- 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 (5–9).
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.
