Ceruloplasmin

Synonym/Acronym

copper oxidase, Cp.

Rationale

To assist in the evaluation of copper intoxication and liver disease, especially Wilson disease.

Patient Preparation

There are no food, fluid, activity, or medication restrictions unless by medical direction.

Normal Findings

Method: Nephelometry.

Age	Conventional Units	SI Units (Conventional Units × 10)
Newborn–3 mo	5–18 mg/dL	50–180 mg/L
6 mo–6 yr	14–43 mg/dL	140–430 mg/L
7–17 yr	20–43 mg/dL	200–430 mg/L
18 yr–older adult	20–50 mg/dL	200–500 mg/L

Critical Findings and Potential Interventions ⬆ ⬇

Overview ⬆ ⬇

(Study type: Blood collected in a gold-, red-, or red/gray-top tube; related body system: Circulatory/hematopoietic and digestive systems.)

Ceruloplasmin is an alpha₂-globulin produced by the liver that binds copper for transport in the blood after it is absorbed from the gastrointestinal system. Decreased production of this transport protein results in the deposition of unbound copper in body tissues such as the brain, liver, corneas, and kidneys. Ceruloplasmin, a ferroxidase, also plays a role in regulating iron homeostasis.

Knowledge of genetics assists in identifying those who may benefit from additional education, risk assessment, and counseling. Genetics is the study and identification of genes, genetic sequence variations, and inheritance. For example, genetics provides some insight into the likelihood of inheriting a medical condition such as Menkes disease (syndrome) or Wilson disease. Some conditions are the result of sequence variations involving a single gene, whereas other conditions may involve multiple genes and/or multiple chromosomes. Menkes disease is an example of a recessive sex-linked genetic disorder passed from a mother to a male child; approximately 30% of cases result from “new” sequence variations in the affected gene, which means those patients will not have a family history of the disease. Wilson disease is an example of an autosomal recessive disorder in which the offspring inherits a copy of the defective gene from each parent. Molecular genetic testing for the respective gene sequence variations can confirm a diagnosis of Menkes and Wilson disease. Further information regarding inheritance of genes can be found in the study titled “Genetic Testing.”

Indications ⬆ ⬇

Assist in the diagnosis of Menkes (kinky hair) disease.
Assist in the diagnosis of Wilson disease.
Determine genetic predisposition to Wilson disease.
Monitor patient response to total parenteral nutrition (hyperalimentation).

Interfering Factors ⬆ ⬇

Drugs and other substances that may increase ceruloplasmin levels include anticonvulsants, oral contraceptives, and tamoxifen.
Drugs and other substances that may decrease ceruloplasmin levels include asparaginase and levonorgestrel.

Other Considerations

Excessive therapeutic intake of zinc may interfere with intestinal absorption of copper.

Potential Medical Diagnosis: Clinical Significance of Results ⬆ ⬇

Increased In

Ceruloplasmin is an acute-phase reactant protein and will be increased in many inflammatory conditions, including cancer

Acute infections
Biliary cholangitis
Cancer of the bone, lung, stomach
Copper intoxication
Hodgkin disease
Leukemia
Pregnancy (last trimester) (estrogen increases copper levels)
Rheumatoid arthritis
Tissue necrosis

Decreased In

Menkes disease (severe X-linked defect causing failed transport to the liver and tissues)
Nutritional deficiency of copper
Wilson disease (genetic defect causing failed transport to the liver and tissues)

Nursing Implications ⬆

Before the Study: Planning and Implementation

Teaching the Patient What to Expect

Explain that a blood sample is needed for the test.
Discuss how this test can determine copper levels in the blood.

After the Study: Implementation & Evaluation Potential Nursing Actions

Treatment Considerations

Discuss the symptoms of Wilson disease that may present themselves relative to the location of copper accumulation within the organs.
Symptoms of copper accumulation include jaundice; issues with speech, swallowing, and coordination; eye discoloration (golden-brown); muscle stiffness; uncontrolled muscle movement; edema; ascites; fatigue; appetite loss.
Discuss the complications associated with Wilson disease: cirrhosis; liver failure; ongoing neurological problems; renal disease; hemolysis; psychological changes such as depression, psychosis, and bipolar disorder.

Nutritional Considerations

Note that copper deficiency does not normally occur in adults; however, patients receiving long-term total parenteral nutrition should be evaluated if signs and symptoms of copper deficiency appear, such as jaundice or eye color changes.
Dietary consultation can assist the patient to identify culturally appropriate copper-rich foods including organ meats, shellfish, nuts, and legumes.
Emphasize a high intake of zinc, iron, calcium, and manganese interferes with copper absorption.
Evaluate home plumbing for copper tubing that should be changed to prevent unintended copper ingestion.

Clinical Judgement

Consider the best cultural approach toward ensuring lifestyle changes necessary to alter copper consumption.

Follow-Up Evaluation and Desired Outcomes

Understands that Kayser-Fleischer rings (green-gold rings) in the cornea and a liver biopsy specimen showing elevated copper levels are findings indicative of Wilson disease.
Acknowledges that depending on the results of this procedure, additional testing may be performed to evaluate or monitor progression of the disease process and determine the need for a change in therapy.
Understands that Wilson disease is an inherited genetic disorder and agrees to genetic counseling.