Ceruloplasmin is a copper-containing glycoprotein primarily synthesized in the liver. It plays a crucial role in iron metabolism, acting as a ferroxidase enzyme that helps convert Fe²⁺ (ferrous iron) to Fe³⁺ (ferric iron) for transport in the blood.
Copper Transport: Binds and transports ~95% of plasma copper.
Iron Metabolism: Facilitates iron mobilization from tissues by oxidizing Fe²⁺ to Fe³⁺ for binding to transferrin.
Antioxidant Properties: Scavenges free radicals and protects against oxidative stress.
Inflammatory Response: Functions as an acute-phase protein, increasing in response to infections or inflammation.
Normal Levels:
Adults: 20–60 mg/dL (200–600 mg/L)
Newborns: 5–18 mg/dL (lower than adults)
Measurement Methods:
Immunoturbidimetry
Nephelometry
Colorimetric assays
🔻 Causes:
Wilson’s Disease (autosomal recessive disorder causing copper accumulation)
Menkes Disease (genetic disorder of copper metabolism)
Malnutrition or Liver Disease (e.g., cirrhosis, hepatitis)
Nephrotic Syndrome (protein loss in urine)
🔬 Associated Symptoms:
Neurological symptoms (tremors, dystonia, psychiatric changes)
Hepatic dysfunction (jaundice, liver failure)
Kayser-Fleischer rings (copper deposits in the cornea)
🩺 Diagnosis & Follow-Up:
Serum copper levels (low in Wilson’s Disease)
24-hour urinary copper (high in Wilson’s Disease)
Genetic testing for ATP7B mutation
🔺 Causes:
Acute and chronic inflammation (infection, rheumatoid arthritis)
Pregnancy or Estrogen Therapy
Liver Disease (hepatitis, cholestasis)
Certain cancers (lymphoma, hepatocellular carcinoma)
✅ Ceruloplasmin is crucial for copper transport and iron metabolism.
✅ Low levels are significant in Wilson’s Disease and liver disorders.
✅ High levels are linked to inflammation and hormonal changes.
✅ Measurement is important in diagnosing copper metabolism disorders.