SERUM COPPER (By ICPMS)

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Copper level in serum.

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Serum Copper (By ICPMS) - Comprehensive Test Guide

Section 1: Why is it done?
- Test Description: Measures the concentration of copper in the blood serum using Inductively Coupled Plasma Mass Spectrometry (ICPMS), a highly sensitive analytical technique that provides precise quantification of this essential trace element.
- Primary Indications: Diagnosis and monitoring of Wilson disease, copper toxicity assessment, evaluation of malabsorption syndromes, assessment of nutritional status in chronic illness, investigation of unexplained neurological or hepatic symptoms, and monitoring during long-term parenteral nutrition.
- Clinical Circumstances: When patients present with progressive neurological deterioration, hepatitis of unknown etiology, Kayser-Fleischer rings on slit-lamp examination, or when family history suggests inherited copper metabolism disorders. Also performed during initial screening for occupational copper exposure or assessment of supplementation efficacy.
Section 2: Normal Range
- Reference Range Values: Typically 70-175 µg/dL (11-27 µmol/L) in adults. Values may vary slightly between laboratories depending on methodology and population demographics. Ranges are generally higher in women (80-155 µg/dL) compared to men (70-140 µg/dL). Neonates and young children may have different reference intervals.
- Units of Measurement: µg/dL (micrograms per deciliter) or µmol/L (micromoles per liter). Conversion factor: 1 µg/dL = 0.157 µmol/L.
- Interpretation of Results: Normal Range = Adequate copper status with balanced metabolism; Low (<70 µg/dL) = Copper deficiency, malabsorption, or excessive supplementation; High (>175 µg/dL) = Possible copper toxicity, Wilson disease, cholestasis, or inflammation; Borderline = Warrants repeat testing and clinical correlation with symptoms and other investigations.
- Clinical Significance: Copper is essential for cytochrome c oxidase, lysyl oxidase, and ceruloplasmin synthesis. Normal levels indicate proper enzymatic function and oxidative metabolism. Abnormal results suggest copper homeostasis disruption requiring further investigation.
Section 3: Interpretation
- Low Copper Levels (<70 µg/dL): May indicate copper deficiency associated with malabsorption (celiac disease, inflammatory bowel disease), zinc supplementation interference, parenteral nutrition without adequate copper supplementation, or genetic disorders affecting copper transport. Clinical manifestations may include anemia, neutropenia, hypercholesterolemia, and neurological symptoms.
- High Copper Levels (>175 µg/dL): Suggests copper accumulation, potentially due to Wilson disease, chronic liver disease with cholestasis, inflammation (acute phase reactant), or occupational/dietary copper overload. In Wilson disease, serum copper alone may be falsely elevated due to ceruloplasmin-bound copper; free copper calculation is essential.
- Factors Affecting Results: Estrogen/oral contraceptives increase copper; circadian variation (morning samples lower); menstrual cycle effects; pregnancy increases copper significantly; hepatic synthetic dysfunction; infection and inflammation raise levels; hemolysis may cause falsely elevated results; sample contamination with copper-containing equipment; recent copper-containing medication or supplementation.
- Clinical Significance of Patterns: Elevated serum copper with low ceruloplasmin suggests Wilson disease; elevated copper with elevated ceruloplasmin indicates cholestasis or inflammation; discordant results warrant investigation of free copper and 24-hour urine copper excretion; serial monitoring trends are more informative than single values for assessing therapeutic response.
Section 4: Associated Organs
- Primary Organ Systems: Hepatic system (primary copper storage and metabolism), central nervous system (copper-dependent enzymatic function and myelin formation), gastrointestinal tract (copper absorption), bone marrow (copper-dependent hematopoiesis), connective tissue (copper-dependent collagen cross-linking).
- Associated Diseases and Conditions: Wilson disease (autosomal recessive copper metabolism disorder), Menkes disease (X-linked copper malabsorption), primary biliary cholangitis, hemochromatosis with hepatic involvement, celiac disease, Crohn's disease and ulcerative colitis, short bowel syndrome, cystic fibrosis, cirrhosis, chronic pancreatitis, and neoplastic conditions.
- Potential Complications: Copper toxicity causing hepatic cirrhosis, progressive neurological deterioration, hemolytic anemia, acute liver failure, Parkinson-like symptoms, dystonia, tremor, cognitive decline, ataxia, and behavioral changes. Copper deficiency leading to peripheral neuropathy, myelopathy, anemia, and immunosuppression.
- Diagnostic Significance: Helps differentiate Wilson disease from other causes of hepatosplenomegaly and neuropsychiatric disease; identifies copper-responsive conditions for targeted therapy; monitors response to copper chelation therapy; evaluates nutritional adequacy in patients at risk for copper deficiency.
Section 5: Follow-up Tests
- Recommended Complementary Tests: Serum ceruloplasmin (critical for Wilson disease evaluation), 24-hour urine copper excretion (identifies excessive renal copper loss), free (non-ceruloplasmin-bound) serum copper calculation, serum zinc levels (zinc supplementation affects copper absorption), serum iron studies and ferritin.
- Hepatic Function Assessment: Liver function tests (AST, ALT, bilirubin, alkaline phosphatase), prothrombin time/INR, hepatic imaging (ultrasound or MRI) to assess for cirrhosis, hepatitis serology panels, and liver biopsy with copper quantification when diagnosis remains uncertain.
- Neurological Investigations: Slit-lamp examination for Kayser-Fleischer rings, brain MRI (T2-weighted imaging showing brainstem hyperintensity in Wilson disease), electromyography and nerve conduction studies if neuropathy suspected, psychometric testing for cognitive dysfunction.
- Monitoring Frequency: For Wilson disease on chelation therapy: serum copper and ceruloplasmin every 3-6 months initially, then every 6-12 months when stable; 24-hour urine copper every 3-6 months. For copper supplementation: baseline and repeat testing at 4-6 weeks, then every 3 months. For occupational exposure: annually or when symptoms develop.
- Related Trace Element Studies: Serum zinc, molybdenum, selenium, and iron panels (comprehensive trace element evaluation); chromium and manganese if malabsorption syndrome suspected.
Section 6: Fasting Required?
- Fasting Requirement: NO - Fasting is not required for serum copper testing. The test can be performed in both fasted and non-fasted states without affecting accuracy.
- Sample Collection Requirements: Collect blood in a trace-element-free, non-heparinized serum separator tube (SST) or gold-top tube, NOT in serum tubes that may contain copper-containing additives. Use plastic or stainless steel needles, avoiding traditional brass needles that may contaminate sample. Handle with copper-free equipment to prevent contamination during collection and processing.
- Medications and Preparations: No need to discontinue routine medications. However, inform healthcare provider of: current copper supplementation, zinc supplements (interfere with copper absorption), chelating agents (penicillamine, dimercaprol), estrogen-containing medications (increase copper), or recent occupational copper exposure.
- Timing Considerations: Morning samples preferred due to circadian variation (copper levels typically lower in morning). For accurate serial monitoring, collect samples at consistent times. Allow at least 48 hours between test and any previous copper-containing interventions (contrast studies, occupational exposures).
- General Patient Instructions: Avoid dietary copper supplements for 24 hours prior to testing if possible; inform phlebotomist about any skin sensitivities to antiseptics; ensure adequate hydration; rest comfortably before collection; notify staff of any relevant medical history or recent illness; provide list of all current medications and supplements.

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