Evidence map›Paper›PMID 27386506›Full record

ArticleNeurology(R) neuroimmunology & neuroinflammation2016

Absence of systemic oxidative stress and increased CSF prostaglandin F2α in progressive MS.

Magda A Lam, Ghassan J Maghzal, Mohsen Khademi, Fredik Piehl, Rikke Ratzer, Jeppe Romme Christensen, Finn Thorup Sellebjerg, Tomas Olsson, Roland Stocker

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology(R) neuroimmunology & neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Oxidative Stress Markers in Multiple Sclerosis.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Magda A LamVascular Biology Division (M.A.L., G.J.M., R.S.), Victor Chang Cardiac Research Institute, Sydney; School of Medical Sciences (G.J.M., R.S.), University of New South Wales, Sydney, Australia; Neuroimmunology Unit (M.K., F.P., T.O.), Department of Clinical Neurosciences, Centre for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden; and Department of Neurology (R.R., J.R.C., F.T.S.), Copenhagen University Hospital, Copenhagen, Denmark.
Ghassan J MaghzalVascular Biology Division (M.A.L., G.J.M., R.S.), Victor Chang Cardiac Research Institute, Sydney; School of Medical Sciences (G.J.M., R.S.), University of New South Wales, Sydney, Australia; Neuroimmunology Unit (M.K., F.P., T.O.), Department of Clinical Neurosciences, Centre for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden; and Department of Neurology (R.R., J.R.C., F.T.S.), Copenhagen University Hospital, Copenhagen, Denmark.
Mohsen KhademiVascular Biology Division (M.A.L., G.J.M., R.S.), Victor Chang Cardiac Research Institute, Sydney; School of Medical Sciences (G.J.M., R.S.), University of New South Wales, Sydney, Australia; Neuroimmunology Unit (M.K., F.P., T.O.), Department of Clinical Neurosciences, Centre for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden; and Department of Neurology (R.R., J.R.C., F.T.S.), Copenhagen University Hospital, Copenhagen, Denmark.
Fredik PiehlVascular Biology Division (M.A.L., G.J.M., R.S.), Victor Chang Cardiac Research Institute, Sydney; School of Medical Sciences (G.J.M., R.S.), University of New South Wales, Sydney, Australia; Neuroimmunology Unit (M.K., F.P., T.O.), Department of Clinical Neurosciences, Centre for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden; and Department of Neurology (R.R., J.R.C., F.T.S.), Copenhagen University Hospital, Copenhagen, Denmark.
Rikke RatzerVascular Biology Division (M.A.L., G.J.M., R.S.), Victor Chang Cardiac Research Institute, Sydney; School of Medical Sciences (G.J.M., R.S.), University of New South Wales, Sydney, Australia; Neuroimmunology Unit (M.K., F.P., T.O.), Department of Clinical Neurosciences, Centre for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden; and Department of Neurology (R.R., J.R.C., F.T.S.), Copenhagen University Hospital, Copenhagen, Denmark.
Jeppe Romme ChristensenVascular Biology Division (M.A.L., G.J.M., R.S.), Victor Chang Cardiac Research Institute, Sydney; School of Medical Sciences (G.J.M., R.S.), University of New South Wales, Sydney, Australia; Neuroimmunology Unit (M.K., F.P., T.O.), Department of Clinical Neurosciences, Centre for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden; and Department of Neurology (R.R., J.R.C., F.T.S.), Copenhagen University Hospital, Copenhagen, Denmark.
Finn Thorup SellebjergVascular Biology Division (M.A.L., G.J.M., R.S.), Victor Chang Cardiac Research Institute, Sydney; School of Medical Sciences (G.J.M., R.S.), University of New South Wales, Sydney, Australia; Neuroimmunology Unit (M.K., F.P., T.O.), Department of Clinical Neurosciences, Centre for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden; and Department of Neurology (R.R., J.R.C., F.T.S.), Copenhagen University Hospital, Copenhagen, Denmark.
Tomas OlssonVascular Biology Division (M.A.L., G.J.M., R.S.), Victor Chang Cardiac Research Institute, Sydney; School of Medical Sciences (G.J.M., R.S.), University of New South Wales, Sydney, Australia; Neuroimmunology Unit (M.K., F.P., T.O.), Department of Clinical Neurosciences, Centre for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden; and Department of Neurology (R.R., J.R.C., F.T.S.), Copenhagen University Hospital, Copenhagen, Denmark.
Roland StockerVascular Biology Division (M.A.L., G.J.M., R.S.), Victor Chang Cardiac Research Institute, Sydney; School of Medical Sciences (G.J.M., R.S.), University of New South Wales, Sydney, Australia; Neuroimmunology Unit (M.K., F.P., T.O.), Department of Clinical Neurosciences, Centre for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden; and Department of Neurology (R.R., J.R.C., F.T.S.), Copenhagen University Hospital, Copenhagen, Denmark.
Victor Chang Cardiac Research Institute · AUUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveWe aimed to investigate the role of oxidative stress in the progression of multiple sclerosis (MS).

methodsWe determined by liquid chromatography-tandem mass spectrometry nonenzymatic (F2-isoprostanes) and enzymatic oxidation products of arachidonic acid (prostaglandin F2α [PGF2α]) in plasma and CSF of 45 controls (other neurologic disease [OND] with no signs of inflammation) and 62 patients with MS. Oxidation products were correlated with disease severity and validated biomarkers of inflammation (chemokine ligand 13; matrix metalloproteinase-9; osteopontin) and axonal damage (neurofilament light protein).

resultsCompared with OND controls, plasma concentrations of F2-isoprostanes and PGF2α were significantly lower in patients with progressive disease, and decreased with increasing disability score (Expanded Disability Status Scale). In contrast, CSF concentrations of PGF2α, but not F2-isoprostanes, were significantly higher in patients with progressive disease than OND controls (p < 0.01). The content of PGF2α in CSF increased with disease severity (p = 0.044) and patient age (p = 0.022), although this increase could not be explained by age. CSF PGF2α decreased with natalizumab and methylprednisolone treatment and was unaffected by the use of nonsteroidal anti-inflammatory drug in secondary progressive MS. CSF PGF2α did not associate with validated CSF markers of inflammation and axonal damage that themselves did not associate with the Expanded Disability Status Scale.

conclusionsOur data suggest that MS progression is associated with low systemic oxidative activity. This may contribute to immune dysregulation with CNS inflammation accompanied by increased local cyclooxygenase-dependent lipid oxidation.

Identifiers

PMID27386506
PMCPMC4929888
OpenAlexW2463565282

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.