Serum uric acid and multiple sclerosis

Rentzos, Michael; Nikolaou, Chryssoula; Anagnostouli, Maria; Rombos, A.; Tsakanikas, K.; Economou, Marina; Dimitrakopoulos, Antonios; Karouli, M; Vassilopoulos, Dimitrios

doi:10.1016/j.clineuro.2005.08.004

Cited by 92 publications

(77 citation statements)

References 31 publications

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“…Studies in twins showed that siblings with MS had lower serum UA concentrations compared with the healthy individual (22). Additionally, lower serum UA concentrations have been found in patients with optic neuritis (34), and in patients with other forms of the clinically isolated syndrome (CIS) (23). In accordance with these findings, we have previously demonstrated significantly lower mean serum UA concentrations in MS patients compared with NIND controls (21).…”

Section: Discussionsupporting

confidence: 80%

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Cerebrospinal fluid and serum uric acid levels in patients with multiple sclerosis

Dujmović¹,

Gazibara²,

Obrenović³

et al. 2009

Clinical Chemistry and Laboratory Medicine

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Background: Peroxynitrite was hypothesized to be involved in the pathogenesis of multiple sclerosis (MS) through its various neurotoxic effects. Uric acid (UA) was shown to be a strong peroxynitrite scavenger. Methods: We analyzed cerebrospinal fluid (CSF) and serum UA concentrations in 30 MS patients and 20 controls with non-inflammatory neurological diseases (NIND) and correlated these findings with demographic and clinical characteristics of MS patients. Disease activity was assessed by brain magnetic resonance imaging (MRI) and the CSF/serum albumin quotient as an indicator of the state of blood-brainbarrier (BBB). Results: Serum UA concentrations were found to be significantly lower in MS patients compared with controls (ps0.019). CSF UA concentrations were lower in MS patients as compared to controls, as well as in patients with active MS (clinical and/or MRI activity) in comparison to patients with inactive MS or controls, but these differences were not statistically significant. Significant correlation was found between CSF and serum UA concentrations (ps0.016) in MS patients, but not in controls; and between CSF UA concentrations and the CSF/serum albumin quotient in MS patients (ps0.043), but not in controls. Conclusions: Our results support the significance of UA in the pathogenesis of MS. Decreased serum UA concentrations in MS patients might be due to both intrinsically reduced antioxidant capacity and increased UA consumption in MS. CSF UA concentrations may not be a reliable marker of disease activity in MS since its concentration is dependent on leakage

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Section: Discussionsupporting

confidence: 80%

“…Protective effects of UA on the blood-CNS barrier in EAE have been also demonstrated (20). Significantly lower serum UA concentrations were found in MS patients compared to controls in some studies (21)(22)(23), and low serum UA concentrations have been suggested to be a potential marker of disease activity in some MS patients (24).…”

Section: Introductionmentioning

confidence: 94%

Cerebrospinal fluid and serum uric acid levels in patients with multiple sclerosis

Dujmović¹,

Gazibara²,

Obrenović³

et al. 2009

Clinical Chemistry and Laboratory Medicine

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“…13,14 It is also interesting to note that, in persons with multiple sclerosis, a group characterized by hypouricemia, the incidence of CVD events appears to be lower than expected. 15 Attempts to understand the causal pathway through which elevated uric acid might contribute to CVD have included studies to determine the relation of SUA to target organ damage. The results have been mixed.…”

Section: Article P 894mentioning

confidence: 99%

Podagra, Uric Acid, and Cardiovascular Disease

Alderman

2007

Circulation

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Hippocrates would not be surprised to read that persons with gout had higher mortality, and particularly cardiovascular-related mortality, than persons without gout. 1 On the other hand, he might well have been bemused, nearly 2500 years after he described the syndrome, that this made news. Article p 894He should not have been. All too often, rigorous examination debunks conventional wisdom. Reassuringly, in this case, Drs Choi and Curhan found evidence to support long-standing belief. These dedicated and productive students of the pathogenesis and natural history of gout have here reported empiric data from the 51 000 male nonphysician health professionals who participated in the Health Professions Follow-up Study. From initial examination in 1986 through nearly 600 000 person-years of follow-up, 5825 deaths occurred, of which 2132 were cardiovascular and 1576 were ascribed to coronary heart disease, rates that attest to the generally good health of the group.The Ϸ6% prevalence of gout, at baseline, in men in their mid-50s, who mirror the general US population in body mass index, reported history of hypertension, hypercholesterolemia, and diabetes mellitus, was higher than expected. Interim biennial questionnaires identified incident cases of gout. Participants with gout were both more likely to report coronary heart disease (CHD) at baseline and, regardless of CHD status, more likely than gout-free persons to have cardiovascular disease (CVD) risk factors. Results were presented after stratification by CHD status at baseline. As expected, the incidence of all-cause and CHD mortality was much greater in those with than in those without prevalent CHD. The adjusted increased relative risk of those with gout (compared with those without) for all-cause, CVD, and CHD mortality was Ϸ25%. The single exception was a near doubling of increased relative risk of CHD mortality among those free of CHD at baseline. Neither the inclusion of incident cases of gout nor stratification by CVD risk factors yielded significantly different results. In fact, inclusion of incident cases actually increased the relative risk of those with gout. The relation of gout to stroke was not reported.The report assessed mortality for persons with prevalent gout at baseline and also for the combination of incident and prevalent cases. The actual incidence of gout was not reported. However, the comparison of deaths in the 2 analyses is puzzling. Total deaths among participants with gout at baseline for no CHD and CHD cases were 410 and 235, respectively. The inclusion of incident gout cases increased those figures to 451 and 456, respectively. If my understanding is correct, this means that a remarkable number of incident cases must have occurred over 10 years among the CHD group to generate the additional 221 deaths.In any event, like Hippocrates, most present-day clinicians would be surprised that this is the first prospective study linking gout to mortality. As coronary artery disease has become more prevalent and its behavioral characteristics...

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“…So me studies have also demonstrated a correlation between serum UA concentration and certain disorders of the central nervous system, including mu ltip le sclerosis (MS) and Parkinson's disease (PD), and strongly suggest that the antioxidant effect of urate is important in protecting against MS and PD [2,5,6,7,8,9,10]. Un like MS and PD, in wh ich serum UA levels are low fro m the beginning and do not change much through the course of disease, the UA levels in A LS patients are higher in the early stage and then decrease through the course.…”

Section: Discussionmentioning

confidence: 99%

The Correlation between Uric Acid Levels and Amyotrophic Lateral Sclerosis

Lin¹,

Lin²,

Lai³

2013

AJCMR

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Introduction Uric acid (UA) may act as an antioxidant in ALS pathophysiology. This study examined whether serum UA concentration correlates to clinical course in the ALS patients. Methods We measured serum UA levels in 51 sporadic ALS patients, and compared them to 51 age-and-gender-matched healthy subjects. We analyzed the correlation between serum UA levels, illness duration, and disease "course factors" (defined as "disease duration" over "terminal time") in the ALS patients. Results The mean serum UA levels in the ALS groups were higher than the control groups in both genders. Serum UA levels were inversely correlated with the disease "course factors" in the ALS male patients. Discussion The elevation of serum UA concentration in ALS patients may be related to oxidative stress. The reasons that serum UA levels inversely correlated with ALS "course factors" include: muscle wasting, poor nutrition, reduced antioxidant reserve, or increased UA consumption in end -stage patients.

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Serum uric acid and multiple sclerosis

Cited by 92 publications

References 31 publications

Cerebrospinal fluid and serum uric acid levels in patients with multiple sclerosis

Cerebrospinal fluid and serum uric acid levels in patients with multiple sclerosis

Podagra, Uric Acid, and Cardiovascular Disease

The Correlation between Uric Acid Levels and Amyotrophic Lateral Sclerosis

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