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Alpha 1 Antitrypsin

Liver
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Report in 48Hrs

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At Home

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No Fasting Required

Details

Protein produced by liver that protects lungs.

₹2,908₹4,155

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Alpha 1 Antitrypsin Test Guide

  • Why is it done?
    • Measures the level of alpha 1 antitrypsin, a protective protein produced by the liver that prevents lung and liver tissue damage
    • Screens for alpha 1 antitrypsin deficiency (AAT deficiency), a genetic disorder that increases risk of early-onset emphysema and chronic obstructive pulmonary disease (COPD)
    • Evaluates patients with unexplained emphysema, bronchiectasis, or COPD, particularly those under age 45 or with a family history of lung disease
    • Assesses individuals with cirrhosis or chronic liver disease of unknown etiology
    • Monitors relatives of patients diagnosed with AAT deficiency
    • Investigates patients with vasculitis or necrotizing vasculitis (anti-neutrophil cytoplasmic antibody [ANCA]-associated)
  • Normal Range
    • Normal/Adequate Level: Greater than 57 micromoles per liter (µmol/L) or greater than 150 mg/dL
    • Borderline/Intermediate Level: 32-57 µmol/L (85-150 mg/dL) - indicates carrier status; heterozygous for AAT deficiency
    • Deficient Level: Less than 32 µmol/L (less than 85 mg/dL) - indicates significant AAT deficiency; homozygous condition carries clinical risk
    • Critical/Severely Deficient: Less than 11 µmol/L (less than 30 mg/dL) - very high risk for early-onset emphysema and liver disease
    • Note: Reference ranges may vary slightly between laboratories; always refer to the specific laboratory's reference range provided with test results
  • Interpretation
    • Normal Results (>57 µmol/L): Adequate protective levels of AAT; patient is at normal risk for AAT deficiency-related diseases; lungs and liver have sufficient protection
    • Carrier/Heterozygous (32-57 µmol/L): Patient carries one copy of the deficiency gene; typically asymptomatic; minimal lung disease risk unless combined with smoking or other environmental exposures; important for genetic counseling and family screening
    • Deficient (< 32 µmol/L): Significant AAT deficiency confirmed; homozygous or compound heterozygous genotype; markedly increased risk of early-onset emphysema (especially if smoker or occupational exposure); liver cirrhosis possible; requires phenotyping or genotyping; augmentation therapy may be considered
    • Severely Deficient (<11 µmol/L): Critical AAT deficiency; very high risk for early-onset emphysema and progressive lung disease; significant risk for neonatal hepatitis and childhood cirrhosis; immediate clinical intervention and specialist referral recommended; AAT replacement therapy indicated
    • Factors Affecting Results:
    • Acute inflammation, infection, or stress can temporarily elevate AAT levels (acute phase reactant)
    • Estrogen therapy and oral contraceptives may slightly increase AAT levels
    • Smoking significantly accelerates lung damage in deficient individuals
    • Occupational exposures (dust, fumes) increase disease progression risk
    • Recent blood transfusion may affect results; test should be delayed 2-3 months
  • Associated Organs
    • Primary Organs Involved:
    • Lungs - most common site of AAT deficiency manifestation
    • Liver - site of AAT production and secondary target organ
    • Associated Diseases and Conditions:
    • Early-onset emphysema (typically before age 45) - progressive lung destruction and air sac damage
    • Chronic obstructive pulmonary disease (COPD) - airway obstruction and airflow limitation
    • Bronchiectasis - chronic widening and damage of airways
    • Neonatal hepatitis - inflammation of liver in newborns
    • Cirrhosis and liver failure - progressive liver scarring and dysfunction
    • Hepatocellular carcinoma - increased risk in patients with AAT-related cirrhosis
    • Vasculitis - particularly ANCA-associated vasculitis affecting small vessels
    • Panniculitis - inflammation of subcutaneous fat tissue
    • Complications of Abnormal Results:
    • Respiratory failure and need for supplemental oxygen
    • Lung transplantation requirement in severe cases
    • Portal hypertension and esophageal varices bleeding
    • Hepatic encephalopathy and liver transplantation need
  • Follow-up Tests
    • Confirmatory/Additional Testing:
    • AAT Phenotyping - identifies specific AAT variants (Pi typing) to confirm genotype, especially if borderline or deficient results
    • AAT Genotyping - genetic testing to identify specific mutations (SERPINA1 gene) for definitive diagnosis and family counseling
    • Pulmonary Function Tests:
    • Spirometry - measures lung function and airflow obstruction
    • Lung diffusion capacity (DLCO) - assesses oxygen transfer capability
    • Imaging Studies:
    • High-resolution CT scan of chest - evaluates for emphysema and bronchiectasis
    • Abdominal imaging - ultrasound or CT to assess liver for cirrhosis if indicated
    • Liver Function Tests:
    • Liver enzymes (ALT, AST, alkaline phosphatase, bilirubin) - assess hepatic function and damage
    • Albumin and prothrombin time (PT/INR) - evaluate synthetic liver function
    • Additional Investigations:
    • Bronchoscopy with bronchoalveolar lavage - if pulmonary infection or malignancy suspected
    • Liver biopsy - if cirrhosis or significant hepatic disease suspected
    • Serologic testing for viral hepatitis and autoimmune markers - if liver disease present
    • 6-minute walk test - assesses exercise tolerance and oxygen requirement
    • Monitoring Frequency:
    • Annual spirometry - for diagnosed AAT deficiency to monitor lung function decline
    • Quarterly or biannual chest imaging - if progressive emphysema documented
    • Annual liver function tests - for patients with evidence of hepatic involvement
    • Family member screening - first-degree relatives should be tested within 1 year of index diagnosis
  • Fasting Required?
    • Fasting Required: No - fasting is not necessary for AAT testing
    • Patient Preparation Instructions:
    • No dietary restrictions - patient can eat and drink normally before the test
    • Inform healthcare provider of recent illnesses - fever, infection, or acute inflammatory conditions within the past 2-4 weeks can transiently elevate AAT
    • List all current medications - particularly estrogen-based therapies and oral contraceptives which may affect results
    • Timing after transfusion - if blood transfusion received, test should be delayed 2-3 months for accurate AAT measurement
    • Standard blood draw preparation - wear loose, comfortable sleeves to facilitate venipuncture
    • Hydration - maintain normal fluid intake before the test
    • Medications:
    • Continue taking regular medications as prescribed unless otherwise instructed
    • No medications need to be withheld for this test
    • Specimen collection involves standard venipuncture requiring 5-10 mL of blood in serum separator tube (SST); results typically available within 24-72 hours

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