Evidence map›Paper›PMID 35585918›Full record

ArticleFrontiers in neuroscience2022

A New Pathogenic Missense Variant in a Consanguineous North-African Family Responsible for a Highly Variable Aceruloplasminemia Phenotype: A Case-Report.

Hervé Lobbes, Quitterie Reynaud, Sabine Mainbourg, Claire Savy-Stortz, Martine Ropert, Edouard Bardou-Jacquet, Stéphane Durupt

Open access · goldAbstract readCase Reports
In one paragraph

Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 47% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Review
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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 4 institutions in 1 country.

Hervé LobbesService de Médecine Interne, Hôpital Estaing, CHU de Clermont-Ferrand, Clermont-Ferrand, France.
Quitterie ReynaudDépartement de Médecine Interne et Centre de Référence Mucoviscidose, Centre Hospitalier Lyon Sud, Hospices Civils de Lyon, Pierre-Bénite, France.
Sabine MainbourgDépartement de Médecine Interne et Centre de Référence Mucoviscidose, Centre Hospitalier Lyon Sud, Hospices Civils de Lyon, Pierre-Bénite, France.
Claire Savy-StortzMédecine interne et médecine vasculaire, Groupe Hospitalier les Portes du Sud, Vénissieux, France.
Martine RopertINSERM, University of Rennes, INRAE, UMR 1241, AEM2 Platform, Nutrition Metabolisms and Cancer (NuMeCan) Institute, Rennes, France.
Edouard Bardou-JacquetLiver Disease Department, French Reference Center for Hemochromatosis and Iron Metabolism Disease, CHU de Rennes, Rennes, France.
Stéphane DuruptDépartement de Médecine Interne et Centre de Référence Mucoviscidose, Centre Hospitalier Lyon Sud, Hospices Civils de Lyon, Pierre-Bénite, France.
Inserm · FRUniversité Claude Bernard Lyon 1 · FRCentre National de la Recherche Scientifique · FRHospices Civils de Lyon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aceruloplasminemia is a rare autosomal recessive inherited disorder. Mutations in the ceruloplasmin gene cause depressed ferroxidase activity leading to iron accumulation. The clinical phenotype is highly variable: anemia, retinopathy, diabetes mellitus, psychiatric disorders, and neurological symptoms including parkinsonian disorders and dementia are the main features of this disease. Characterized by high serum ferritin with low transferrin saturation, aceruloplasminemia uniquely combines brain, liver and systemic iron overload. We report here four new cases of aceruloplasminemia in a consanguineous North-African family. Genetic sequencing revealed a homozygous missense variant c.656T>A in exon 4 of the ceruloplasmin gene, which had been described previously as of "unknown significance" in the dbSNP database and never associated with ACP in the HGMD database. Ferroxidase activity was strongly depressed. Clinical manifestations varied among cases. The proband exhibited mild microcytic anemia, diabetes mellitus, psychosis and parkinsonism, whereas the other cases were asymptomatic or mildly anemic, although high serum ferritin and brain iron deposition were documented in all of them. Therapeutic management was complex. The proband started deferoxamine treatment when already symptomatic and he rapidly declined. In the asymptomatic cases, the treatment was associated with poor tolerance and was discontinued due to anemia requiring red blood cell transfusion. Our series illustrates the need for new therapeutic approaches to aceruloplasminemia.

Indexed as

aceruloplasminemiaferroxidasegenetic variationiron overloadneurodegenerative disease

Identifiers

PMID35585918
PMCPMC9108494
OpenAlexW4225261976

What OpenQuestion holds

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Registered trials

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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.