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Updated: Aug 3, 2025

Positron Emission Tomography Using 64-Copper as a Tracer for the Study of Copper-Related Disorders
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Wilson's disease: best practice.

Aidan Ryan1,2, Patrick J Twomey3,4, Paul Cook5

  • 1Chemical Pathology, Cork University Hospital, Cork, Ireland, Cork University Hospital Biochemistry Laboratory, Cork, Ireland aidan.ryan1@hse.ie.

Journal of Clinical Pathology
|April 12, 2023
PubMed
Summary
This summary is machine-generated.

Wilson's disease, caused by ATP7B gene mutations, leads to copper accumulation and organ damage. This review updates understanding of its biomarkers, pathogenesis, clinical features, and therapeutic advancements.

Keywords:
DIAGNOSISEDUCATIONGENETICSNEUROPATHOLOGY

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Area of Science:

  • Genetics and Molecular Biology
  • Hepatology
  • Neurology

Background:

  • Wilson's disease is an inherited autosomal recessive disorder resulting from mutations in the ATP7B gene.
  • Defective copper transport leads to toxic copper accumulation, primarily affecting the liver and subsequently other organs.
  • This review addresses the 20-year gap since the last Best Practice publication on Wilson's disease.

Approach:

  • Comprehensive literature review of recent advancements.
  • Analysis of new diagnostic biomarkers.
  • Evaluation of current and emerging therapeutic strategies.

Key Points:

  • Novel biomarkers are enhancing early diagnosis and monitoring of Wilson's disease.
  • Updated understanding of pathogenesis reveals complex cellular mechanisms of copper toxicity.
  • Clinical features require re-evaluation based on new evidence.
  • Therapeutic developments offer improved management options.

Conclusions:

  • This review provides an updated perspective on Wilson's disease, integrating recent research.
  • It highlights the importance of novel biomarkers and refined therapeutic approaches for patient care.
  • The findings aim to guide clinicians in managing this complex genetic disorder.