A ceruloplasmin test measures the amount of ceruloplasmin (CP), a protein produced predominantly by the liver. Its primary function is to bind to and carry copper throughout the body. Measuring the concentration of this protein provides insight into how the body is managing and metabolizing copper. Abnormal levels, whether too high or too low, often suggest underlying problems with copper regulation or significant systemic inflammation.
The Biological Role of Ceruloplasmin
Ceruloplasmin is the main transport vehicle for copper in the blood, carrying approximately 95% of the plasma copper. It functions as a ferroxidase enzyme, connecting the metabolism of copper and iron. Ceruloplasmin catalyzes the conversion of ferrous iron (Fe2+) into its ferric form (Fe3+).
This oxidation step is necessary because ferric iron is the only form that can bind to the transport protein transferrin. Without adequate ceruloplasmin activity, iron cannot be properly mobilized from storage cells. Ceruloplasmin also possesses antioxidant properties, protecting cells from damage caused by free radicals.
Key Conditions Associated with Low Levels
The most important clinical use of the ceruloplasmin test is diagnosing inherited disorders that disrupt copper metabolism, which typically cause low ceruloplasmin levels. Wilson’s Disease is the most recognized condition, an autosomal recessive genetic disorder causing copper to accumulate excessively in the liver, brain, and other organs. This buildup occurs because the liver cannot properly incorporate copper into ceruloplasmin or excrete excess copper into bile.
The amount of ceruloplasmin released into the blood is greatly reduced, often falling below 20 milligrams per deciliter, which strongly suggests the disease. This low ceruloplasmin, combined with high copper excretion in a 24-hour urine sample, forms a standard diagnostic pattern. However, some patients with acute liver failure related to Wilson’s Disease may have ceruloplasmin levels within the normal range.
Another, much rarer, inherited copper disorder associated with low ceruloplasmin is Menkes Disease, a severe X-linked condition. This disorder impairs the body’s ability to absorb copper from the gut and transport it to the liver and brain. In Menkes Disease, low ceruloplasmin results from systemic copper deficiency, as the liver cannot acquire enough copper to synthesize the protein. Unlike Wilson’s Disease, Menkes Disease presents with symptoms of copper deficiency due to poor distribution, not copper toxicity from accumulation.
Interpreting Results Beyond Copper Disorders
While low levels indicate genetic copper disorders, interpreting results requires considering other physiological states, particularly those causing high levels. Ceruloplasmin is classified as a positive acute-phase reactant, meaning its concentration rises rapidly in response to inflammation, infection, or tissue damage. This increase is a non-specific response, seen in numerous conditions such as rheumatoid arthritis, certain cancers, and cardiovascular disease.
High ceruloplasmin levels are also commonly observed during periods of high estrogen, such as pregnancy or in women using oral contraceptives or estrogen therapy. This elevation is less helpful for diagnosis than a low result, as it indicates a systemic reaction rather than a specific metabolic defect.
Conversely, low ceruloplasmin levels not related to Wilson’s or Menkes Disease can point to other health issues. Severe liver disease impairs the liver’s ability to synthesize proteins, leading to reduced ceruloplasmin production. Other causes include malnutrition, malabsorption syndromes, or conditions causing protein loss, like nephrotic syndrome. The ceruloplasmin test is almost never used in isolation; it is evaluated alongside other measurements, such as serum copper and 24-hour urine copper excretion, to provide a complete picture of copper status.