Alpha-1 Antitrypsin (A1AT)
Alpha-1 antitrypsin is a protease inhibitor made by the liver that protects lung tissue from damage by neutrophil elastase. Congenital A1AT deficiency (due to SERPINA1 gene mutations) causes early-onset emphysema (especially in smokers), chronic liver disease in both children and adults, and less commonly, panniculitis. A1AT is also an acute-phase reactant and rises with inflammation — useful to remember when interpreting borderline values.
Reference Ranges
Male
90 – 200
mg/dL
Female
90 – 200
mg/dL
Child
90 – 200
mg/dL
Reference ranges may vary by laboratory. Always compare with the range printed on your lab report.
What Low Levels Mean
A1AT below 90 mg/dL suggests deficiency and triggers phenotyping (SERPINA1 gene testing or protease inhibitor typing). The most severe deficiency state is ZZ (Pi*ZZ) phenotype, with levels typically 10–15% of normal. Smokers with A1AT deficiency develop panacinar emphysema by age 30–40. A1AT deficiency is also the most common genetic cause of liver disease in children and can cause cirrhosis and hepatocellular carcinoma in adults.
What High Levels Mean
Elevated A1AT is usually non-specific — it is an acute-phase reactant and rises with inflammation, infection, cancer, trauma, pregnancy, and oral contraceptive use. High A1AT rarely has its own clinical significance. However, a 'normal' A1AT during acute illness can mask underlying deficiency — retesting after the acute illness resolves is important if deficiency is suspected.
Frequently Asked Questions
Who should be tested for A1AT deficiency?
Anyone with: early-onset emphysema (especially <45 years), basilar-predominant emphysema on CT, unexplained adult liver disease, unexplained chronic liver disease in children, necrotizing panniculitis, or a family history of A1AT deficiency. Many patients are never diagnosed — under-diagnosis is a recognized problem globally, including in India.
What treatments exist for A1AT deficiency?
Smoking cessation is by far the most important intervention — smokers with A1AT deficiency lose lung function 10× faster than non-smokers with the same deficiency. Intravenous A1AT augmentation therapy (weekly infusion of pooled human A1AT) is available in some countries but expensive and not widely available in India. Standard COPD management applies. Lung and liver transplantation are options for end-stage disease.
Is A1AT deficiency inherited?
Yes — autosomal co-dominant. The SERPINA1 gene has many variants; Pi*Z is the most common clinically important deficiency allele. Pi*ZZ homozygotes have severe deficiency and disease; Pi*MZ heterozygotes have intermediate levels and modestly increased risk, especially with smoking. Family members of an affected patient should be tested — early smoking cessation in carriers may prevent disease.
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mg/dLThis information is for educational purposes only and should not replace professional medical advice. Always consult your doctor for interpretation of your test results.
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