Effects of Albumin, Uric Acid, Hemoglobin, and C-Reactive Protein Levels on Rehabilitation Outcomes in Stroke: A Retrospective Clinical Study

 Your competent? doctor has been working on Uric acid, albumin, C-reactive protein and hemoglobin a long time already, right? Oh no, you DON'T have a functioning stroke doctor, do you? And they still haven't been fired yet?

• Uric acid (11 posts to February 2014)

• albumin (5 posts to October 2011)

• C-reactive protein(18 posts to October 2012)
  • hemoglobin A1c (1 post to December 2017)
  • hemoglobin levels (3 posts to February 2024)
  • hemoglobin-albumin cluster (1 post to July 2018)
  • hemoglobin-to-red cell distribution width ratio (1 post to March 2025)
  • oxygenated hemoglobin concentration (1 post to June 2017)
  • glycated hemoglobin levels (1 post to April 2025)

 Effects of Albumin, Uric Acid, Hemoglobin, and C-Reactive Protein Levels on Rehabilitation Outcomes in Stroke: A Retrospective Clinical Study

y Selda Ciftci Inceoglu,1 Aylin Ayyildiz,2 Cansu Adikti,1 Banu Kuran1 1Department of Physical Medicine and Rehabilitation, University of Health Sciences, Sisli Hamidiye Etfal Training and Research Hospital, Istanbul, Türkiye 2Department of Physical Medicine and Rehabilitation, Basaksehir Cam & Sakura City Hospital, Istanbul, Türkiye 

 Objective: 

The aim was to explain the relationship between recovery in motor functions and ambulation skills after stroke and albumin, uric acid, C-reactive protein (CRP), and hemoglobin levels. 

 Materials and Methods: 

Patients who received inpatient rehabilitation in the physical medicine and rehabilitation (PM&R) clinic within the past 2 years were included in the study. Patients’ discharge report, albumin, CRP, uric acid, and hemoglobin levels were obtained from the blood tests taken during hospitalization through the hospital system. The relationship between Brunnstrom staging (BS) and functional ambulation category (FAC) assessments before treatment and on the 15th day of rehabilitation, and the initial albumin, CRP, uric acid, and hemoglobin levels was investigated. 

 Results: 

The files of 135 patients were accessed. Six patients were excluded because they did not meet the inclusion criteria, and 4 patients were excluded because their data were incomplete. The study was completed with 125 patients. Albumin levels were low in 22 (17.6%) patients, and hemoglobin levels were low in 75 (60%) patients. CRP levels were above normal in 53 (42.4%) patients. When uric acid levels were examined, 1 (0.8%) patient was below normal, and 15 (12%) patients were above normal. There was no significant relationship between BS and albumin, CRP, uric acid, and hemoglobin levels (p>0.05). There was a significant positive relationship between improvements in FAC and albumin and hemoglobin levels (p<0.05). 

 Conclusion: 

Post-stroke FAC recovery is associated with albumin and hemoglobin levels. 

 Keywords: 

Albumin, C-reactive protein, Hemoglobin, Stroke, Uric acid 

 Address for correspondence: Selda Ciftci Inceoglu, Department of Physical Medicine and Rehabilitation, University of Health Sciences, Sisli Hamidiye Etfal Training and Research Hospital, Istanbul, Türkiye E-mail: seldavd@gmail.com ORCID ID: 0000-0002-0387-3558 Submitted: 19.05.2025 Revised: 20.05.2025 Accepted: 14.07.2025 Available Online: 12.09.2025 European Archives of Medical Research – Available online at www.eurarchmedres.org OPEN ACCESS This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. ABSTRACT European Archives of Medical Research DOI: 10.14744/eamr.2025.20082 Eur Arch Med Res 2025;41(3):183–192 ORIGINAL ARTICLE INTRODUCTION Stroke is a cerebrovascular disease (CVD) that causes loss of brain function due to interruption of blood flow to the brain or bleeding.[1] It is a significant health problem worldwide. It is a significant cause of morbidity and mortality acquired in adulthood.[2] Most patients develop hemiplegia, affecting upper extremity functions and ambulation skills.[3] Stroke re habilitation is the primary treatment option recommended for functional limitations and disabilities that occur after a stroke.[4] Cite this article as: Ciftci Inceoglu S, Ayyildiz A, Adikti C, Kuran B. Effects of Albumin, Uric Acid, Hemoglobin, and C-Reactive Protein Levels on Rehabilitation Outcomes in Stroke: A Retrospective Clinical Study. Eur Arch Med Res 2025;41(3):183–192.

Uric Acid Stimulates PINK1/Parkin-Mediated Mitophagy via Nrf2/HO-1 Pathway to Protect Against Neuronal Apoptosis in Alzheimer’s Disease

 

 So what the fuck do we do with this information? With nothing to suggest this is totally fucking useless.

But do you want gout because of this?

Gout may lessen Alzheimer risk

Or take this for gout?

Could Old Gout Drug Offer New CV Benefits?

And all this information for your incompetent? doctor to digest, I bet s/he throws up with info overload! Can your doctor get human testing going?

Middle cerebral artery remodeling following transient brain ischemia is linked to early postischemic hyperemia: a target of uric acid treatment February 2015 

Uric Acid Therapy Improves Clinical Outcome in Women With Acute Ischemic Stroke July 2015 

Uric Acid Boosts 'Clot-Busting' Therapy for Stroke July 2015 

Gout Culprit Promising as Acute Stroke Tx - Uric acid February 2014

Uric Acid Contributes to Obesity-Paradox of the Outcome of Ischemic Stroke January 2020  

The latest here:

Uric Acid Stimulates PINK1/Parkin-Mediated Mitophagy via Nrf2/HO-1 Pathway to Protect Against Neuronal Apoptosis in Alzheimer’s Disease

Authors: Qian Zhang https://orcid.org/0009-0005-5231-9229, De Xie, Binyang Chen, Linqian Yu, Jiayu Chen, Yunbo Yan, Mingyan Zhang, Qiang Wang, Yuemei Xi, Tetsuya Yamamoto, Hidenori Koyama, and Jidong Cheng https://orcid.org/0000-0002-5909-5759 jidongcheng36@hotmail.com

Authors Info & Affiliations

Publication: Antioxidants & Redox Signaling

https://doi.org/10.1089/ars.2024.0837

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Abstract

Aims: Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder among the elderly. Uric acid (UA), the end product of purine metabolism, functions as a potent free radical scavenger and helps mitigate oxidative stress. Several epidemiological studies revealed that serum UA levels are negatively correlated with the risk of AD; however, the molecular mechanisms remain unclear. Notably, β-amyloid (Aβ) deposition is implicated in the disruption of mitophagy, leading to neuronal apoptosis. In this study, we aim to elucidate the link between UA and AD and explore the underlying mechanisms.

Results: We demonstrated that UA improved cognitive impairment in 5×FAD mice and reduced neuronal apoptosis both in vivo and in vitro. UA reversed the expression of phosphatase and tensin homolog (PTEN)-induced kinase 1 (PINK1), p-ParkinS65, parkin, microtubule-associated protein 1 light chain 3 II/I, and p62 proteins inhibited by Aβ treatment, alleviated Aβ induced mitochondrial dysfunction, and disturbed dynamics. We found that UA activated nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1(HO-1) signaling both in vivo and in vitro. Furthermore, ML385, a Nrf2-specific inhibitor, reversed the increase in mitochondrial membrane potential and mitophagy promoted by UA and increased neuronal apoptosis in HT22 cells. The antiapoptotic effects of UA in HT22 cells were prevented by treatment with small interfering RNAs targeting PINK1.

Conclusions and Innovation: These data suggest that UA stimulates PINK1/parkin-mediated mitophagy reducing Aβ-induced neuronal apoptosis through the Nrf2/HO-1 pathway, which plays a neuroprotective role in AD. Our findings confirmed that UA effectively reduces neuronal damage and cognitive impairment, highlighting its potential clinical applications in the treatment of AD. Antioxid. Redox Signal. 00, 000–000.

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Increased uric acid to high-density lipoprotein ratio positively correlated with stroke risk

 Your competent? doctor has been working on Uric acid a long time already, right? Oh no, you DON'T have a functioning stroke doctor, do you? And they still haven't been fired yet?

• Uric acid (11 posts to February 2014)

Increased uric acid to high-density lipoprotein ratio positively correlated with stroke risk

Tieshi Zhu^1†Yong He^2†Erxinxian Bei^1,3*

• ¹Department of Neurology, Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, China
• ²Department of Neurology, Liuyang Jili Hospital, Changsha, China
• ³Department of Neurology, Haikou Affiliated Hospital of Central South University Xiangya School of Medicine, Haikou, China

Background: The Uric Acid-to-HDL Ratio (UHR), a novel index derived from serum uric acid and high-density lipoprotein, has been linked to hypertension and poor diabetes control. It has also been shown to predict ischemic heart disease and is strongly associated with collateral circulation and coronary artery flow reserve. However, fewer studies have focused on the relationship between UHR and stroke, highlighting the need for further research in this area.

Methods: The study included 33,192 individuals from the NHANES 1999–2023, of whom 1,363 had a history of stroke. The nonlinear relationship between UHR and stroke risk was assessed using restricted cubic spline (RCS) analysis, and the robustness of the findings was further tested through stratified analysis. Logistic regression was employed to analyze the relationship between UHR and stroke risk, considering both UHR as a continuous variable and its categorization into quartiles (Q1–Q4).

Results: UHR was not nonlinearly associated with stroke (p for overall <0.01; p for nonlinearity = 0.65), and the RCS graph approximated a straight line with a positive slope. UHR was significantly associated with an increased risk of stroke, both when analyzed as a continuous variable (Model 4: OR = 1.02, 95% CI 1.01–1.03, p < 0.01) and when categorized into quartiles (Q4, OR = 1.31, 95% CI 1.11–1.55, p < 0.01).

Conclusion: There was a significant positive correlation between UHR and stroke risk.

Introduction

Stroke remains a leading cause of mortality and disability worldwide, placing a substantial burden on individuals, families, and healthcare systems (1, 2). Given its unfavorable prognosis and the long-term functional impairments experienced by many survivors, a comprehensive understanding and identification of risk factors are essential for effective prevention strategies (3–5).

Traditional risk factors for stroke include hypertension, diabetes mellitus, dyslipidemia, smoking, and alcohol consumption (6–10). Beyond these established factors, elevated serum uric acid (UA) and reduced high-density lipoprotein (HDL) levels have also been implicated in stroke pathogenesis (11, 12). The Uric Acid-to-HDL Ratio (UHR) is a novel and easily accessible index that integrates these two parameters, providing a potential marker for systemic inflammatory and metabolic conditions (13, 14). Studies have demonstrated that UHR outperforms serum uric acid and HDL alone in predicting coronary artery disease and the severity of coronary stenosis (15). Furthermore, UHR has been associated with an increased risk of type 2 diabetes mellitus, metabolic syndrome, myocardial infarction, and all-cause mortality in individuals with diabetes (16–19). However, its relationship with stroke remains inadequately explored. Therefore, this study aims to investigate the association between UHR and stroke using data from the National Health and Nutrition Examination Survey (NHANES) 1999–2023, providing a foundation for future prospective research.

More at link.

Study shows potential of uric acid as add-on therapy for stroke

 
Several earlier studies that your doctor and hospital probably did nothing on to get more research done and protocols created. How fucking incompetent can your stroke medical team be and still be employed?  Human testing needed. Will your doctors and hospital DO ANYTHING AT ALL to get that done? If not, your board of directors is completely incompetent.

Middle cerebral artery remodeling following transient brain ischemia is linked to early postischemic hyperemia: a target of uric acid treatment February 2015 

Uric Acid Therapy Improves Clinical Outcome in Women With Acute Ischemic Stroke July 2015 

Uric Acid Boosts 'Clot-Busting' Therapy for Stroke July 2015 

Gout Culprit Promising as Acute Stroke Tx - Uric acid February 2014

Uric Acid Contributes to Obesity-Paradox of the Outcome of Ischemic Stroke January 2020 

SPAN Study Finds a Winner for Treating Stroke in Rodents February 2023

The latest here:

Study shows potential of uric acid as add-on therapy for stroke

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National Institute of Neurological Disorders and Stroke (NINDS)Mar 17 2025

In a preclinical study, rodents treated with uric acid showed improved long-term outcomes after acute ischemic stroke. The findings suggest that the treatment may work as an add-on therapy to standard stroke treatments in humans. The study was funded by the National Institutes of Health (NIH) and published in Stroke.(Why was this study needed when the February 2023 study already proved that? Everyone in stroke is a complete blithering idiot because they don't know about earlier research? I'd fire everyone in this!) 

Led by Enrique Leira, M.D., and Anil Chauhan, Ph.D., at the University of Iowa, Iowa City, researchers used a well-established rodent model of stroke that closely simulates stroke in humans. They administered intravenous uric acid or saline control and monitored animals' recovery over one month. Behavioral and neurological assessments, including MRI scans, were used to evaluate the treatment's effects.

Mice treated with uric acid had better sensorimotor function—the primary outcome measure—30 days after stroke. More animals in the uric acid group also survived their stroke compared to control animals. However, some secondary outcome measures, such as brain damage, were not reduced.

The research teams used equal numbers of male and female animals and studied older, young, and obese mice, as well as rats with hypertension. Uric acid was efficacious across all groups, suggesting that the treatment could potentially perform well in human trials, including in people with stroke comorbidities.

Ischemic stroke, a leading cause of disability and death in the United States, occurs when a blood clot or other blockage in an artery cuts off blood supply to the brain. Strokes are treated with medications or surgery aimed to break up clots and restore blood flow to affected brain areas. These therapies are highly effective, but not all people fully recover. Using additional treatments that protect brain tissue from damage, either immediately before or during clot removal, could boost the effects of standard treatments and greatly improve recovery in patients.

The study was part of the NIH's Stroke Preclinical Assessment Network (SPAN), a rigorous, transparent approach to preclinical research that mimics clinical trials. SPAN applies standard clinical practices, like randomization and blinded analysis, to animal studies, with the goal of finding agents that are likely to succeed in clinical trials. Recently, the network tested six promising stroke treatments and found one, uric acid, that showed efficacy. The current study described the results of this trial.

The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS) (U01NS113388, U24NS113452) and the National Heart Lung and Blood Institute (R35HL139926).

Source:

National Institute of Neurological Disorders and Stroke (NINDS)

Journal reference:

Patel, R. B., et al. (2025). Uric Acid Stroke Cerebroprotection Transcended Sex, Age, and Comorbidities in a Multicenter Preclinical Trial. Stroke. doi.org/10.1161/strokeaha.124.048748.

Fructose may be fueling the formation of Alzheimer’s disease

How long before your doctor and nutritionist update your stroke diet protocol? Oh wait, I bet you don't have one. Or did you just get the generic crap of do the DASH or Mediterranean diets?
Does your doctor have any stroke rehab knowledge at all? Mine didn't.

• fructose (5 posts to November 2014) In here is where a naked mole rat survives low oxygen levels due to switching from glucose energy in the brain to fructose. Has your doctor or hospital done any followup on this?
  

• High-fructose diet (2 posts to October 2015)

 I bet your doctor and hospital have done nothing on this for these many years.

Fructose may be fueling the formation of Alzheimer’s disease

An ancient human foraging instinct, fueled by fructose production in the brain, may hold clues to the development and possible treatment of Alzheimer's disease (AD), according to researchers at the University of Colorado Anschutz Medical Campus.

The study, published recently in The American Journal of Clinical Nutrition, offers a new way of looking at a fatal disease characterized by abnormal accumulations of proteins in the brain that slowly erode memory and cognition.

"We make the case that Alzheimer's disease is driven by diet," said the study's lead author Richard Johnson, MD, professor at the University of Colorado School of Medicine specializing in renal disease and hypertension. The study co-authors include Maria Nagel, MD, research professor of neurology at the CU School of Medicine.

Johnson and his team suggest that AD is a harmful adaptation of an evolutionary survival pathway used in animals and our distant ancestors during times of scarcity.

"A basic tenet of life is to assure enough food, water and oxygen for survival," the study said. "Much attention has focused on the acute survival responses to hypoxia and starvation. However, nature has developed a clever way to protect animals before the crisis actually occurs."

When threatened with the possibility of starvation, early humans developed a survival response which sent them foraging for food. Yet foraging is only effective if metabolism is inhibited in various parts of the brain. Foraging requires focus, rapid assessment, impulsivity, exploratory behavior and risk taking. It is enhanced by blocking whatever gets in the way, like recent memories and attention to time. Fructose, a kind of sugar, helps damp down these centers, allowing more focus on food gathering.

In fact, the researchers found the entire foraging response was set in motion by the metabolism of fructose whether it was eaten or produced in the body. Metabolizing fructose and its byproduct, intracellular uric acid, was critical to the survival of both humans and animals.

The researchers noted that fructose reduces blood flow to the brain's cerebral cortex involved in self-control, as well as the hippocampus and thalamus. Meanwhile, blood flow increased around the visual cortex associated with food reward. All of this stimulated the foraging response.

We believe that initially the fructose-dependent reduction in cerebral metabolism in these regions was reversible and meant to be beneficial. But chronic and persistent reduction in cerebral metabolism driven by recurrent fructose metabolism leads to progressive brain atrophy and neuron loss with all of the features of AD."

Richard Johnson, MD,Professor, University of Colorado School of Medicine

Johnson suspects the survival response, what he calls the `survival switch,' that helped ancient humans get through periods of scarcity, is now stuck in the `on' position in a time of relative abundance. This leads to the overeating of high fat, sugary and salty food prompting excess fructose production.

Fructose produced in the brain can lead to inflammation and ultimately Alzheimer's disease, the study said. Animals given fructose show memory lapses, a loss in the ability to navigate a maze and inflammation of the neurons.

"A study found that if you keep laboratory rats on fructose long enough they get tau and amyloid beta proteins in the brain, the same proteins seen in Alzheimer's disease," Johnson said. "You can find high fructose levels in the brains of people with Alzheimer's as well."

Johnson suspects that the tendency of some AD patients to wander off might be a vestige of the ancient foraging response.

The study said more research is needed on the role of fructose and uric acid metabolism in AD.

"We suggest that both dietary and pharmacologic trials to reduce fructose exposure or block fructose metabolism should be performed to determine if there is potential benefit in the prevention, management or treatment of this disease," Johnson said.

The study's co-authors include Dean R. Tolan, Dale Bredesen, Laura G. Sanchez-Lozada, Mehdi Fini, Scott Burtis, Miguel A. Lanaspa and David Pearlmutter.

Source:

University of Colorado Anschutz

Journal reference:

Johnson, R.J., et al. (2023) Could Alzheimer's disease be a maladaptation of an evolutionary survival pathway mediated by intracerebral fructose and uric acid metabolism?. American Journal of Clinical Nutrition. doi.org/10.1016/j.ajcnut.2023.01.002

SPAN Study Finds a Winner for Treating Stroke in Rodents

Several earlier studies that your doctor and hospital probably did nothing on to get more research done and protocols created. How fucking incompetent can your stroke medical team be and still be employed?  Human testing needed. Will your doctors and hospital DO ANYTHING AT ALL to get that done? If not, your board of directors is completely incompetent.

Middle cerebral artery remodeling following transient brain ischemia is linked to early postischemic hyperemia: a target of uric acid treatment February 2015 

Uric Acid Therapy Improves Clinical Outcome in Women With Acute Ischemic Stroke July 2015 

Uric Acid Boosts 'Clot-Busting' Therapy for Stroke July 2015 

Gout Culprit Promising as Acute Stroke Tx - Uric acid February 2014

Uric Acid Contributes to Obesity-Paradox of the Outcome of Ischemic Stroke January 2020 

The latest here:

SPAN Study Finds a Winner for Treating Stroke in Rodents

Among six interventions, uric acid exceeded efficacy boundaries

by Elizabeth Short, Staff Writer, MedPage Today February 10, 2023

DALLAS -- Uric acid was shown to be the most successful neuroprotectant among rodents in a study from the Stroke Preclinical Assessment Network (SPAN), a nationwide trial platform that applies clinical research practices to preclinical studies in hopes of better informing human studies.

Of the six interventions studied in the randomized rodent trial, uric acid 16 mg/kg administered intravenously at the time of reperfusion exceeded the efficacy boundaries, reported Lauren H. Sansing, MD, of Yale University in New Haven, Connecticut, and colleagues during the American Stroke Association's International Stroke Conferenceopens in a new tab or window.

The other interventions included the Rho-associated kinase inhibitor fasudil, the PARP inhibitor veliparib, the immunosuppressive drug tocilizumab (Actemra), the S1P analogue fingolimod (Gilenya), and remote ischemic conditioning, which were analyzed via corner test at 28 days.

Three interventions fell below SPAN's inferiority barriers after just the first stage. Only uric acid remained within the study's efficacy boundaries after four stages, ultimately surpassing their original acceptable outcomes.

The study showed that SPAN is an effective preclinical research tool, noted James C. Grotta, MD, a vascular neurologist at Memorial Hermann-Texas Medical Center in Houston, who was not involved in the study.

"The SPAN project entailed a tremendous amount of careful planning and meticulous work by a large team, and kudos to the network for a successful result. The 'winner,' e.g., uric acid, has withstood rigorous testing and the stroke community is now looking forward to the clinical trial of this approach that may complement existing reperfusion strategies," he told MedPage Today.

During a press conference, Sansing explained that "experimental rigor is something we can control. SPAN embraced all of the rigor of a clinical trial."

The study also aimed to "embrace heterogeneity," allowing for some variation in its subjects in an effort to mimic clinical trials, she and her colleagues noted.

Sansing cited growing public distrust in scientific research, recently exacerbated by the COVID-19 pandemic, as part of the reason behind the development of SPAN. Stroke research is no exception. Several neuroprotectant agents have performed well during the course of preclinical trials, but failed to prove effective when introduced in human trials -- a trend that has been documented for decades.

Sansing also pointed to an opinion piece published in Trends in Neurosciencesopens in a new tab or window in 2007 that cited research that showed that as the quality or rigor of a preclinical study on treatments for stroke increased, their efficacy decreased, with the authors noting that animal models for stroke research were "profoundly biased by aspects of study design."

More recent researchopens in a new tab or window compiled evidence listing albumin, the potassium channel activator BMS-204352, and the sodium channel blocker lubeluzole as just a few of many therapies that showed promise as neuroprotectors in animal studies, which then fell short in clinical research on humans.

For this National Institute of Neurological Disorders and Stroke (NINDS)-funded study, six independent labs were used to conduct the research, including Yale University, Massachusetts General Hospital, Johns Hopkins University, the University of Texas Health Science Center at Houston, the Medical College of Georgia at Augusta University, and the University of Iowa.

A total of 2,651 rodents were included in the study, including young mice, aging mice, mice experiencing diet-induced obesity or hyperglycemia, young rats, and spontaneously hypertensive rats, with an equal number of male and female rodents.

After receiving more funding from NINDS, SPAN 2.0 will continue to test neuroprotectants, utilizing six more experimental sites.

The positive results for uric acid, the experimental rigor present in the trials, and the renewal of the SPAN program may bring change to years of issues regarding neuroprotectants, commented Gregory Albers, MD, director of the Stanford Stroke Center in Palo Alto, California, during a Q&A session on SPAN's results.

"I think it's really exciting that the winning drug had a lot of clinical data prior to going into SPAN," he said. "We have seen a number of these agents that have gotten into the human trials where the trial was close but didn't quite make it, some subgroups looked great, and then you repeat, focusing on those subgroups, and then again they didn't make it. What I think we now have is a much higher level of enthusiasm for this drug than what we just had from the prior clinical work that was done for that."

• 

  Elizabeth Short is a staff writer for MedPage Today. She often covers pulmonology and allergy & immunology. Follow

Disclosures

The study was funded by the National Institute of Neurological Disorders and Stroke.

Sansing reported no disclosures. Co-authors reported several relationships with industry.

Primary Source

International Stroke Conference

Source Reference: opens in a new tab or windowSansing LH, et al "Primary results of the Stroke Preclinical Assessment Network" ISC 2023.

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Carotid Plaques From Symptomatic Patients Are Characterized by Local Increase in Xanthine Oxidase Expression

But what about asymptomatic patients? I had zero symptoms until my stroke and yet carotid plaque tore loose which caused a clot to form and them break off and lodge someplace in my middle cerebral artery on my right side. My doctor never told me where  it lodged or what parts of the brain were damaged. In my opinion he was totally fucking useless, knew nothing, did nothing.

 

Carotid Plaques From Symptomatic Patients Are Characterized by Local Increase in Xanthine Oxidase Expression

Morsaleh Ganji

,

Valentina Nardi

,

Megha Prasad

,

Kyra L. Jordan

,

Melanie C. Bois

,

Federico Franchi

,

Xiang Y. Zhu

,

Hui Tang

,

Melissa D. Young

,

Lilach O. Lerman

,

Amir Lerman

Originally published10 Jun 2021https://doi.org/10.1161/STROKEAHA.120.032964Stroke. 2021;52:2792–2801

Abstract

• Download figure
• Download PowerPoint

Background and Purpose:

XO (xanthine oxidase) is a key enzyme of uric acid metabolism and is thought to contribute to oxidative pathways that promote atherosclerotic plaque progression, yet its role in plaque destabilization is not well elucidated. We hypothesized that XO is expressed in carotid plaque from symptomatic patients in association with cardiovascular risk factors.

Methods:

Patients were stratified by symptoms, defined as presentation with an ipsilateral cerebral ischemic event. Carotid atherosclerotic plaques were obtained from 44 patients with symptomatic plaque and 44 patients without ischemic cerebral events. Protein expression of XO was evaluated by immunohistochemical staining and the percentage of cells expressing XO and CD68 (macrophage marker) compared between the groups. Biochemical and demographic cardiometabolic risk factors of study participants also were measured.

Results:

Carotid atherosclerotic plaques from symptomatic patients were associated with significantly higher XO expression versus asymptomatic plaque (median [interquartile range]: 1.24 [2.09] versus 0.16 [0.34]; P<0.001) and with significantly higher circulating uric acid levels (mean±SD: 7.36±2.10 versus 5.37±1.79 mg/dL; P<0.001, respectively). In addition, XO expression in atherosclerotic carotid plaque was inversely associated with serum high-density lipoproteins cholesterol levels (P=0.010, r=−0.30) and directly with circulating uric acid levels (P<0.001, r=0.45). The average percentage of macrophages that expressed XO was significantly higher in symptomatic versus asymptomatic plaques (median [interquartile range]: 93.37% [25] versus 46.15% [21], respectively; P<0.001).

Conclusions:

XO overexpression in macrophages is associated with increased serum uric acid and low high-density lipoproteins cholesterol levels and may potentially have a mechanistic role in carotid plaque destabilization. The current study supports a potential role for uric acid synthesis pathway as a target for management of carotid atherosclerosis in humans.

 

Carotid Plaques From Symptomatic Patients Are Characterized by Local Increase in Xanthine Oxidase Expression

But what about asymptomatic patients? I had zero symptoms until my stroke and yet carotid plaque tore loose which caused a clot to form and them break off and lodge someplace in my middle cerebral artery on my right side. My doctor never told me where  it lodged or what parts of the brain were damaged. In my opinion he was totally fucking useless, knew nothing, did nothing.

Carotid Plaques From Symptomatic Patients Are Characterized by Local Increase in Xanthine Oxidase Expression

Morsaleh Ganji

,

Valentina Nardi

,

Megha Prasad

,

Kyra L. Jordan

,

Melanie C. Bois

,

Federico Franchi

,

Xiang Y. Zhu

,

Hui Tang

,

Melissa D. Young

,

Lilach O. Lerman

,

Amir Lerman

Originally published10 Jun 2021https://doi.org/10.1161/STROKEAHA.120.032964Stroke. ;0:STROKEAHA.120.032964

Abstract

Background and Purpose:

XO (xanthine oxidase) is a key enzyme of uric acid metabolism and is thought to contribute to oxidative pathways that promote atherosclerotic plaque progression, yet its role in plaque destabilization is not well elucidated. We hypothesized that XO is expressed in carotid plaque from symptomatic patients in association with cardiovascular risk factors.

Methods:

Patients were stratified by symptoms, defined as presentation with an ipsilateral cerebral ischemic event. Carotid atherosclerotic plaques were obtained from 44 patients with symptomatic plaque and 44 patients without ischemic cerebral events. Protein expression of XO was evaluated by immunohistochemical staining and the percentage of cells expressing XO and CD68 (macrophage marker) compared between the groups. Biochemical and demographic cardiometabolic risk factors of study participants also were measured.

Results:

Carotid atherosclerotic plaques from symptomatic patients were associated with significantly higher XO expression versus asymptomatic plaque (median [interquartile range]: 1.24 [2.09] versus 0.16 [0.34]; P<0.001) and with significantly higher circulating uric acid levels (mean±SD: 7.36±2.10 versus 5.37±1.79 mg/dL; P<0.001, respectively). In addition, XO expression in atherosclerotic carotid plaque was inversely associated with serum high-density lipoproteins cholesterol levels (P=0.010, r=−0.30) and directly with circulating uric acid levels (P<0.001, r=0.45). The average percentage of macrophages that expressed XO was significantly higher in symptomatic versus asymptomatic plaques (median [interquartile range]: 93.37% [25] versus 46.15% [21], respectively; P<0.001).

Conclusions:

XO overexpression in macrophages is associated with increased serum uric acid and low high-density lipoproteins cholesterol levels and may potentially have a mechanistic role in carotid plaque destabilization. The current study supports a potential role for uric acid synthesis pathway as a target for management of carotid atherosclerosis in humans.

• Download figure
• Download PowerPoint