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Assessment of Serum Nitrogen Species and Inflammatory Parameters in Relapsing-Remitting Multiple Sclerosis Patients Treated with Different Therapeutic Approaches

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      Abstract

      The role of nitric oxide and its reactive derivatives (NOx) is well known in the pathogenesis of multiple sclerosis, which is an inflammatory disease while NOx seems to be important in coordinating inflammatory response. The purpose of the present study was to assess serum NOx as one of the nitrogen species and inflammatory parameters in relapsing-remitting multiple sclerosis patients and to compare the effectiveness of various types of disease-modifying therapies that reduce nitric oxide and inflammatory biomarkers. Elevated NOx level was observed in patients who received the first-line disease-modifying therapy (interferons beta-1a and beta-1b) in comparison with the subjects treated with the second-line disease-modifying therapy (natalizumab; fingolimod) and healthy controls without significant differences in C-reactive protein and interleukin-1 beta. A negative correlation was observed between serum NOx level and the duration of multiple sclerosis confirmed in the whole study population and in subjects treated with the first-line agents. Only serum NOx, concentration could reveal a potential efficacy of disease-modifying therapy with a better reduction in NOx level due to the second-line agents of disease-modifying therapy.

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      Most cited references 65

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      The L-arginine-nitric oxide pathway.

       S Moncada,  A Higgs (1993)
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        Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination.

        Multiple sclerosis (MS) is a disease with profound heterogeneity in clinical course, neuroradiological appearance of the lesions, involvement of susceptibility gene loci, and response to therapy. These features are supported by experimental evidence, which demonstrates that fundamentally different processes, such as autoimmunity or virus infection, may induce MS-like inflammatory demyelinating plaques and suggest that MS may be a disease with heterogeneous pathogenetic mechanisms. From a large pathology sample of MS, collected in three international centers, we selected 51 biopsies and 32 autopsies that contained actively demyelinating lesions defined by stringent criteria. The pathology of the lesions was analyzed using a broad spectrum of immunological and neurobiological markers. Four fundamentally different patterns of demyelination were found, defined on the basis of myelin protein loss, the geography and extension of plaques, the patterns of oligodendrocyte destruction, and the immunopathological evidence of complement activation. Two patterns (I and II) showed close similarities to T-cell-mediated or T-cell plus antibody-mediated autoimmune encephalomyelitis, respectively. The other patterns (III and IV) were highly suggestive of a primary oligodendrocyte dystrophy, reminiscent of virus- or toxin-induced demyelination rather than autoimmunity. At a given time point of the disease--as reflected in autopsy cases--the patterns of demyelination were heterogeneous between patients, but were homogenous within multiple active lesions from the same patient. This pathogenetic heterogeneity of plaques from different MS patients may have fundamental implications for the diagnosis and therapy of this disease.
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          Risk alleles for multiple sclerosis identified by a genomewide study.

          Multiple sclerosis has a clinically significant heritable component. We conducted a genomewide association study to identify alleles associated with the risk of multiple sclerosis. We used DNA microarray technology to identify common DNA sequence variants in 931 family trios (consisting of an affected child and both parents) and tested them for association. For replication, we genotyped another 609 family trios, 2322 case subjects, and 789 control subjects and used genotyping data from two external control data sets. A joint analysis of data from 12,360 subjects was performed to estimate the overall significance and effect size of associations between alleles and the risk of multiple sclerosis. A transmission disequilibrium test of 334,923 single-nucleotide polymorphisms (SNPs) in 931 family trios revealed 49 SNPs having an association with multiple sclerosis (P<1x10(-4)); of these SNPs, 38 were selected for the second-stage analysis. A comparison between the 931 case subjects from the family trios and 2431 control subjects identified an additional nonoverlapping 32 SNPs (P<0.001). An additional 40 SNPs with less stringent P values (<0.01) were also selected, for a total of 110 SNPs for the second-stage analysis. Of these SNPs, two within the interleukin-2 receptor alpha gene (IL2RA) were strongly associated with multiple sclerosis (P=2.96x10(-8)), as were a nonsynonymous SNP in the interleukin-7 receptor alpha gene (IL7RA) (P=2.94x10(-7)) and multiple SNPs in the HLA-DRA locus (P=8.94x10(-81)). Alleles of IL2RA and IL7RA and those in the HLA locus are identified as heritable risk factors for multiple sclerosis. Copyright 2007 Massachusetts Medical Society.
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            Author and article information

            Affiliations
            1Department of Neurology in Zabrze, Medical University of Silesia, ul. 3-go Maja 13–15, 41-800 Zabrze, Poland
            23rd Department of Cardiology, SMDZ in Zabrze, Medical University of Silesia, Silesian Centre for Heart Disease, ul. Curie-Skłodowskiej 9, 41-800 Zabrze, Poland
            3Department of Microbiology and Immunology in Zabrze, Medical University of Silesia, ul. Jordana 19, 41-808 Zabrze, Poland
            4Department of Radiology in Zabrze, Medical University of Silesia, ul. 3-go Maja 13–15, 41-800 Zabrze, Poland
            5Department of Laryngology in Zabrze, Medical University of Silesia, ul. Curie-Skłodowskiej 10, 41-800 Zabrze, Poland
            Author notes
            *Natalia Niedziela: natalia@ 123456niedziela.org

            Academic Editor: Markus Kipp

            Journal
            Biomed Res Int
            Biomed Res Int
            BMRI
            BioMed Research International
            Hindawi Publishing Corporation
            2314-6133
            2314-6141
            2016
            19 December 2016
            : 2016
            5204117
            10.1155/2016/4570351
            Copyright © 2016 Natalia Niedziela et al.

            This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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            Research Article

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