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A very rare inherited multisystemic disease presenting non-specific neurological, hepatic, psychiatric or osseo-muscular manifestations due to excessive copper deposition in the body.
Features include always present findings: Muscle stiffness (rigidity), Hypoalbuminemia, Abdominal distention, and High nonceruloplasmin-bound serum copper and others; and very common findings: Jaundice, Elevated circulating aspartate aminotransferase concentration, and Elevated circulating alanine aminotransferase concentration. 68 total HPO annotations.
Organ System | Phenotype Count | Example Features |
|---|---|---|
Brain and nerves | 16 | Dystonia, Seizure, Muscle stiffness (rigidity) |
Digestive system | 14 | Abdominal distention, Acute hepatic failure, Jaundice |
Lab test results | 5 | Elevated circulating aspartate aminotransferase concentration, Increased urinary copper concentration, Hyperbilirubinemia |
Bones and joints | 4 | Joint hypermobility, Osteomalacia, Weak and brittle bones (osteoporosis) |
Kidneys and urinary system | 4 | Increased urinary copper concentration, Protein in the urine (proteinuria), Renal tubular dysfunction |
Blood and immune system | 4 | Low red blood cell count (anemia), Enlarged spleen (splenomegaly), Red blood cell destruction (hemolytic anemia) |
Arms and legs | 3 | Limb muscle weakness, Hand tremor, Limb dystonia |
Eyes | 1 | Sunflower cataract |
Muscles | 1 | Limb muscle weakness |
Head and neck | 1 | Face of the giant panda sign |
Age of onset: adolescence.
Untreated symptomatic Wilson disease can manifest in individuals ages three years to older than 70 years as hepatic, neurologic, psychiatric, or hematologic disturbances, or a combination of these. Phenotypic expression varies even within families. The understanding of the phenotypic spectrum has further expanded through the widespread use of molecular genetic testing, which has confirmed the diagnosis in individuals with atypical clinical and biochemical findings. outlines the typical presenting clinical findings of untreated Wilson disease. Of note, the "classic triad" of liver disease, movement disorder, and Kayser-Fleischer ring is uncommon. Table 3. Clinical Findings in Individuals with Untreated Symptomatic Wilson Disease by Presenting Finding
Presenting Finding | % of Persons | Typical Age of Presentation (Range) | Liver Disease | Neurologic Disease |
|---|
ATP7B encodes ATPase copper transporting beta (1,465 aa). Copper ion transmembrane transporter involved in the export of copper out of the cells. Highest expression in Testis (28.3 TPM) and Brain Cerebellum (13.5 TPM).
Wilson disease is caused by mutations in the ATP7B gene on chromosome 13.
The ATP7B protein participates in ATP7B transports cytosolic Cu1+ to Golgi lumen and ATP7A transports cytosolic Cu2+ to phagosomal lumen pathways.
ATP7B is classified as a druggable target (Clinically Actionable, Druggable Genome, Enzyme, and Transporter categories) with score 4.4.
No genotype-phenotype correlations for ATP7B have been identified .
Source: GeneReviews — "Wilson Disease"
The diagnostic algorithm for Wilson disease in the European Association for Study of Liver (EASL) Clinical Practice Guidelines is based on a diagnostic index ("Leipzig" score) proposed by an expert panel . This score includes clinical, biochemical, and molecular findings, but has not been validated in large patient series. The most recent diagnostic pathway of the American Association for Study of the Liver Diseases (AASLD) highlights diagnostic approaches when clinical and biochemical evaluations are ambiguous .
Wilson disease should be suspected in individuals ages three to 45 years, but age alone should not exclude consideration of the diagnosis, as affected individuals have been diagnosed in their early 70s.
Source: GeneReviews — "Wilson Disease"
The complete differential diagnosis of Wilson disease is extensive and includes: • Copper metabolism disorders; • Hereditary disorders involving the liver; • Hereditary disorders involving the nervous system; and • Acquired conditions such as viral hepatitis, severe drug toxicity, and nonalcoholic steatohepatitis (NASH). Note: Wilson disease must be specifically excluded in individuals thought to have NASH, or the opportunity for life-saving treatment will be missed. lists selected genetic disorders of interest in the differential diagnosis of Wilson disease (see also , Table 5). Table 4. Hereditary Disorders of Known Genetic Cause in the Differential Diagnosis of Wilson Disease
Gene(s) | Disorder | MOI | Copper Metabolism |
|---|---|---|---|
MEDNIK syndrome | AR | Low ceruloplasmin |
Genetic testing for ATP7B is available. Testing is considered confirmatory for diagnosis.
Biomarker and diagnostic research for Wilson disease has been reported in the published literature.
2 FDA-approved treatments are available for Wilson disease, including ZINC ACETATE (GALZIN, approved 1997) and TRIENTINE TETRAHYDROCHLORIDE (CUVRIOR, approved 2022). An additional 8 compounds hold orphan drug designation.
Brand Name | Generic Name | Mechanism | Approved | Market Status |
|---|---|---|---|---|
CUVRIOR | TRIENTINE TETRAHYDROCHLORIDE | — | 2022 | Available |
GALZIN | ZINC ACETATE | — | 1997 | Available |
The following drugs have received orphan drug designation from the FDA for Wilson disease. Orphan designation reflects regulatory interest and does not indicate approval for treatment.
Brand Name | Generic Name | Sponsor | Designated | Exclusivity End | Designation Status |
|---|---|---|---|---|---|
recombinant adeno-associated virus serotype 5 vector carrying the codon-optimized and truncated human ATP7B gene | recombinant adeno-associated virus serotype 5 vector carrying the codon-optimized and truncated human ATP7B gene | Beijing Genecradle Therapeutics Co., Ltd. | 2025 | — | Designated |
methanobactin SB2 | methanobactin SB2 | ArborMed Co., Ltd | 2024 | — | Designated |
Evaluations Following Initial Diagnosis To establish the extent of disease and needs in an individual with symptomatic untreated Wilson disease, the evaluations summarized (if not performed as part of the evaluation that led to the diagnosis) are recommended. Table 5. Recommended Evaluations Following Initial Diagnosis in Individuals with Symptomatic Untreated Wilson Disease
System/Concern | Evaluation | Comment |
|---|---|---|
Liver disease | Liver biopsy or biochemical testing imaging of liver | Establish baseline copper studies (serum ceruloplasmin serum copper 24-hr urinary copper excretion).; Consider additional upper GI endoscopy to exclude or confirm esophageal varices. Neurologic |
Speech | For those w/dysarthria: eval by speech-language pathologist |
Foods very high in copper (liver, brain, chocolate, mushrooms, shellfish, and nuts) should be avoided, especially at the beginning of treatment. In case of biochemical abnormalities in liver function tests or transaminases, alcohol consumption is strongly discouraged.
Source: GeneReviews — "Wilson Disease"
Tetrathiomolybdate (TTM) is an orally administered chelating agent proposed to work by multiple mechanisms including:
Detoxifying non-ceruloplasmin-bound copper by creating a nonreactive tripartite complex with albumin and copper;
Extracting copper from the endogenous cellular chelator metallothionein (based on its high affinity for copper); and
Interfering with the intestinal uptake of copper when administered with food.
Source: GeneReviews — "Wilson Disease"
32 trials found
Assessment of Treatment Effectiveness and Adherence to Medical Interventions to Prevent/Treat Copper Accumulation Monitoring of individuals under therapy should include routine assessments of treatment efficacy by biochemical testing and clinical evaluation.
Insufficient therapy, underdosage, or poor adherence could lead to reaccumulation of copper and development of new symptoms.
Adverse events related to medical treatment (especially under D-penicillamine treatment) should be evaluated.
Excessive long-term treatment could result in copper deficiency, leading to immobilization of iron (as observed in aceruloplasminemia) and neurologic symptoms of copper deficiency .
According to current guidelines (AASLD and EASL Clinical Practice Guidelines ), routine monitoring should include the following examinations:
At least twice annually: serum copper and ceruloplasmin, liver biochemistries, international normalized ratio, complete blood count, urinalysis, and physical examination including neurologic assessment
Note: Individuals receiving chelation therapy require a complete blood count and urinalysis regularly, no matter how long they have been on treatment.
At least once annually: 24-hour urinary excretion of copper
Note: Measurements are recommended more frequently if there are questions on adherence or if dosage of medications is adjusted.
To monitor the individual's response to supportive care and the emergence of new manifestations, the evaluations in are recommended b...
Source: GeneReviews — "Wilson Disease"
Phenotype severity distribution: 30 always present features, 3 very common features, 6 common features.
Estimated prevalence: 1-9 in 100,000 (Uncommon).
32 clinical trials registered, 17 recruiting. Interventions under study include other interventions, gene therapy, drug therapy, and medical devices. Pipeline includes 1 PHASE3, 5 PHASE1, 1 EARLY_PHASE1. Research is sponsored by a mix of industry and academic institutions.
NCT ID | Title | Phase | Sponsor | Status |
|---|---|---|---|---|
[NCT06945081](https://clinicaltrials.gov/study/NCT06945081) | Wilson's Disease Treated With D-Penicillamine: Characterization of Skin Damage Secondary to Treatment by Measuring Skin Elasticity | NA | Centre Hospitalier Universitaire de Saint Etienne | RECRUITING |
[NCT06573723](https://clinicaltrials.gov/study/NCT06573723) | Institutional Registry of Rare Diseases | — | Hospital Italiano de Buenos Aires | RECRUITING |
[NCT03334292](https://clinicaltrials.gov/study/NCT03334292) | Natural History of Wilson Disease | — | Yale University | RECRUITING |
[NCT06466291](https://clinicaltrials.gov/study/NCT06466291) | Spanish Wilson Disease Registry | — | Asociación Española para el Estudio del Hígado | RECRUITING |
[NCT04012658](https://clinicaltrials.gov/study/NCT04012658) | A Registered Cohort Study on Wilson's Disease | — | Wan-Jin Chen | RECRUITING |
500 publications have been identified in PubMed for Wilson disease. Research spans Review / Meta-Analysis (21%), Case Report / Case Series (19%), and Epidemiology / Natural History (18%).
Research Type | Count | % of Total |
|---|---|---|
Research summaries | 105 | 21% |
Patient case studies | 97 | 19% |
Disease patterns and progression | 89 | 18% |
Laboratory research | 79 | 16% |
Testing and diagnosis research | 49 | 10% |
Clinical study results | 28 |
Wang G (2027). [PMID: 42892985](https://pubmed.ncbi.nlm.nih.gov/42892985/). *J Clin Exp Hepatol*. [Review / Meta-Analysis]
Zhang L (2026). [PMID: 42237336](https://pubmed.ncbi.nlm.nih.gov/42237336/). *Orphanet J Rare Dis*. [Epidemiology / Natural History]
Berenguer M (2026). [PMID: 42758868](https://pubmed.ncbi.nlm.nih.gov/42758868/). *Hepatol Commun*. [Diagnostic / Biomarker]
Kunwar D (2026). [PMID: 42501667](https://pubmed.ncbi.nlm.nih.gov/42501667/). *J Trace Elem Med Biol*. [Review / Meta-Analysis]
Cheng T (2026). [PMID: 42866034](https://pubmed.ncbi.nlm.nih.gov/42866034/). *Front Immunol*. [Review / Meta-Analysis]
Chen J (2026). [PMID: 42551357](https://pubmed.ncbi.nlm.nih.gov/42551357/). *J Trace Elem Med Biol*. [Review / Meta-Analysis]
Einsiedler M (2026). [PMID: 42533190](https://pubmed.ncbi.nlm.nih.gov/42533190/). *Neurol Sci*. [Case Report / Case Series]
Ban R (2026). [PMID: 42582392](https://pubmed.ncbi.nlm.nih.gov/42582392/). *Front Neurol*. [Other]
Aldiabat M (2026). [PMID: 41729169](https://pubmed.ncbi.nlm.nih.gov/41729169/). *Clin Transplant*. [Epidemiology / Natural History]
Fang S (2026). [PMID: 42027254](https://pubmed.ncbi.nlm.nih.gov/42027254/). *Food Sci Nutr*. [Basic Science / Preclinical]
Data assembled from 10 of 12 sources · Last updated Nov 3, 2026, 8:41 AM UTC
Patient Advocacy Groups (PAGs) provide support, resources, and community for patients and caregivers.
Online Mendelian Inheritance in Man
European rare disease database
Genetic and Rare Diseases Info Center
Common questions about Wilson disease
Kayser-Fleischer Rings |
|---|
Liver disease | ~40% | 6-45 yrs (3-70 yrs) | + | +/– | +/– | ~50% |
Neurologic disease | ~40% | Mid-teen to mid-adult (6-50 yrs) | –/mild | + | +/– | ~90% |
Psychiatric disturbance | ~20% | Adolescent to young adult | –/mild | +/– | + | ~90% |
Hemolytic anemia | Few | + | – | – | + , , , Liver disease. Untreated Wilson disease manifests as liver disease more commonly in children and younger adults, typically between ages six and 45 years; however, severe liver disease can be the initial finding in preschool-aged children and in older adults. | — |
Source: GeneReviews — "Wilson Disease"
ATP7A | Menkes disease (See ATP7A-Related Copper Transport Disorders.)1 | XL | Low serum copper low ceruloplasmin |
Occipital horn syndrome (See ATP7A-Related Copper Transport Disorders.) | XL ATP7A-related distal motor neuropathy (See ATP7A-Related Copper Transport Disorders.) | XL | Normal |
CP | Aceruloplasminemia2 | AR | Low ceruloplasmin |
SLC33A1 | Huppke-Brendel syndrome3 | AR | Low serum copper low ceruloplasmin Liver diseases4 |
ABCB4 | MDR3 deficiency (PFIC3) (See Pediatric Genetic Cholestatic Liver Disease Overview.) | AR | Hepatic copper retention due to cholestasis |
HFE | HFE hemochromatosis5 | AR | Hepatic copper retention due to cholestasis is possible. |
SERPINA1 | Alpha-1 antitrypsin deficiency5 | AD6 Neurologic disorders ATN1 | — |
DRPLA | AD | Normal DNAJC6 FBXO7 PARK7 PINK1 PRKN SYNJ1 | — |
VPS13C | Early-onset Parkinson disease (See Parkinson Disease Overview.) | AR GCH1 | — |
TOR1A | Inherited forms of dystonia incl DYT1 early-onset isolated dystonia GTPCH1-deficient dopa-responsive dystonia | AD HTT | Huntington disease |
Source: GeneReviews — "Wilson Disease"
recombinant adeno-associated viral vector of serotype 8 carrying the coding sequence of human ATP7B gene and a hepatic-specific promoter
recombinant adeno-associated viral vector of serotype 8 carrying the coding sequence of human ATP7B gene and a hepatic-specific promoter |
Lingyi Biotech Co., Ltd |
2024 |
— |
Designated |
methyl (R)-4-((3S,5R,7R,8R,9S,10S,13R,14S,17R)-7-hydroxy-10,13-dimethyl-3-((4-((pyridin-2-ylmethyl)amino)butyl)amino)hexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)pentanoate | methyl (R)-4-((3S,5R,7R,8R,9S,10S,13R,14S,17R)-7-hydroxy-10,13-dimethyl-3-((4-((pyridin-2-ylmethyl)amino)butyl)amino)hexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)pentanoate | DepYmed Inc. | 2022 | — | Designated |
Adeno-associated viral vector serotype 9 encoding human ATP7B | Adeno-associated viral vector serotype 9 encoding human ATP7B | Ultragenyx Pharmaceutical Inc. | 2020 | — | Designated |
adeno-associated viral vector serotype 3B encoding shortened human ATP7B | adeno-associated viral vector serotype 3B encoding shortened human ATP7B | Vivet Therapeutics SAS | 2017 | — | Designated |
choline tetrathiomolybdate | choline tetrathiomolybdate | Monopar Therapeutics, Inc. | 2011 | — | Designated |
Ammonium tetrathiomolybdate | Ammonium tetrathiomolybdate | Pipex Pharmaceuticals, Inc. | 1994 | — | Designated |
— |
Musculoskeletal/ADL | Eval by physiatrist/OT/PT | To assess gross motor fine motor skills, gait, ambulation, need for adaptive devices |
Cognitive | Assess for cognitive dysfunction. | — |
Psychiatric | Eval by psychiatrist, psychologist, neuropsychologist if needed | For personality mood disorders |
Eyes | Complete eye exam | To incl assessment for Kayser-Fleischer rings, sunflower cataracts Possible secondary manifestations |
Endocrine disorders | Glucose intolerance | Basic biochemical profile |
Cardiac involvement | Cardiac arrhythmia | By cardiolologist |
Renal involvement | By nephrologist | Assess for:; Tubular dysfunction (e.g., aminoaciduria, hypercalcuria, hyperphosphaturia); Nephrolithiasis, nephrocalcinosis |
Genetic counseling | By genetics professionals2 | To obtain a pedigree inform affected persons their families re nature, MOI, implications of Wilson disease to facilitate medical personal decision making Family support |
resources | By treating clinicians, social workers | Assess need for:; Community or ;; Social work involvement for parental/caregiver support;; Home nursing referral. ADL = activities of daily living; GI = gastrointestinal; OT = occupational therapist; PT = physical therapist Adapted from 1. , 2. |
Source: GeneReviews — "Wilson Disease"
Other research | 27 | 5% |
New treatment approaches | 26 | 5% |
AI-curated news mentioning Wilson disease
Updated Oct 23, 2026
preclinical models of wilson s disease from pathogenesis to clinical translation
Recent research highlights the effectiveness of non-invasive fibrosis tests in assessing liver damage in Wilson disease. Insights were drawn from the international Wilson Disease Registry and the Barcelona Cohort, contributing valuable data to improve patient management.
The Wilson disease market assessment ... emerging therapies, treatment guidelines, unmet needs, and potential growth opportunities. Individual pipeline drug profiles feature mechanisms of action, clinical trial activity, regulatory designations, development technologies, collaborations, licensing agreements, funding, mergers and acquisitions, and NDA approvals, where applicable. ... Wilson disease is a rare autosomal ... The Wilson disease market assessment includes clinical and commercial analysis of emerging therapies, treatment guidelines, unmet needs, and potential growth opportunities. Individual pipeline drug profiles feature mechanisms of action, clinical trial activity, regulatory designations, development technologies, collaborations, licensing agreements, funding, mergers and acquisitions, and NDA approvals, where applicable. ... Wilson disease is a rare autosomal recessive genetic disorder associated with pathogenic variants in the ATP7B gene. The report supports pharmaceutical companies, biotechnology organizations, investors, researchers, and other stakeholders seeking actionable intelligence on the Wilson disease treatment pipeline. It addresses the number of companies and candidates in development, distribution of therapies by clinical phase, recent research trends, clinical trial progress, strategic partnerships, regulatory designations, and the technologies shaping future Wilson disease treatment. Explore Wilson Disease pipeline innovation, including gene therapy, clinical and nonclinical candidates, unmet needs, collaborations, licensing and... This single-dose intravenous therapy targets the underlying genetic cause of Wilson disease. Preclinical and early findings indicate potential improvements in liver enzymes and copper levels. GC310 has received FDA Orphan Drug Designation and is being evaluated in a Phase I/II clinical trial.
A recent study published in PubMed explores non-invasive methods for assessing hepatic steatosis in Wilson disease, utilizing data from an international registry. This research could enhance diagnostic approaches and patient management for those affected by this rare condition.
Prime Medicine has initiated a global Phase 1/2 trial for PM577a, a novel genetic therapy for Wilson disease, and received FDA Rare Pediatric Disease Designation. Initial clinical data is expected by 2027, emphasizing the urgent need for effective treatments in younger patients.