Molybdenum

Hormone/ Element

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No Fasting Required

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Trace element analysis.

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Molybdenum Test Information Guide

Why is it done?
- Measures serum or urinary molybdenum levels to assess molybdenum nutritional status and metabolic function
- Evaluates for molybdenum deficiency in patients with parenteral nutrition or total parenteral nutrition (TPN) requiring long-term supplementation
- Assesses for molybdenum toxicity in patients with excessive occupational or environmental exposure
- Investigates suspected molybdenum cofactor deficiency, a rare genetic disorder affecting metabolic enzymes
- Monitors molybdenum status in patients with malabsorption syndromes or chronic gastrointestinal disorders
- Evaluates metabolic dysfunction symptoms such as neurological abnormalities, intellectual disability, or developmental delays in infants and children
- Typically performed when clinical suspicion of molybdenum imbalance exists or as part of micronutrient profiling in specialized clinical settings
Normal Range
- Serum Molybdenum: 0.3-3.0 ng/mL (nanograms per milliliter) or 3-30 μmol/L (micromoles per liter), depending on laboratory and methodology
- Urinary Molybdenum: 10-100 ng/day or 0.1-1.0 μmol/day (24-hour urine collection)
- Interpretation:
- Normal: Molybdenum levels within established reference range indicate adequate nutritional status and normal metabolic function
- Low/Deficient: Serum molybdenum <0.3 ng/mL suggests deficiency; associated with enzyme dysfunction and metabolic disorders
- Elevated/Toxic: Serum molybdenum >3.0 ng/mL or significantly elevated levels may indicate toxicity from occupational exposure or excessive supplementation
- Note: Reference ranges vary significantly among laboratories; always consult your laboratory's specific reference values as measurement methods differ
Interpretation
- Low Molybdenum (Deficiency):
- Indicates molybdenum deficiency, leading to impaired function of molybdenum-dependent enzymes (sulfite oxidase, xanthine oxidase, aldehyde oxidase)
- Associated with neurological symptoms, developmental delays, intellectual disability, seizures, and cerebral palsy-like manifestations in severe cases
- May occur in patients on prolonged TPN without molybdenum supplementation or in malabsorption syndromes
- Normal Molybdenum:
- Reflects adequate enzyme cofactor availability for normal metabolic functions including purine and sulfite metabolism
- Suggests adequate nutritional intake and proper gastrointestinal absorption or supplementation regimen
- Elevated Molybdenum (Toxicity):
- May indicate occupational or environmental exposure in workers (mining, smelting, welding industries)
- Elevated levels may interfere with copper metabolism, causing secondary copper deficiency with associated neurological symptoms
- Can result from excessive supplementation or long-term high-dose therapeutic administration
- Factors Affecting Results:
- Dietary intake: Foods high in molybdenum (legumes, grains, nuts) increase serum levels
- Kidney function: Renal impairment may affect molybdenum excretion and serum accumulation
- Gastrointestinal health: Malabsorption, inflammatory bowel disease, and short bowel syndrome reduce absorption
- Supplementation status: TPN formulations with or without molybdenum directly influence serum levels
- Occupational/environmental exposure: Industrial work or contaminated water sources increase levels
Associated Organs
- Primary Organ Systems:
- Central Nervous System: Molybdenum-dependent enzymes critical for neurological function; deficiency causes seizures, developmental delays, intellectual disability, cerebral palsy-like manifestations, and lactic acidosis
- Hepatic System: Liver is a major metabolic site for molybdenum-dependent enzymes; dysfunction impairs detoxification and metabolic processes
- Renal System: Kidneys regulate molybdenum excretion; renal disease affects molybdenum homeostasis and accumulation
- Gastrointestinal System: Site of molybdenum absorption; malabsorption conditions reduce bioavailability
- Associated Medical Conditions:
- Molybdenum Cofactor Deficiency (MoCoD): Rare autosomal recessive genetic disorder affecting sulfite oxidase and other molybdenum enzymes; characterized by severe developmental delays, seizures, cerebral palsy, lactic acidosis, and early neonatal or infantile death
- Isolated Molybdenum Deficiency: Rare condition occurring in TPN patients without molybdenum supplementation; presents with neurological dysfunction and enzyme deficiencies
- Molybdenum-Induced Copper Deficiency: Excessive molybdenum antagonizes copper absorption, leading to copper deficiency neurological complications including myelopathy and peripheral neuropathy
- Occupational Molybdenum Toxicity: Chronic exposure in industrial workers associated with respiratory symptoms, elevated serum uric acid, and gout-like arthralgia
- Inflammatory Bowel Disease (IBD): Crohn's disease and ulcerative colitis impair molybdenum absorption and increase requirements
- Short Bowel Syndrome: Reduced intestinal surface area decreases molybdenum absorption capacity
- Chronic Kidney Disease: Impaired renal excretion leads to molybdenum accumulation and potential toxicity
- Potential Complications:
- Neurotoxicity: Severe developmental and progressive neurological impairment with seizures and encephalopathy in deficiency states
- Metabolic Acidosis: Impaired sulfite oxidase function leads to sulfite accumulation and lactic acidosis
- Secondary Copper Deficiency: Molybdenum excess competitively inhibits copper absorption, causing myelopathy and neuropathy
- Hyperuricemia and Gout: Elevated xanthine oxidase activity increases uric acid production in toxicity states
Follow-up Tests
- For Suspected Molybdenum Deficiency:
- Urinary sulfite levels: Elevated in deficiency indicating impaired sulfite oxidase function
- Serum and urine uric acid: Low levels in deficiency due to reduced xanthine oxidase activity
- Serum and urine xanthine: Elevated in deficiency due to enzyme dysfunction
- Plasma lactic acid: Assess for secondary metabolic acidosis
- Serum copper and zinc levels: Evaluate for related micronutrient deficiencies
- Comprehensive metabolic panel (CMP): Assess renal function and electrolyte balance
- Neuroimaging (MRI or CT): Evaluate structural brain abnormalities in pediatric cases with developmental delays
- For Suspected Molybdenum Toxicity:
- Serum copper level: Assess for secondary copper deficiency from competitive inhibition
- Serum uric acid: Elevated in molybdenum toxicity due to xanthine oxidase stimulation
- Renal function tests (creatinine, BUN): Monitor for renal effects of molybdenum accumulation
- Chest imaging: In occupational toxicity cases with respiratory symptoms
- For Suspected Molybdenum Cofactor Deficiency:
- Genetic testing: Identify mutations in MOCS1, MOCS2, or MOCS3 genes
- Urinary sulfite and thiosulfate: Diagnostic markers markedly elevated in cofactor deficiency
- Serum xanthine and hypoxanthine: Elevated in cofactor deficiency
- EEG and neurodiagnostic studies: Assess seizure activity and neurological dysfunction
- Brain MRI: Evaluate for structural abnormalities, periventricular cystic leukomalacia
- General Follow-up Monitoring:
- Repeat molybdenum testing: Every 3-6 months during supplementation therapy to assess response
- Micronutrient panel: Comprehensive assessment of other trace elements and vitamins in TPN patients
- Neurological assessment: Serial evaluations in pediatric patients with developmental concerns
- Hepatic and renal function panels: Routine monitoring in chronically supplemented patients
Fasting Required?
- Fasting Status: No
- Fasting is not required for molybdenum testing. The test can be performed regardless of meal timing or food consumption.
- Patient Preparation Requirements:
- Standard venipuncture: For serum molybdenum collection, standard patient preparation applies with no special pre-test requirements
- 24-hour urine collection: For urinary molybdenum, collect all urine over 24-hour period in laboratory-provided container; no special diet restrictions needed
- Medication considerations: Continue all regularly scheduled medications unless otherwise instructed by healthcare provider; no specific medications require discontinuation
- Supplementation disclosure: Inform laboratory personnel of any molybdenum supplements, multivitamins containing molybdenum, or trace element supplements being taken
- Occupational exposure history: Report any occupational or environmental molybdenum exposure to healthcare provider
- Normal hydration: Ensure adequate hydration prior to 24-hour urine collection for optimal specimen quality
- Specimen handling: Blood specimens should be collected in appropriate trace element-free tubes; urine specimens must be properly preserved according to laboratory specifications
- Timing considerations: For baseline assessment or after therapeutic interventions, coordinate timing with healthcare provider for optimal clinical interpretation

How our test process works!