Evidence map›Paper›PMID 27682263›Full record

ReviewCurrent treatment options in neurology2016

Bioavailable Trace Metals in Neurological Diseases.

Aurélia Poujois, Jean-Christophe Devedjian, Caroline Moreau, David Devos, Pascal Chaine, France Woimant, James A Duce

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current treatment options in neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

8 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Overview of iron metabolism in health and disease.Hemodialysis international. International Symposium on Home Hemodialysis · 2017
    Review
  7. Review
  8. Copper and Zinc Homeostasis: Lessons fromFrontiers in genetics · 2017
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 6 institutions in 3 countries.

Aurélia PoujoisFrench National Reference Centre for Wilson's Disease, University Hospital Lariboisière, Assistance Publique-Hôpitaux de Paris, Paris, France. aurelia.poujois@aphp.fr.
Jean-Christophe DevedjianINSERM U1171, CHU Lille, Lille University, Lille, France.
Caroline MoreauINSERM U1171, CHU Lille, Lille University, Lille, France.
David DevosINSERM U1171, CHU Lille, Lille University, Lille, France.
Pascal ChaineFrench National Reference Centre for Wilson's Disease, University Hospital Lariboisière, Assistance Publique-Hôpitaux de Paris, Paris, France.
France WoimantFrench National Reference Centre for Wilson's Disease, University Hospital Lariboisière, Assistance Publique-Hôpitaux de Paris, Paris, France.
James A DuceSchool of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, Leeds, West Yorkshire, UK.
Hôpital Lariboisière · FRAssistance Publique – Hôpitaux de Paris · FRCentre Hospitalier Universitaire de Lille · FRInserm · FRLille’s Cardiology Hospital · FRUniversity of Leeds · GB

Funding

Parkinson's UK J-1203
6 · The paper itself

Abstract

opinion statementMedical treatment in Wilson's disease includes chelators (D-penicillamine and trientine) or zinc salts that have to be maintain all the lifelong. This pharmacological treatment is categorised into two phases; the first being a de-coppering phase and the second a maintenance one. The best therapeutic approach remains controversial, as only a few non-controlled trials have compared these treatments. During the initial phase, progressive increase of chelators' doses adjusted to exchangeable copper and urinary copper might help to avoid neurological deterioration. Liver transplantation is indicated in acute fulminant liver failure and decompensated cirrhosis; in cases of neurologic deterioration, it must be individually discussed. During the maintenance phase, the most important challenge is to obtain a good adherence to lifelong medical therapy. Neurodegenerative diseases that lead to a mislocalisation of iron can be caused by a culmination of localised overload (pro-oxidant siderosis) and localised deficiency (metabolic distress). A new therapeutic concept with conservative iron chelation rescues iron-overloaded neurons by scavenging labile iron and, by delivering this chelated metal to endogenous apo-transferrin, allows iron redistribution to avoid systemic loss of iron.

Indexed as

Chelation therapyCopperIronManganeseNeurodegenerationReactive species

Identifiers

PMID27682263
OpenAlexW2524396650

What OpenQuestion holds

Textmetadata
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.