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, July 2, 2024

Serum uric acid as a predictor of mortality in patients with stroke: results from National Health and Nutrition Examination Survey 2007–2016

 Who approved this useless research that predicts mortality rather than prevents it? They need to be fired!

Serum uric acid as a predictor of mortality in patients with stroke: results from National Health and Nutrition Examination Survey 2007–2016

Xinyu TongXinyu Tong1Chuxin LyuChuxin Lyu2Minjie GuoMinjie Guo1Jianxiong GuJianxiong Gu1Yichun Zhao
Yichun Zhao1*
  • 1Department of Neurology, Wuxi Traditional Chinese Medicine Hospital, Wuxi, China
  • 2First Clinical Medical School, Nanjing University of Chinese Medicine, Nanjing, China

Objective: This research endeavors to explore the relationship between serum uric acid (SUA) concentration and all-cause mortality in stroke patients.

Methods: We undertook a cross-sectional analysis utilizing data derived from the National Health and Nutrition Examination Survey (NHANES) spanning 2007 to 2016. The concentrations of SUA served as the independent variable, while the dependent variable was defined as all-cause mortality in stroke patients. The quartile method was utilized to classify uric acid levels into four distinct categories. Subsequently, three models were developed, and Cox proportional hazards regression was used to assess the effect of varying uric acid concentrations on the risk of all-cause mortality among stroke patients.

Results: The study included a total of 10,805 participants, of whom 395 were stroke patients. Among all populations, the group with elevated levels of uric acid (Q4) exhibited a significant association with the overall mortality risk among stroke patients in all three models (model 1 p < 0.001, model 2 p < 0.001, model 3 p < 0.001). In the male population, there was no significant correlation observed between uric acid levels and the overall mortality risk among stroke patients in model 3 (Q2 p = 0.8, Q3 p = 0.2, Q4 p = 0.2). However, within the female population, individuals with high uric acid levels (Q4) demonstrated a noteworthy association with the overall mortality risk among stroke patients across all three models (model 1 p < 0.001, model 2 p < 0.001, model 3 p < 0.001).

Conclusion: This cross-sectional investigation reveals a significant correlation between SUA levels and all-cause mortality in stroke patients, with a noticeable trend observed among females. Consequently, SUA may serve as a promising biomarker for assessing the prognosis(Why? So you can tell your patients they are going to DIE!) of individuals affected by stroke.

Introduction

Stroke, a term encompassing sudden localized or diffuse neurological deficits, is attributed to the disturbance of blood circulation. Sometimes stroke is covert. According to the Global Burden of Diseases, Injuries and Risk Factors Study (GBD) 2017, stroke is ranked as the third leading cause of mortality and disability, quantified by disability-adjusted life years (DALY). Furthermore, it is the second most significant contributor to death and disability (1, 2). In 2017, the global incidence of acute ischemic strokes was approximately 950 per 100,000 individuals (3).

Following a significant long cessation of oxygen supply resulting from blood inflow or outflow disturbance, a sequence of cascading events (4) is initiated, which includes ATP depletion, alterations in sodium, potassium, and calcium ion concentrations, an increase in lactic acid, acidosis, the accumulation of oxygen free radicals, cell edema, and proteolysis. These processes ultimately result in cell death and neurological deficits. Prior research has identified numerous contributing factors to these neurological deficits after a stroke. It has been found that hypertension, suboptimal blood glucose control, smoking, alcohol consumption, and other unhealthy lifestyle habits significantly influence neurological deficits following a stroke (59). Serum uric acid (SUA) serves as a prevalent index in serological tests. Its impact on blood pressure and renal function is notable, particularly due to its role in generating oxidative stress via xanthine oxidase. This enzyme binds with endothelial cells, thereby inhibiting the activity of nitric oxide (NO), which results in vascular damage. Inflammation and damage of blood vessels lead to atherosclerosis, thereby promoting the occurrence and development of stroke.

Several prior meta-analyses have demonstrated that hyperuricemia marginally elevates the risk of stroke morbidity and mortality (10, 11). However, contrasting findings suggest the potential beneficial effects of SUA on the central nervous system (12, 13). Reactive oxygen species, induced by ischemia/reperfusion injury, play a significant role in neuronal cell death. Consequently, the antioxidant properties of SUA may be advantageous for neuronal survival. Currently, only a handful of small-scale studies have indicated that a reduction in serum uric acid (SUA) levels is independently linked to adverse outcomes following acute ischemic stroke (14). Therefore, further research is required to substantiate whether SUA levels can effectively influence the prognosis of stroke patients.

However, limited research has been conducted to explore the relationship between SUA levels and all-cause mortality. The optimal range of SUA levels that could prevent death remains ambiguous, necessitating substantial evidence from the general population to fill these knowledge gaps. Consequently, this study will utilize the public NHANES database, which boasts a large sample size. We conducted a cross-sectional study utilizing pooled data from the NHANES spanning 2007 to 2016, aiming to elucidate the specific association between SUA levels and all-cause mortality in patients with stroke.

More at link.

No comments:

Post a Comment