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Active, not recruitingNCT07765472Updated Aug 14, 2026

Subclinical Myocardial Dysfunction in Children With Wilson's Disease

An observational study in Wilson's Disease, Myocardial Dysfunction and Children, sponsored by Hebatullah Fawzy. Active, not recruiting at 2 sites in Egypt. Open to participants aged 4 Years to 18 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2026-08-14.

Sponsored by Hebatullah Fawzy · Observational

Study type
Observational
Model
Case-control
Time perspective
Cross-sectional
Enrollment
72
Ages
4 Years to 18 Years
Sex
All
01

Study summary

Wilson's disease (WD) is one of the most common metabolic liver diseases in older children. The most frequent clinical presentation is liver disease. However, Wilson's disease (WD) is a multisystem disorder. It is concluded that four modes of cardiac manifestations in Wilson's disease (WD) include arrhythmias, cardiomyopathy, cardiac death, and autonomic dysfunction. Such possible cardiac involvement should be added to the clinical picture of Wilson's disease (WD) involving the hepatic and central nervous system(CNS).

The data on cardiac manifestations in children is very limited and only few adult studies are available.

In this study, the investigators aim to unveil subclinical cardiac dysfunction in children with Wilson's disease with apparently normal cardiac functions by conventional assessment.

Read the detailed description

Wilson's disease (WD) is an autosomal recessive metabolic liver disorder caused by toxic copper accumulation. While hepatic and neurological manifestations are well recognized, copper can also accumulate in cardiac tissue, potentially leading to subtle myocardial changes, arrhythmias, and heart failure. Traditional two-dimensional (2D) echocardiography often appears normal in early stages. This study aims to evaluate early left ventricular (LV) systolic and diastolic dysfunction in pediatric patients with Wilson's disease using speckle tracking echocardiography (STE) and tissue Doppler imaging, and to correlate these findings with serum levels of Pro-Brain Natriuretic Peptide (Pro-BNP) and ceruloplasmin.

02

Conditions studied

  • Wilson's Disease
  • Myocardial Dysfunction
  • Children
  • Wilson Disease
  • Speckle Tracking Echocardiography
  • Electrocardiographic Changes

Keywords

  • WD
  • pedia
  • cardiac
  • childern
  • LV dysfunction
  • Wilson
  • BNP
  • ceruloplasmin
  • Speckled tracking
  • Pro-BNP
  • STE
03

Who can participate

Ages eligible
4 Years to 18 Years
Sexes eligible
All
Accepts healthy volunteers
Yes
Sampling method
Non-probability sample

Study population

They will be divided in to 2 groups: - Group 1: Patients confirmed Wilson's disease. - Group 2: Controls.

  • Patients group: Patient diagnosed as WD patients, following up in Pediatric Hepatology Clinic in NHTMRI.

According to Criteria of diagnosis based on Leipzig scoring system (11,12): Typical clinical symptoms and signs, as: Kayser-Fleischer rings, neurological symptoms, serum ceruloplasmin, Coombs-negative hemolytic anemia. Other tests: Liver biopsy, 24hr urinary Cu, gene analysis.

Inclusion criteria

  1. Confirmed diagnosis of Wilson's disease based on Leipzig scoring criteria (including clinical signs, Kayser-Fleischer rings, low ceruloplasmin, or genetic analysis).
  2. Age between 4 years and 18 years.
  3. Written informed consent obtained from parents or legal guardians.

Exclusion criteria

Exclusion Criteria

  1. Children with clinical evidence of overt heart failure or known congenital heart disease.
  2. Children suffering from fulminant hepatitis.
  3. Known co-existing primary liver diseases other than Wilson's disease.
  4. Presence of syndromic disorders or major congenital anomalies.
04

Study design

Observational model
Case-control
Time perspective
Cross-sectional
Enrollment
72 participants (estimated)
Patient registry
No

Groups and cohorts

  • Group 1 (Cases)

    Children aged 4-18 years with confirmed Wilson's disease recruited from the Pediatric Hepatology Clinic at the National Hepatology and Tropical Medicine Research Institute (NHTMRI).

    Device: Echocardiography · Device: Electrocardiography · Diagnostic Test: N-terminal pro b- type natriuretic peptide

  • Group 2 (Controls)

    Age- and sex-matched control children without chronic liver or cardiac illness recruited from the outpatient clinic.

    Device: Echocardiography

Interventions

  • DeviceEchocardiography

    a safe, painless test that uses sound waves to create moving pictures of your heart's structure and pumping function.

    Also known as: Echo

  • DeviceElectrocardiography

    a quick, painless test that records the electrical signals in the heart.

    Also known as: ECG

  • Diagnostic testN-terminal pro b- type natriuretic peptide

    a protein made by our heart, examined by peripheral blood sample.

    Also known as: pro BNP

05

What researchers measure

Primary outcomes

  1. Left Ventricular Peak Longitudinal Strain (LV-PLS)

    Left Ventricular Peak Longitudinal Strain (LV-PLS) assessed by Speckle Tracking Echocardiography (STE) to evaluate subclinical LV systolic dysfunction. Expressed as a negative percentage (%), where a less negative percentage indicates impaired function.

    Time frame: Baseline (Day 1 , at single cross-sectional evaluation).

Secondary outcomes

  1. Serum Pro-Brain Natriuretic Peptide (Pro-BNP) Level

    Quantitative measurement of serum Pro-BNP assessed via ELISA (pg/mL) as a circulating biomarker of cardiac wall stress.

    Time frame: Baseline (Day 1 , at single cross-sectional evaluation).

  2. Tissue Doppler LV Filling Pressure (E/e' Ratio)

    Ratio of early mitral inflow velocity (E) measured by conventional Doppler to early diastolic mitral annular velocity (e') measured by tissue Doppler imaging to evaluate LV diastolic function.

    Time frame: Baseline (Day 1 , at single cross-sectional evaluation).

  3. Serum Ceruloplasmin Level Correlation

    Serum ceruloplasmin levels (mg/dL) measured within 6 months of cardiac evaluation to correlate hepatic copper transport marker levels with cardiac function parameters.

    Time frame: Baseline (Day 1,at time of cardiac evaluation or within 6 months preceding cardiac evaluation).

  4. Frequency of Electrocardiographic (ECG) Abnormalities

    Presence or absence of cardiac electrical abnormalities, including conduction delays, ST-T wave changes, and arrhythmias recorded on standard 12-lead ECG.

    Time frame: Baseline (Day 1 , at single cross-sectional evaluation).

06

Study locations

2 sites
  • Faculty of medicine AinShams U
    Cairo, Egypt
  • National Hepatology and Tropical Research Institute (NHTMRI)
    Giza, Egypt
07

References and documents

Publications

  • Wiernicka A, Dadalski M, Janczyk W, Kaminska D, Naorniakowska M, Husing-Kabar A, Schmidt H, Socha P. Early Onset of Wilson Disease: Diagnostic Challenges. J Pediatr Gastroenterol Nutr. 2017 Nov;65(5):555-560. doi: 10.1097/MPG.0000000000001700. PubMed 28753182 ↗
  • European Association for the Study of the Liver. EASL-ERN Clinical Practice Guidelines on Wilson's disease. J Hepatol. 2025 Feb 22:S0168-8278(24)02706-5. doi: 10.1016/j.jhep.2024.11.007. Online ahead of print. PubMed 40089450 ↗
  • European Association for Study of Liver. EASL Clinical Practice Guidelines: Wilson's disease. J Hepatol. 2012 Mar;56(3):671-85. doi: 10.1016/j.jhep.2011.11.007. PubMed 22340672 ↗
  • https://ebm.one/en/chapter-table/scoring-system-developed-8th-international-meeting-wilson-disease-leipzig-2001
  • https://doi.org/10.4236/wjcd.2019.93018
  • Romuk E, Jachec W, Zbrojkiewicz E, Mroczek A, Niedziela J, Gasior M, Rozentryt P, Wojciechowska C. Ceruloplasmin, NT-proBNP, and Clinical Data as Risk Factors of Death or Heart Transplantation in a 1-Year Follow-Up of Heart Failure Patients. J Clin Med. 2020 Jan 3;9(1):137. doi: 10.3390/jcm9010137. PubMed 31947878 ↗
  • Salatzki J, Mohr I, Heins J, Cerci MH, Ochs A, Paul O, Riffel J, Andre F, Hirschberg K, Muller-Hennessen M, Giannitsis E, Friedrich MG, Merle U, Weiss KH, Katus HA, Ochs M. The impact of Wilson disease on myocardial tissue and function: a cardiovascular magnetic resonance study. J Cardiovasc Magn Reson. 2021 Jun 24;23(1):84. doi: 10.1186/s12968-021-00760-1. PubMed 34162411 ↗
  • Chevalier K, Benyounes N, Obadia MA, Van Der Vynckt C, Morvan E, Tibi T, Poujois A. Cardiac involvement in Wilson disease: Review of the literature and description of three cases of sudden death. J Inherit Metab Dis. 2021 Sep;44(5):1099-1112. doi: 10.1002/jimd.12418. Epub 2021 Aug 2. PubMed 34286869 ↗
  • Quick S, Reuner U, Weidauer M, Hempel C, Heidrich FM, Mues C, Sveric KM, Ibrahim K, Reichmann H, Linke A, Speiser U. Cardiac and autonomic function in patients with Wilson's disease. Orphanet J Rare Dis. 2019 Jan 28;14(1):22. doi: 10.1186/s13023-019-1007-7. PubMed 30691535 ↗
  • https://doi.org/10.21608/cupsj.2021.71046.1018
  • Sanchez-Monteagudo A, Ripolles E, Berenguer M, Espinos C. Wilson's Disease: Facing the Challenge of Diagnosing a Rare Disease. Biomedicines. 2021 Aug 28;9(9):1100. doi: 10.3390/biomedicines9091100. PubMed 34572285 ↗
  • Ovchinnikova EV, Garbuz MM, Ovchinnikova AA, Kumeiko VV. Epidemiology of Wilson's Disease and Pathogenic Variants of the ATP7B Gene Leading to Diversified Protein Disfunctions. Int J Mol Sci. 2024 Feb 18;25(4):2402. doi: 10.3390/ijms25042402. PubMed 38397079 ↗
  • https://doi.org/10.1038/s41598-024-59377-w
  • Dang J, Chevalier K, Letavernier E, Tissandier C, Mouawad S, Debray D, Obadia M, Poujois A. Kidney involvement in Wilson's disease: a review of the literature. Clin Kidney J. 2024 Mar 9;17(4):sfae058. doi: 10.1093/ckj/sfae058. eCollection 2024 Apr. PubMed 38660122 ↗

Study documents

  • Study protocol · Jul 25, 2025
  • Study protocol · Jul 25, 2025

Documents are hosted by the registry — open the source record to download them.

Individual participant data

Plan to share: Undecided

08

Registry details

Key details

Study ID
NCT07765472
Lead sponsor
Hebatullah Fawzy
Responsible party
Hebatullah Fawzy ((Principal Investigator / Postgraduate Master's Student / ASU / Pediatric Resident /NHTMRI), Ain Shams University) — Sponsor-investigator
First posted
Aug 14, 2026
Start date
Oct 1, 2025
Primary completion
Oct 30, 2026 (estimated)
Completion
Nov 30, 2026 (estimated)
Last update
Aug 14, 2026

Study contacts

Hebatullah I Fawzy, Msc Student
principal investigator · Faculty of medicine AinShams U,National Hepatology and Tropical Research Institute (NHTMRI)
Eman M ElSayed (Assistant Professor of Pediatrics), AssProfessor
study chair · Faculty of Medicine AinShams U
Mona AH Khafagy (Lecturer of Pediatrics), Lecturer
study director · Faculty of Medicine AinShams U
Sara M Osman (Teaching Fellow of Pediatrics), PedFellow
study director · National Hepatology and Tropical Research Institute (NHTMRI)

Oversight

Data monitoring committee
No
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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This study is active, not recruiting, as verified in Aug 2026. You cannot join it, but the record below documents what was studied.

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