Serum uric acid and multiple sclerosis

Sotgiu, Stefano; Pugliatti, Maura; Sanna, Alessandra; Sotgiu, A.; Fois, Maria Laura; Arru, Giannina; Rosati, Giulio

doi:10.1007/s100720200059

Cited by 73 publications

(61 citation statements)

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“…Some studies have suggested that serum or CSF UA levels decrease in MS (Dujmovic et al., 2009; Peng et al., 2008; Sotgiu et al., 2002), while others show increased UA and purine compounds in biological fluids of MS patients (Amorini et al., 2009; Langemann, Kabiersch, & Newcombe, 1992; Lazzarino et al., 2010). Min et al.…”

Section: Discussionmentioning

confidence: 98%

“…Oxidative stress is also thought to be involved in NMO and MS (Gonsette, 2008; Haider, 2015; Lassmann & van Horssen, 2016; Penton‐Rol et al., 2009). Previous studies have focused more on serum UA in NMO/MS patients (Ashtari, Bahar, Aghaei, & Zahed, 2013; Liu et al., 2013; Min et al., 2012; Peng et al., 2008; Sotgiu et al., 2002), although cerebrospinal fluid (CSF) UA levels might more directly reflect CNS. However, very little is known about CSF UA levels in NMOSDs.…”

Section: Introductionmentioning

confidence: 99%

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Elevated cerebrospinal fluid uric acid during relapse of neuromyelitis optica spectrum disorders

Shu

Zhang

et al. 2016

Brain and Behavior

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IntroductionPrevious studies have shown that serum uric acid (UA) modulates outcomes of neurological diseases, although little is known about cerebrospinal fluid (CSF) UA levels in neuromyelitis optica spectrum disorders (NMOSDs).MethodsCerebrospinal fluid and serum UA levels were measured in samples from 68 patients, including NMOSDs during relapse (n = 38) and controls with noninflammatory and non‐neurodegenerative diseases (CTLs, n = 30). Correlation analysis was performed between CSF UA and clinical characteristics, serum UA, and blood–brain barrier integrity in NMOSDs.ResultsCerebrospinal fluid UA levels in NMOSDs were significantly higher than in CTLs (p = .002), while serum UA differences between NMOSDs and CTLs were not statistically significant. In NMOSDs, CSF UA levels were significantly higher in patients with an impaired blood–brain barrier than in patients with an intact one (p < .001), and significantly higher in longer disease duration than in shorter disease duration patients (p = .002). CSF UA levels were also significantly higher in active patients upon MRI than in inactive patients (p < .001), and significantly higher in patients with brain lesions than without brain lesions (p = .024). CSF UA was significantly associated with the serum UA levels (r = .454, p = .002), disease duration (r = .383, p = .018), and blood–brain barrier index (r = .805, p < .001), but did not correlate with age, gender, annualized relapse rate, duration, or severity of NMOSD. Multiple regression analysis demonstrated that CSF UA was independent of the blood–brain barrier index (β = .765, p < .001) and serum UA levels (β = .01, p = .019) in NMOSDs.ConclusionsCerebrospinal fluid UA levels were elevated in NMOSD patients during relapse, and were likely modified by serum UA levels and blood–brain barrier integrity.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Elevated cerebrospinal fluid uric acid during relapse of neuromyelitis optica spectrum disorders

Shu

Zhang

et al. 2016

Brain and Behavior

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“…Changes of uric acid: in the course of MS a reduced value of uric acid (UA) was found, in normal range, compared to healthy subjects, in the absence of correlations with disease activity, duration, course or degree of disability [10]. This study favored the view that reduced UA in MS acts as a primary, constitutive loss of protection against oxidative agents.…”

Section: Introductionmentioning

confidence: 56%

Biochemical Parameters Alterations in Multiple Sclerosis: A Longitudinal Study and Review of the Literature

Orefice

Ferraro²,

Barbato³

et al. 2012

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Multiple Sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) and is characterized by inflammation, demyelination and desctruction of oligodendrocytes and axons. The immunology of MS is complex, involving autoreactive Th1 and Th17 lymphocytes, cells of the innate immune system including dedritic, natural killer (NK) and microglia cells, as well as vascular endothelial cells. Multiple Sclerosis (MS) is based by a series of biochemical changes affecting to different extent neuronal functions; great attention has been focused on: liver enzymes, thyroid function tests, autoantibodies, lipid profile and uric acid levels. Following the introduction of therapy with drugs that modify the course of disease, more attention has been paid to the change of biochemical parameters, in particular to evaluate possible adverse effects. Aim of this study was to perform a review of the literature on biochemical alterations in treated and untreated MS patients and to assess laboratory parameters alterations in a cohort of MS patients, before and during treatment. On a total of 624 patients followed at our center, we selected those who practiced for the first time a therapy with IFN beta 1a at various doses, IFN beta 1b and Glatiramer acetate, that were 595 (95%), with baseline biochemical evaluation available in 488 (82%) (307 females, mean age 36.6 years). We considered the evolution of various biochemical parameters during treatment. The following outcome variables were evaluated: laboratory changes, in particular liver function, thyroid function, lipids and blood cell count. Percentages were compared using the chisquare test. ANOVA was performed to evaluate changes of laboratory tests over time between therapy groups. Our finding confirm the presence of biochemical alterations at baseline, in particular regarding liver enzymes, thyroid hormones and lipids. Treatment effects were more evident on liver enzymes elevation, anti thyroid antibodies production and blood cholesterol decrease. These effects were mainly transient and self remitting without suspension of therapy. Biochemical alterations, mainly related to autoimmune pathology and lipid metabolism change were encountered. Treatments increased transient biochemical alterations particulary in patients with baseline changes, suggesting a stricter monitoring of blood exams in this category of patients.

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“…This product may be responsible for a significant proportion of the damage attributed to NO and therefore may be an important factor in the generation of CNS lesions. Several studies suggest lower levels of serum UA in MS patients (7)(8)(9). In the other hand, there were several reports concerning no correlation with lower levels of serum UA, in the literature (10).…”

Section: Introductionmentioning

confidence: 99%