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SERUM COPPER (By Photometry)

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Report in 12Hrs

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Details

Measures the concentration of copper in the blood serum using photometric methods

149300

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SERUM COPPER (By Photometry) - Comprehensive Test Guide

  • Why is it done?
    • Test Description: Measures the level of copper in the blood serum using photometric analysis to assess copper metabolism and identify copper-related disorders
    • Primary Indications: Suspected Wilson's disease (genetic copper accumulation disorder); Menkes disease screening (copper deficiency); Evaluation of unexplained neurological symptoms; Assessment of chronic liver disease; Investigation of anemia or bleeding disorders; Monitoring copper status in patients with malabsorption syndromes; Evaluation of immune system dysfunction
    • Typical Timing/Circumstances: Ordered when Wilson's disease is suspected based on clinical presentation; During routine screening of family members of Wilson's disease patients; When patients present with hepatic dysfunction without clear etiology; In cases of unexplained movement disorders, tremors, or behavioral changes; For monitoring patients already diagnosed with copper metabolism disorders; During evaluation of nutritional deficiencies in premature infants or patients on parenteral nutrition
  • Normal Range
    • Reference Range Values: Adults: 70-150 µg/dL (11-24 µmol/L); Children: 90-190 µg/dL (14-30 µmol/L); Infants: 30-190 µg/dL (5-30 µmol/L)
    • 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: Serum copper within established reference range indicates adequate copper status and proper copper metabolism; Low (Below 70 µg/dL): May indicate copper deficiency, malabsorption, or Menkes disease; High (Above 150 µg/dL in adults): May suggest Wilson's disease, hepatic dysfunction, inflammation, or copper supplementation; Borderline Values: May require repeat testing and correlation with clinical findings, ceruloplasmin levels, and 24-hour urinary copper excretion
    • What Normal vs Abnormal Means: Normal: Adequate copper stores and metabolism without significant accumulation or deficiency; Abnormal: May indicate metabolic disorder, nutritional imbalance, or underlying systemic disease requiring further investigation and intervention
  • Interpretation
    • Elevated Serum Copper (>150 µg/dL): Suggests Wilson's disease (genetic disorder of copper metabolism); Indicates hepatic cirrhosis or chronic liver disease; Associated with inflammation, acute phase response, or infection; May result from copper supplementation or occupational exposure; Requires confirmation with ceruloplasmin level, 24-hour urinary copper excretion, and slit-lamp examination for Kayser-Fleischer rings
    • Low Serum Copper (<70 µg/dL): Indicates copper deficiency; Associated with Menkes disease (X-linked genetic disorder affecting copper absorption); Seen in malabsorption syndromes (celiac disease, cystic fibrosis); Related to prolonged parenteral nutrition without adequate copper supplementation; Causes anemia, neutropenia, bone demineralization, and neurological symptoms; Requires copper supplementation and investigation of underlying cause
    • Factors Affecting Readings: Estrogen therapy (increases copper levels); Infections and inflammatory conditions (acute phase response increases copper); Pregnancy (physiological increase); Time of day (diurnal variation); Hemolysis of blood sample (falsely elevated); Contamination during collection; Ceruloplasmin levels affect total serum copper; Albumin concentration (binds copper); Medications (zinc supplementation decreases copper absorption); Dietary intake and supplementation
    • Clinical Significance of Result Patterns: High copper + Low ceruloplasmin = Strong indicator of Wilson's disease; High copper + High ceruloplasmin = Suggests inflammation, acute phase response, or pregnancy; Low copper + Normal ceruloplasmin = Consider malabsorption or dietary deficiency; Low copper + Low ceruloplasmin = May indicate Menkes disease or severe copper depletion; Serial measurements show treatment response in Wilson's disease or copper supplementation efficacy
  • Associated Organs
    • Primary Organ Systems: Liver (primary site of copper metabolism and storage); Brain and Central Nervous System (vulnerable to copper toxicity); Gastrointestinal System (copper absorption site); Red Blood Cells (copper essential for hemoglobin synthesis)
    • Conditions Associated with Abnormal Results: Wilson's Disease: Autosomal recessive genetic disorder causing toxic copper accumulation in liver, brain, and cornea; Menkes Disease: X-linked recessive disorder causing severe copper deficiency; Hepatic Cirrhosis: Advanced liver disease with altered copper metabolism; Hemolytic Anemia: Related to copper toxicity or deficiency; Chronic Cholestasis: Impaired biliary copper excretion; Celiac Disease: Malabsorption of copper; Cystic Fibrosis: Copper deficiency due to fat malabsorption; Rheumatoid Arthritis: Associated with elevated copper levels; Schizophrenia and Other Psychiatric Disorders: Possible association with copper metabolism abnormalities
    • Diseases Diagnosed or Monitored: Wilson's Disease: Primary diagnosis and ongoing monitoring of treatment efficacy; Menkes Disease: Neonatal and early childhood diagnosis; Copper Deficiency Syndromes: Associated with parenteral nutrition or malabsorption; Chronic Liver Disease: Assessment of hepatic synthetic function and copper handling; Nutritional Disorders: Evaluation of mineral status in at-risk populations
    • Potential Complications from Abnormal Results: From Copper Toxicity (High Levels): Fulminant hepatic failure; Hemolytic anemia; Neurological deterioration (tremors, dystonia, rigidity); Psychiatric manifestations; Corneal Kayser-Fleischer rings (permanent); From Copper Deficiency (Low Levels): Microcytic anemia; Neutropenia with increased infection risk; Osteoporosis and bone demineralization; Neurological symptoms including myelopathy; Impaired immune function; Growth retardation in children
  • Follow-up Tests
    • Recommended Additional Tests: Serum Ceruloplasmin: Essential for Wilson's disease diagnosis (typically low in Wilson's disease); 24-Hour Urinary Copper Excretion: Gold standard for assessing body copper burden; Slit-Lamp Examination: Detection of Kayser-Fleischer rings in eyes; Liver Function Tests (AST, ALT, alkaline phosphatase, bilirubin); Albumin and Total Protein: Assessment of liver synthetic function; Complete Blood Count: Evaluate for anemia, hemolysis, or neutropenia; Neuroimaging (MRI of brain): If neurological symptoms present
    • Further Investigations Based on Results: If Elevated Copper: Genetic testing for ATP7B gene mutations (Wilson's disease); Liver biopsy if diagnosis unclear; Hepatic ultrasound or CT imaging; Ophthalmology referral for slit-lamp examination; If Decreased Copper: Genetic testing for ATP7A gene (Menkes disease); Evaluation for malabsorption disorders (celiac serology, fecal fat); Assessment of nutritional intake and supplementation; If borderline or equivocal: Repeat testing after addressing confounding factors
    • Monitoring Frequency for Ongoing Conditions: Wilson's Disease on Treatment: Every 3-6 months initially, then every 6-12 months; More frequently if medication changes or symptoms develop; After treatment stabilization: Annually; Copper Deficiency on Supplementation: Every 1-3 months during therapy; Post-correction: Every 6-12 months; Family Screening in Wilson's Disease: Initial screening of siblings and children; Then periodically based on clinical status; Patients on Parenteral Nutrition: Every 1-3 months for copper monitoring
    • Related Tests Providing Complementary Information: Serum Zinc: Competes with copper absorption; useful in Wilson's disease management; Iron Studies: Related to copper metabolism and anemia assessment; Serum Transferrin and Ferritin: Associated with copper in iron metabolism; Prealbumin: Marker of nutritional and liver synthetic status; Immunoglobulin Levels: Copper important for immune function; Hemoglobin Electrophoresis: Assessment of hemolysis in copper toxicity; Liver Biopsy Copper Content: Confirmatory test for Wilson's disease (>250 µg/g dry weight suggests diagnosis)
  • Fasting Required?
    • Fasting Requirement: NO - Fasting is NOT required for serum copper testing. The test can be performed on random serum samples without dietary restriction.
    • Patient Preparation Requirements: Patient may eat and drink normally before the test; No specific dietary modifications necessary; Standard timing: Morning collection preferred for consistency (diurnal variation exists); Patient should remain seated for 5 minutes before collection to minimize stress effects; Report current medications to laboratory technician
    • Medications to Avoid or Report: Do NOT discontinue medications unless specifically instructed by physician; Medications affecting copper levels (report to laboratory): Zinc supplements (decreases copper absorption); Estrogen therapy (increases serum copper); Corticosteroids (may increase levels during acute phase response); Copper supplementation or chelating agents (D-penicillamine, trientine); Iron supplements (competitive absorption); Do not require medication cessation for test accuracy
    • Special Specimen Collection Instructions: Use only trace-metal-free collection tubes (copper-free) to avoid contamination; Whole blood drawn into appropriate vacutainer; Allow proper clotting time (5-10 minutes); Centrifuge at appropriate speed to separate serum; Avoid hemolysis (release of RBC hemoglobin falsely elevates copper); Refrigerate sample if delay in processing expected; Transport to laboratory promptly; Label specimen with patient identification and collection time; Inform laboratory of any copper supplementation or occupational copper exposure

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