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  1. Sabrina Paganoni, May Zhang, Alejandro Quiroz Zárate, Matthew Jaffa, Hong Yu, Merit E Cudkowicz and Anne-Marie Wills.
    Uric acid levels predict survival in men with amyotrophic lateral sclerosis.. Journal of neurology 259(9):1923–8, 2012.
    Abstract {Elevated uric acid levels have recently been found to be associated with slower disease progression in Parkinson's disease, Huntington's disease, multiple system atrophy, and mild cognitive impairment. The aim of this study is to determine whether serum uric acid levels predict survival in amyotrophic lateral sclerosis (ALS). A total of 251 people with ALS enrolled in two multicenter clinical trials were included in our analysis. The main outcome measure was survival time, which was calculated as time to death, tracheostomy, or permanent assistive ventilation, with any event considered a survival endpoint. Cox proportional hazards models were used to estimate the hazard ratio (HR) of reaching a survival endpoint according to baseline uric acid levels after adjusting for markers of disease severity (FVC, total ALSFRS-R score, time since symptom onset, diagnostic delay, BMI, bulbar vs. spinal onset, age, and riluzole use). There was a dose-dependent survival advantage in men, but not women, with higher baseline uric acid levels (logrank test: p = 0.018 for men
    URL, DOI BibTeX

    @article{Paganoni2012,
    	abstract = "{Elevated uric acid levels have recently been found to be associated with slower disease progression in Parkinson's disease, Huntington's disease, multiple system atrophy, and mild cognitive impairment. The aim of this study is to determine whether serum uric acid levels predict survival in amyotrophic lateral sclerosis (ALS). A total of 251 people with ALS enrolled in two multicenter clinical trials were included in our analysis. The main outcome measure was survival time, which was calculated as time to death, tracheostomy, or permanent assistive ventilation, with any event considered a survival endpoint. Cox proportional hazards models were used to estimate the hazard ratio (HR) of reaching a survival endpoint according to baseline uric acid levels after adjusting for markers of disease severity (FVC, total ALSFRS-R score, time since symptom onset, diagnostic delay, BMI, bulbar vs. spinal onset, age, and riluzole use). There was a dose-dependent survival advantage in men, but not women, with higher baseline uric acid levels (logrank test: p = 0.018 for men",
    	p = "",
    	author = "Paganoni, Sabrina and Zhang, May and {Quiroz Z\'{a}rate}, Alejandro and Jaffa, Matthew and Yu, Hong and Cudkowicz, Merit E and Wills, Anne-Marie",
    	doi = "10.1007/s00415-012-6440-7",
    	issn = "1432-1459",
    	journal = "Journal of neurology",
    	keywords = "Adult,Aged,Amyotrophic Lateral Sclerosis,Amyotrophic Lateral Sclerosis: blood,Amyotrophic Lateral Sclerosis: mortality,Female,Humans,Male,Middle Aged,Neuroprotective Agents,Proportional Hazards Models,Sex Characteristics,Survival Analysis,Uric Acid,Uric Acid: blood",
    	month = "",
    	number = 9,
    	pages = "1923--8",
    	pmid = 22323210,
    	title = "{Uric acid levels predict survival in men with amyotrophic lateral sclerosis.}",
    	url = "http://www.mendeley.com/research/uric-acid-levels-predict-survival-men-amyotrophic-lateral-sclerosis/",
    	volume = 259,
    	year = 2012
    }
    
  2. Daniel I Feig.
    Uric acid and hypertension.. Seminars in nephrology 31(5):441–6, September 2011.
    Abstract A link between serum uric acid and the development of hypertension was first hypothesized in the 1870s. Although numerous epidemiologic studies in the 1980s and 1990s suggested an association, relatively little attention was paid to it until recently. Animal models have suggested a two-step pathogenesis by which uric acid initially activates the renin angiotensin system and suppresses nitric oxide, leading to uric acid-dependent increase in systemic vascular resistance, followed by a uric acid-mediated vasculopathy, involving renal afferent arterioles, resulting in a late sodium-sensitive hypertension. Initial clinical trials in young patients have supported these mechanisms in young patients but do not yet support pharmacologic reduction of serum uric acid as first-line therapy for hypertension.
    URL, DOI BibTeX

    @article{Feig2011,
    	abstract = "A link between serum uric acid and the development of hypertension was first hypothesized in the 1870s. Although numerous epidemiologic studies in the 1980s and 1990s suggested an association, relatively little attention was paid to it until recently. Animal models have suggested a two-step pathogenesis by which uric acid initially activates the renin angiotensin system and suppresses nitric oxide, leading to uric acid-dependent increase in systemic vascular resistance, followed by a uric acid-mediated vasculopathy, involving renal afferent arterioles, resulting in a late sodium-sensitive hypertension. Initial clinical trials in young patients have supported these mechanisms in young patients but do not yet support pharmacologic reduction of serum uric acid as first-line therapy for hypertension.",
    	author = "Feig, Daniel I",
    	doi = "10.1016/j.semnephrol.2011.08.008",
    	issn = "1558-4488",
    	journal = "Seminars in nephrology",
    	keywords = "Animals,Humans,Hypertension,Hypertension: etiology,Hyperuricemia,Hyperuricemia: complications,Uric Acid,Uric Acid: metabolism",
    	month = "sep",
    	number = 5,
    	pages = "441--6",
    	pmid = 22000651,
    	title = "{Uric acid and hypertension.}",
    	url = "http://www.mendeley.com/research/uric-acid-hypertension/",
    	volume = 31,
    	year = 2011
    }
    
  3. Alexander So and Bernard Thorens.
    Uric acid transport and disease.. The Journal of clinical investigation 120(6):1791–9, June 2010.
    Abstract Uric acid is the metabolic end product of purine metabolism in humans. It has antioxidant properties that may be protective but can also be pro-oxidant, depending on its chemical microenvironment. Hyperuricemia predisposes to disease through the formation of urate crystals that cause gout, but hyperuricemia, independent of crystal formation, has also been linked with hypertension, atherosclerosis, insulin resistance, and diabetes. We discuss here the biology of urate metabolism and its role in disease. We also cover the genetics of urate transport, including URAT1, and recent studies identifying SLC2A9, which encodes the glucose transporter family isoform Glut9, as a major determinant of plasma uric acid levels and of gout development.
    URL, DOI BibTeX

    @article{So2010,
    	abstract = "Uric acid is the metabolic end product of purine metabolism in humans. It has antioxidant properties that may be protective but can also be pro-oxidant, depending on its chemical microenvironment. Hyperuricemia predisposes to disease through the formation of urate crystals that cause gout, but hyperuricemia, independent of crystal formation, has also been linked with hypertension, atherosclerosis, insulin resistance, and diabetes. We discuss here the biology of urate metabolism and its role in disease. We also cover the genetics of urate transport, including URAT1, and recent studies identifying SLC2A9, which encodes the glucose transporter family isoform Glut9, as a major determinant of plasma uric acid levels and of gout development.",
    	author = "So, Alexander and Thorens, Bernard",
    	doi = "10.1172/JCI42344",
    	file = ":C$\backslash$:/Users/riku/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/So, Thorens - 2010 - Uric acid transport and disease.pdf:pdf",
    	issn = "1558-8238",
    	journal = "The Journal of clinical investigation",
    	keywords = "Animals,Biological Transport,Biological Transport: genetics,Glucose Transport Proteins, Facilitative,Glucose Transport Proteins, Facilitative: genetics,Glucose Transport Proteins, Facilitative: metaboli,Gout,Gout: etiology,Gout: genetics,Gout: metabolism,Humans,Hypertension,Hypertension: complications,Hypertension: genetics,Hypertension: metabolism,Hyperuricemia,Hyperuricemia: etiology,Hyperuricemia: genetics,Hyperuricemia: metabolism,Uric Acid,Uric Acid: blood,Uric Acid: metabolism",
    	month = "jun",
    	number = 6,
    	pages = "1791--9",
    	pmid = 20516647,
    	title = "{Uric acid transport and disease.}",
    	url = "http://www.mendeley.com/research/uric-acid-transport-disease/",
    	volume = 120,
    	year = 2010
    }
    
  4. Marilda Mazzali, Mehmet Kanbay, Mark S Segal, Mohamed Shafiu, Diana Jalal, Daniel I Feig and Richard J Johnson.
    Uric acid and hypertension: cause or effect?. Current rheumatology reports 12(2):108–17, 2010.
    Abstract Uric acid was first associated with primary hypertension in 1874, yet its role in this condition remains unclear. Historically, uric acid was thought to be a secondary response to hypertension or its associated conditions. However, more recent experimental and clinical studies suggest that uric acid could have a contributory role in the pathogenesis of elevated blood pressure. More studies are needed to help dissect the potential mechanisms by which uric acid could initiate this response. It remains possible that uric acid is a marker for xanthine oxidase-associated oxidants and that the latter could be driving the hypertensive response. However, the weight of the evidence suggests that uric acid is a true modifying and possibly causal factor for human primary hypertension. Hence, early management of hyperuricemia might delay the development of essential hypertension.
    URL, DOI BibTeX

    @article{Mazzali2010,
    	abstract = "Uric acid was first associated with primary hypertension in 1874, yet its role in this condition remains unclear. Historically, uric acid was thought to be a secondary response to hypertension or its associated conditions. However, more recent experimental and clinical studies suggest that uric acid could have a contributory role in the pathogenesis of elevated blood pressure. More studies are needed to help dissect the potential mechanisms by which uric acid could initiate this response. It remains possible that uric acid is a marker for xanthine oxidase-associated oxidants and that the latter could be driving the hypertensive response. However, the weight of the evidence suggests that uric acid is a true modifying and possibly causal factor for human primary hypertension. Hence, early management of hyperuricemia might delay the development of essential hypertension.",
    	author = "Mazzali, Marilda and Kanbay, Mehmet and Segal, Mark S and Shafiu, Mohamed and Jalal, Diana and Feig, Daniel I and Johnson, Richard J",
    	doi = "10.1007/s11926-010-0094-1",
    	issn = "1534-6307",
    	journal = "Current rheumatology reports",
    	keywords = "Allopurinol,Allopurinol: therapeutic use,Blood Pressure,Blood Pressure: physiology,Gout Suppressants,Gout Suppressants: therapeutic use,Humans,Hypertension,Hypertension: blood,Hypertension: complications,Hypertension: physiopathology,Hyperuricemia,Hyperuricemia: complications,Hyperuricemia: drug therapy,Hyperuricemia: physiopathology,Uric Acid,Uric Acid: blood",
    	month = "",
    	number = 2,
    	pages = "108--17",
    	pmid = 20425019,
    	title = "{Uric acid and hypertension: cause or effect?}",
    	url = "http://www.mendeley.com/research/uric-acid-hypertension-cause-effect/",
    	volume = 12,
    	year = 2010
    }
    
  5. Fabio Martinon.
    Mechanisms of uric acid crystal-mediated autoinflammation.. Immunological reviews 233(1):218–32, January 2010.
    Abstract Gout is an arthritis characterized by elevated uric acid in the bloodstream. In this condition, crystals of uric acid are formed and accumulate in the synovial fluids. Crystal deposition leads to acute inflammation, which is associated with the spontaneous resolution of the disease. Recent studies have led to significant advances in the understanding of the basic biology of crystal-mediated inflammation. Uric acid has been identified as a danger signal that triggers a cytosolic sensor, the inflammasome. This signaling platform is required for the activation of interleukin-1, a cytokine that is critical to the initiation of acute inflammation in gout. Importantly, both molecular and pathological evidence support the notion that gout is a prototypical member of the growing family of autoinflammatory diseases. This review discusses the role of the inflammasome in gout and the emerging new therapeutic strategies aimed at controlling inflammation in crystal arthritis.
    URL, DOI BibTeX

    @article{Martinon2010,
    	abstract = "Gout is an arthritis characterized by elevated uric acid in the bloodstream. In this condition, crystals of uric acid are formed and accumulate in the synovial fluids. Crystal deposition leads to acute inflammation, which is associated with the spontaneous resolution of the disease. Recent studies have led to significant advances in the understanding of the basic biology of crystal-mediated inflammation. Uric acid has been identified as a danger signal that triggers a cytosolic sensor, the inflammasome. This signaling platform is required for the activation of interleukin-1, a cytokine that is critical to the initiation of acute inflammation in gout. Importantly, both molecular and pathological evidence support the notion that gout is a prototypical member of the growing family of autoinflammatory diseases. This review discusses the role of the inflammasome in gout and the emerging new therapeutic strategies aimed at controlling inflammation in crystal arthritis.",
    	author = "Martinon, Fabio",
    	doi = "10.1111/j.0105-2896.2009.00860.x",
    	issn = "1600-065X",
    	journal = "Immunological reviews",
    	keywords = "Animals,Arthritis, Gouty,Arthritis, Gouty: immunology,Arthritis, Gouty: therapy,Autoimmunity,Crystallization,Humans,Immunity, Innate,Inflammation Mediators,Inflammation Mediators: immunology,Signal Transduction,Signal Transduction: immunology,Uric Acid,Uric Acid: immunology",
    	month = "jan",
    	number = 1,
    	pages = "218--32",
    	pmid = 20193002,
    	title = "{Mechanisms of uric acid crystal-mediated autoinflammation.}",
    	url = "http://www.mendeley.com/research/mechanisms-uric-acid-crystalmediated-autoinflammation/",
    	volume = 233,
    	year = 2010
    }
    
  6. Hajime Kono, Chun-Jen Chen, Fernando Ontiveros and Kenneth L Rock.
    Uric acid promotes an acute inflammatory response to sterile cell death in mice.. The Journal of clinical investigation 120(6):1939–49, 2010.
    Abstract Necrosis stimulates inflammation, and this response is medically relevant because it contributes to the pathogenesis of a number of diseases. It is thought that necrosis stimulates inflammation because dying cells release proinflammatory molecules that are recognized by the immune system. However, relatively little is known about the molecular identity of these molecules and their contribution to responses in vivo. Here, we investigated the role of uric acid in the inflammatory response to necrotic cells in mice. We found that dead cells not only released intracellular stores of uric acid but also produced it in large amounts postmortem as nucleic acids were degraded. Using newly developed Tg mice that have reduced levels of uric acid either intracellularly and/or extracellularly, we found that uric acid depletion substantially reduces the cell death-induced inflammatory response. Similar results were obtained with pharmacological treatments that reduced uric acid levels either by blocking its synthesis or hydrolyzing it in the extracellular fluids. Importantly, uric acid depletion selectively inhibited the inflammatory response to dying cells but not to microbial molecules or sterile irritant particles. Collectively, our data identify uric acid as a proinflammatory molecule released from dying cells that contributes significantly to the cell death-induced inflammatory responses in vivo.
    URL, DOI BibTeX

    @article{Kono2010,
    	abstract = "Necrosis stimulates inflammation, and this response is medically relevant because it contributes to the pathogenesis of a number of diseases. It is thought that necrosis stimulates inflammation because dying cells release proinflammatory molecules that are recognized by the immune system. However, relatively little is known about the molecular identity of these molecules and their contribution to responses in vivo. Here, we investigated the role of uric acid in the inflammatory response to necrotic cells in mice. We found that dead cells not only released intracellular stores of uric acid but also produced it in large amounts postmortem as nucleic acids were degraded. Using newly developed Tg mice that have reduced levels of uric acid either intracellularly and/or extracellularly, we found that uric acid depletion substantially reduces the cell death-induced inflammatory response. Similar results were obtained with pharmacological treatments that reduced uric acid levels either by blocking its synthesis or hydrolyzing it in the extracellular fluids. Importantly, uric acid depletion selectively inhibited the inflammatory response to dying cells but not to microbial molecules or sterile irritant particles. Collectively, our data identify uric acid as a proinflammatory molecule released from dying cells that contributes significantly to the cell death-induced inflammatory responses in vivo.",
    	author = "Kono, Hajime and Chen, Chun-Jen and Ontiveros, Fernando and Rock, Kenneth L",
    	doi = "10.1172/JCI40124",
    	file = ":C$\backslash$:/Users/riku/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Kono et al. - 2010 - Uric acid promotes an acute inflammatory response to sterile cell death in mice.pdf:pdf",
    	isbn = "doi:10.1172/JCI40124",
    	issn = "1558-8238",
    	journal = "The Journal of clinical investigation",
    	keywords = "Animals,Cell Death,Cell Death: drug effects,Cell Death: immunology,Cells,Cells: metabolism,Immune System,Immune System: metabolism,Inflammation,Inflammation: immunology,Inflammation: metabolism,Mice,Mice, Inbred C57BL,Mice, Inbred Strains,Mice, Transgenic,Necrosis,Uric Acid,Uric Acid: metabolism,Uric Acid: pharmacology",
    	month = "",
    	number = 6,
    	pages = "1939--49",
    	pmid = 20501947,
    	title = "{Uric acid promotes an acute inflammatory response to sterile cell death in mice.}",
    	url = "http://www.mendeley.com/research/uric-acid-promotes-acute-inflammatory-response-sterile-cell-death-mice/",
    	volume = 120,
    	year = 2010
    }
    
  7. Gene L Bowman, Jackilen Shannon, Balz Frei, Jeffrey A Kaye and Joseph F Quinn.
    Uric acid as a CNS antioxidant.. Journal of Alzheimer's disease : JAD 19(4):1331–6, 2010.
    Abstract {Oxidative damage is a consistent finding in a number of central nervous system (CNS) disorders. Uric acid (UA) is a potent hydrophilic antioxidant that is modified by diet and drug. Several lines of evidence suggest that plasma UA may modulate outcomes in neurologic disease, but little attention has been paid to CNS levels of UA. Our objective was to test the hypothesis that cerebrospinal fluid (CSF) UA is determined by plasma UA, modified by blood-brain barrier (BBB) integrity and associated with rate of cognitive decline in Alzheimer's disease (AD). Also, since UA and ascorbic acid may act as antioxidants for one another, we also explored a potential interaction between them in the brain. Thirty-two patients with mild to moderate AD (Mini-Mental Status Exam 19 +/- 5) participated in a longitudinal biomarker study for one year involving standardized clinical assessments. CSF and blood were collected at baseline for UA, ascorbic acid, and albumin. Cognitive measures were collected at baseline and again one year later. CSF UA was independent of age, gender, and AD severity. CSF and plasma UA were positively correlated (r=0.669
    URL, DOI BibTeX

    @article{Bowman2010,
    	abstract = "{Oxidative damage is a consistent finding in a number of central nervous system (CNS) disorders. Uric acid (UA) is a potent hydrophilic antioxidant that is modified by diet and drug. Several lines of evidence suggest that plasma UA may modulate outcomes in neurologic disease, but little attention has been paid to CNS levels of UA. Our objective was to test the hypothesis that cerebrospinal fluid (CSF) UA is determined by plasma UA, modified by blood-brain barrier (BBB) integrity and associated with rate of cognitive decline in Alzheimer's disease (AD). Also, since UA and ascorbic acid may act as antioxidants for one another, we also explored a potential interaction between them in the brain. Thirty-two patients with mild to moderate AD (Mini-Mental Status Exam 19 +/- 5) participated in a longitudinal biomarker study for one year involving standardized clinical assessments. CSF and blood were collected at baseline for UA, ascorbic acid, and albumin. Cognitive measures were collected at baseline and again one year later. CSF UA was independent of age, gender, and AD severity. CSF and plasma UA were positively correlated (r=0.669",
    	p = "",
    	author = "Bowman, Gene L and Shannon, Jackilen and Frei, Balz and Kaye, Jeffrey A and Quinn, Joseph F",
    	doi = "10.3233/JAD-2010-1330",
    	file = ":C$\backslash$:/Users/riku/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Bowman et al. - 2010 - Uric acid as a CNS antioxidant.pdf:pdf",
    	issn = "1875-8908",
    	journal = "Journal of Alzheimer's disease : JAD",
    	keywords = "Aged,Alzheimer Disease,Alzheimer Disease: prevention \& control,Antioxidants,Antioxidants: pharmacology,Antioxidants: therapeutic use,Ascorbic Acid,Ascorbic Acid: cerebrospinal fluid,Ascorbic Acid: pharmacology,Ascorbic Acid: therapeutic use,Blood-Brain Barrier,Blood-Brain Barrier: drug effects,Brain,Brain: drug effects,Female,Humans,Male,Uric Acid,Uric Acid: cerebrospinal fluid,Uric Acid: pharmacology,Uric Acid: therapeutic use",
    	month = "",
    	number = 4,
    	pages = "1331--6",
    	pmid = 20061611,
    	title = "{Uric acid as a CNS antioxidant.}",
    	url = "http://www.mendeley.com/research/uric-acid-cns-antioxidant/",
    	volume = 19,
    	year = 2010
    }
    
  8. Mladen Boban and Darko Modun.
    Uric Acid and Antioxidant Effects of Wine. Croatian Medical Journal 51(1):16–22, 2010.
    URL, DOI BibTeX

    @article{Boban2010,
    	author = "Boban, Mladen and Modun, Darko",
    	doi = "10.3325/cmj.2010.51.16",
    	issn = "0353-9504",
    	journal = "Croatian Medical Journal",
    	month = "",
    	number = 1,
    	pages = "16--22",
    	title = "{Uric Acid and Antioxidant Effects of Wine}",
    	url = "http://www.mendeley.com/research/uric-acid-antioxidant-effects-wine/",
    	volume = 51,
    	year = 2010
    }
    
  9. Yuri Y Sautin and Richard J Johnson.
    Uric acid: the oxidant-antioxidant paradox.. Nucleosides, nucleotides & nucleic acids 27(6):608–19, June 2008.
    Abstract Uric acid, despite being a major antioxidant in the human plasma, both correlates and predicts development of obesity, hypertension, and cardiovascular disease, conditions associated with oxidative stress. While one explanation for this paradox could be that a rise in uric acid represents an attempted protective response by the host, we review the evidence that uric acid may function either as an antioxidant (primarily in plasma) or pro-oxidant (primarily within the cell). We suggest that it is the pro-oxidative effects of uric acid that occur in cardiovascular disease and may have a contributory role in the pathogenesis of these conditions.
    URL, DOI BibTeX

    @article{Sautin2008,
    	abstract = "Uric acid, despite being a major antioxidant in the human plasma, both correlates and predicts development of obesity, hypertension, and cardiovascular disease, conditions associated with oxidative stress. While one explanation for this paradox could be that a rise in uric acid represents an attempted protective response by the host, we review the evidence that uric acid may function either as an antioxidant (primarily in plasma) or pro-oxidant (primarily within the cell). We suggest that it is the pro-oxidative effects of uric acid that occur in cardiovascular disease and may have a contributory role in the pathogenesis of these conditions.",
    	author = "Sautin, Yuri Y and Johnson, Richard J",
    	doi = "10.1080/15257770802138558",
    	file = ":C$\backslash$:/Users/riku/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Sautin, Johnson - 2008 - Uric acid the oxidant-antioxidant paradox.pdf:pdf",
    	issn = "1532-2335",
    	journal = "Nucleosides, nucleotides \& nucleic acids",
    	keywords = "Animals,Antioxidants,Antioxidants: metabolism,Humans,Inflammation,Inflammation: metabolism,Oxidants,Oxidants: metabolism,Uric Acid,Uric Acid: metabolism",
    	month = "jun",
    	number = 6,
    	pages = "608--19",
    	pmid = 18600514,
    	title = "{Uric acid: the oxidant-antioxidant paradox.}",
    	url = "http://www.mendeley.com/research/uric-acid-oxidantantioxidant-paradox/",
    	volume = 27,
    	year = 2008
    }
    
  10. R Meral.
    Antioxidant effects of wine polyphenols. Trakia Journal of Sciences 6(1):57–62, 2008.
    URL BibTeX

    @article{Meral2008,
    	author = "Meral, R",
    	journal = "Trakia Journal of Sciences",
    	number = 1,
    	pages = "57--62",
    	title = "{Antioxidant effects of wine polyphenols}",
    	url = "http://www.mendeley.com/research/antioxidant-effects-wine-polyphenols/",
    	volume = 6,
    	year = 2008
    }
    
  11. G Glantzounis, E Tsimoyiannis, A Kappas and D Galaris.
    Uric Acid and Oxidative Stress. Current Pharmaceutical Design 11(32):4145–4151, 2005.
    URL, DOI BibTeX

    @article{Glantzounis2005,
    	author = "Glantzounis, G. and Tsimoyiannis, E. and Kappas, A. and Galaris, D.",
    	doi = "10.2174/138161205774913255",
    	isbn = "doi:10.2174/138161205774913255",
    	issn = 13816128,
    	journal = "Current Pharmaceutical Design",
    	month = "",
    	number = 32,
    	pages = "4145--4151",
    	title = "{Uric Acid and Oxidative Stress}",
    	url = "http://www.mendeley.com/catalog/uric-acid-oxidative-stress-2/",
    	volume = 11,
    	year = 2005
    }
    
  12. BIJAN SHEKARRIZ and MARSHALL L STOLLER.
    Uric Acid Nephrolithiasis: Current Concepts and Controversies. The Journal of Urology 168(4 Pt 1):1307–1314, 2002.
    URL, DOI BibTeX

    @article{SHEKARRIZ2002,
    	author = "SHEKARRIZ, BIJAN and STOLLER, MARSHALL L.",
    	doi = "10.1097/00005392-200210010-00003",
    	issn = "0022-5347",
    	journal = "The Journal of Urology",
    	month = "",
    	number = "4 Pt 1",
    	pages = "1307--1314",
    	title = "{Uric Acid Nephrolithiasis: Current Concepts and Controversies}",
    	url = "http://www.mendeley.com/research/uric-acid-nephrolithiasis-current-concepts-controversies/",
    	volume = 168,
    	year = 2002
    }
    
  13. D C Hooper, S Spitsin, R B Kean, J M Champion, G M Dickson, I Chaudhry and H Koprowski.
    Uric acid, a natural scavenger of peroxynitrite, in experimental allergic encephalomyelitis and multiple sclerosis. Proceedings of the National Academy of Sciences 95(2):675–680, January 1998.
    URL, DOI BibTeX

    @article{Hooper1998,
    	author = "Hooper, D. C. and Spitsin, S. and Kean, R. B. and Champion, J. M. and Dickson, G. M. and Chaudhry, I. and Koprowski, H.",
    	doi = "10.1073/pnas.95.2.675",
    	issn = "0027-8424",
    	journal = "Proceedings of the National Academy of Sciences",
    	month = "jan",
    	number = 2,
    	pages = "675--680",
    	title = "{Uric acid, a natural scavenger of peroxynitrite, in experimental allergic encephalomyelitis and multiple sclerosis}",
    	url = "http://www.mendeley.com/research/uric-acid-natural-scavenger-peroxynitrite-experimental-allergic-encephalomyelitis-multiple-sclerosis/",
    	volume = 95,
    	year = 1998
    }
    

 

Uric acid levels predict survival in men with amyotrophic lateral sclerosis.

http://www.ncbi.nlm.nih.gov/pubmed/22323210

Feb 10, 2012

Abstract

Elevated uric acid levels have recently been found to be associated with slower disease progression in Parkinson's disease, Huntington's disease, multiple system atrophy, and mild cognitive impairment. The aim of this study is to determine whether serum uric acid levels predict survival in amyotrophic lateral sclerosis (ALS). A total of 251 people with ALS enrolled in two multicenter clinical trials were included in our analysis. The main outcome measure was survival time, which was calculated as time to death, tracheostomy, or permanent assistive ventilation, with any event considered a survival endpoint. Cox proportional hazards models were used to estimate the hazard ratio (HR) of reaching a survival endpoint according to baseline uric acid levels after adjusting for markers of disease severity (FVC, total ALSFRS-R score, time since symptom onset, diagnostic delay, BMI, bulbar vs. spinal onset, age, and riluzole use). There was a dose-dependent survival advantage in men, but not women, with higher baseline uric acid levels (logrank test: p = 0.018 for men, p = 0.81 for women). There was a 39% reduction in risk of death during the study for men with each 1 mg/dl increase in uric acid levels (adjusted HR: 0.61, 95% CI 0.39-0.96, p = 0.03). This is the first study to demonstrate that serum uric acid is associated with prolonged survival in ALS, after adjusting for markers of disease severity. Similar to previous reports in Parkinson's disease, this association was seen in male subjects only.