology, People's Hospital of Chongqing Hechuan (PHHC), Chongqing, China
²Neuroscience Center, General Hospital of Ningxia Medical University, Yinchuan, China
³Department of Gerontology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China
⁴Department of Ultrasound, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China

Background: Blood-based prognostic biomarkers of acute ischemic stroke (AIS) are limiting. Calprotectin is suggested to be involved in directing post-stroke inflammatory conditions. However, the pathological alteration of circulating calprotectin in AIS is yet to be thoroughly elucidated. Therefore, this study aimed to investigate the levels and clinical relevance of calprotectin in AIS.

Methods: This study recruited 271 patients with AIS within 24 h since symptom onset and 145 non-stroke healthy controls (HC) from February 1, 2018, to Dec 31, 2020. Patients were followed up for 2 weeks for observation of functional outcomes, as determined by the National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS). Plasma calprotectin concentrations were determined by ELISA.

Results: Plasma calprotectin concentrations were significantly higher in patients with AIS compared with controls [patients vs. control: median (IQR) 54.2 (39.01–99.04) vs. 50.04 (35.42–61.22), p < 0.001]. Besides, patients with poor prognosis, as defined by mRS ≥ 3, had significantly higher calprotectin levels than patients with good prognosis [poor prognosis patients vs. good prognosis patients: median (IQR) 61.99 (47.52–108) vs. 43.36 (33.39–60.2), p < 0.001]. Plasma calprotectin levels were positively associated with the disease severity of AIS, as reflected by infarction volume and NIHSS score at baseline. Furthermore, baseline calprotectin was found to be independently associated with poor prognosis [odds ratio (OR): 1.02, 95% CI: 1.01–1.03] and disease progression (OR: 1.03, 95% CI: 1.02–1.04) of AIS during a 2-week follow-up, with adjustment of possible confounding factors.

Conclusion: Plasma calprotectin is associated with short-term functional outcomes of AIS.

Introduction

Acute ischemic stroke (AIS) is one of the leading causes of mortality and disability worldwide (1). Over the next years, the global AIS burden is expected to increase steadily because of population aging. The pathophysiology of brain ischemia and post-ischemia changes in the brain are not yet fully understood. Inflammation is increasingly recognized as an important element in the pathogenesis of ischemic stroke. Brain ischemia leads to an immediate local inflammatory reaction with activation of microglia, astrocytes, and endothelial cells, as well as the further release of pro-inflammatory cytokines (2). These non-specific alterations post-ischemia could result in blood-brain barrier dysfunction and infiltration of peripheral inflammatory cells and cytokines into the brain, which may further increase tissue injury (3).

A panel of inflammatory molecules are predictive markers of severity and functional outcomes of AIS; such molecules are proposed as potential therapeutic targets in AIS (4). Calprotectin, which is formed by S100A8 and S100A9 heterodimer, plays a pivotal role in promoting inflammation and atherosclerosis progression. Plasma calprotectin is associated with the risk of coronary artery events (5) and peripheral artery diseases (6). Moreover, circulating calprotectin has been demonstrated to be elevated in AIS (7), and inhibition of S100A9 has been found to suppress thrombus formation in experimental models of AIS (8). However, there is limited evidence currently about the predictive effects of calprotectin on short-term functional outcomes of AIS. Therefore, this study aimed to investigate the potential of circulating calprotectin as a short-term prognostic biomarker of AIS.