Evidence map›Paper›PMID 34239699›Full record

ReviewWorld journal of hepatology2021

Wilson's disease: Revisiting an old friend.

Ana Lucena-Valera, Domingo Perez-Palacios, Rocio Muñoz-Hernandez, Manuel Romero-Gómez, Javier Ampuero

Open access · diamondAbstract readReview
In one paragraph

Review in World journal of hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
4.5field-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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Effect of primary copper metabolism disturbance on elemental, protein, and lipid composition of the organs in Jackson toxic milk mouse.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Monitoring of Copper in Wilson Disease.Diagnostics (Basel, Switzerland) · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Biochemical diagnosis of Wilson's disease: an update.Advances in laboratory medicine · 2022
    Review
  18. Article
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

5 authors at 2 institutions in 2 countries.

Ana Lucena-ValeraDepartment of Gastroenterology, Hospital Universitario Virgen del Rocio, Sevilla 41013, Spain.
Domingo Perez-PalaciosDepartment of Gastroenterology, Hospital Universitario Virgen del Rocio, Sevilla 41013, Spain.
Rocio Muñoz-HernandezSeLiver Group, Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Sevilla, España.
Manuel Romero-GómezDepartment of Unit of Digestive Diseases, Hospital Universitario Virgen del Rocio, Sevilla 41014, Spain.
Javier AmpueroDepartment of Unit of Digestive Diseases, Hospital Universitario Virgen del Rocio, Sevilla 41014, Spain. jampuero-ibis@us.es.
Hospital Universitario Virgen del Rocío · ESInstituto de Biomedicina de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wilson's disease (WD) is a rare condition caused by copper accumulation primarily in the liver and secondly in other organs, such as the central nervous system. It is a hereditary autosomal recessive disease caused by a deficiency in the ATP7B transporter. This protein facilitates the incorporation of copper into ceruloplasmin. More than 800 mutations associated with WD have been described. The onset of the disease frequently includes manifestations related to the liver (as chronic liver disease or acute liver failure) and neurological symptoms, although it can sometimes be asymptomatic. Despite it being more frequent in young people, WD has been described in all life stages. Due to its fatal prognosis, WD should be suspected in all patients with unexplained biochemical liver abnormalities or neurological or psychiatric symptoms. The diagnosis is established with a combination of clinical signs and tests, including the measurement of ceruloplasmin, urinary copper excretion, copper quantification in liver biopsy, or genetic assessment. The pharmacological therapies include chelating drugs, such as D-penicillamine or trientine, and zinc salts, which are able to change the natural history of the disease, increasing the survival of these patients. In some cases of end-stage liver disease or acute liver failure, liver transplantation must be an option to increase survival. In this narrative review, we offer an overview of WD, focusing on the importance of clinical suspicion, the correct diagnosis, and treatment.

Indexed as

ATP7BCeruloplasminChelatorCopperLiver diseaseWilson´s disease

Identifiers

PMID34239699
PMCPMC8239488
OpenAlexW3173794300

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.