Is a blood copper level of 67 micromoles per liter (hypocupremia) something to be concerned about?

Assessment and Management of Hypocupremia with Blood Copper Level of 67 μmol/L

A blood copper level of 67 μmol/L indicates hypercupremia (copper excess), not hypocupremia, and requires further evaluation to determine the underlying cause, which may include Wilson's disease or certain malignancies. 1

Diagnostic Interpretation

A blood copper level of 67 μmol/L is above the normal range and indicates hypercupremia (elevated copper), not hypocupremia (copper deficiency). This distinction is critical for proper management:

• Normal serum copper range is typically 12-25 μmol/L (75-145 μg/dL)
• Value of 67 μmol/L suggests pathological copper excess
• This elevation requires further diagnostic workup to determine the underlying cause

Essential Additional Tests

1. Ceruloplasmin measurement:

   • Low ceruloplasmin (<50 mg/L or <5 mg/dL) with elevated copper suggests Wilson's disease 2
   • Normal or elevated ceruloplasmin with high copper suggests other causes

2. Non-ceruloplasmin bound copper calculation:

   • Calculate using: Total serum copper (μg/L) - [3.15 × ceruloplasmin (mg/L)] 2
   • Values >25 μg/dL (>250 μg/L) suggest pathological copper excess 1

3. 24-hour urinary copper excretion:

   • 100 μg/24 hours (>1.6 μmol/24 hours) supports Wilson's disease diagnosis 1

   • May be elevated in other liver diseases and cholestatic conditions 2

4. Liver function tests to assess for liver damage

5. Complete blood count to check for cytopenias that might occur with copper disorders

Differential Diagnosis

Wilson's Disease

• Genetic disorder of copper metabolism
• Presents with liver disease, neurological symptoms, and Kayser-Fleischer rings
• Paradoxically may have low serum copper despite copper overload due to low ceruloplasmin 2

Other Causes of Hypercupremia

• Acute liver failure (copper released from damaged hepatocytes) 2
• Chronic cholestasis 2
• Inflammatory conditions (copper rises as an acute phase reactant) 2
• Malignancies
• Pregnancy (physiological) 2
• Hyperthyroidism 2
• Hemochromatosis 2

Management Approach

If Wilson's Disease is Confirmed:

1. First-line treatment: Chelation therapy with Trientine, 750-1500 mg/day in 2-3 divided doses 1

2. Alternative treatment: Zinc therapy with Zinc acetate, 50 mg three times daily 1

3. Dietary modifications:

   • Avoid foods high in copper: shellfish, nuts, chocolate, mushrooms, and organ meats 1

4. Monitoring parameters:

   • 24-hour urinary copper excretion: 200-500 μg/day for chelation therapy
   • Non-ceruloplasmin bound copper should normalize with effective treatment
   • Regular liver function tests and complete blood count 1

If Other Causes of Hypercupremia:

• Treat the underlying condition
• Monitor copper levels and associated symptoms
• Consider hepatology consultation for persistent unexplained hypercupremia

Monitoring and Follow-up

• Initial phase: Monitor every 1-2 months
• Maintenance phase: Monitor at least twice yearly 1
• Laboratory monitoring should include:
  • Liver function tests
  • Complete blood count
  • Serum copper and ceruloplasmin
  • 24-hour urinary copper excretion
  • Non-ceruloplasmin bound copper calculation 1

Potential Complications

• Overtreatment: Excessive chelation can lead to copper deficiency with neutropenia, anemia, and neurological symptoms 1
• Untreated Wilson's disease: Progressive liver damage, neurological deterioration
• Copper toxicity symptoms: Hematemesis, hypotension, melena, coma, headaches, behavioral changes, fever, diarrhea, abdominal cramps, Kayser-Fleischer rings, and jaundice 2

Important Considerations

• Copper status assessment should always include CRP determination, as inflammatory states can elevate copper levels 2
• Interpretation of copper levels requires consideration of clinical context and other laboratory parameters
• Permanent neurological damage may occur if diagnosis and treatment are delayed in Wilson's disease

Remember that the value of 67 μmol/L represents hypercupremia (excess copper), not hypocupremia (copper deficiency), and requires appropriate evaluation and management to prevent serious complications.