To detect hereditary decreases in the production of alpha-1 antitrypsin. Decreased or nearly absent levels of A1AT can genetically predispose patients to chronic obstructive lung disease and liver disease (cirrhosis in children).
113 - 263 mg/dL
A1AT may be spuriously elevated in heterozygous deficient patients during concurrent infection, pregnancy, estrogen therapy, steroid therapy, cancer, and during postoperative periods. Homozygous deficient patients will not show the spurious elevation. Normal A1AT levels may occur in patients with liver disease who are heterozygotes. In normal patients, pregnancy and contraceptive medication may elevate levels. Levels are normally low at birth but rise soon thereafter.
- A-1 Antitrypsin
- Alpha 1 Antitrypsin
- Antitrypsin, Alpha-1
- ALPHA-1 ANTITRYPSIN, Serum
- ALPHA-1 ANTITRYPSIN
- C-REACTIVE PROTEIN SCREEN
Collect specimen in an SST tube. Centrifuge, aliquot serum into a plastic vial and refrigerate up to 7 days or freeze for up to 3 months. Avoid repeated freezing and thawing of specimen.
CRP (C-Reactive Protein) is run on all patients concurrently with A1AT at no additional charge. CRP is an indicator of infection, inflammation or necrosis, all of which may cause a spurious A1AT elevation. If CRP positive, it is recommended that A1AT be retested in 10-14 days. Alpha-1 antitrypsin (A1AT) is a glycoprotein synthesized in the liver and is the main component of the alpha-1 globulins. A1AT deficiency may be associated with a characteristic lung disease which occurs early in life (i.e., juvenile emphysema). A1AT deficiency is one of the most frequent inborn metabolic errors. A1AT should be considered a positive "acute phase protein" because it rises whenever there is tissue injury, necrosis, inflammation, or infection. In acute phase reactions, A1AT increases within 12-24 hours, reaching maximum levels in 72-96 hours. Therefore, patients with A1AT deficiency who suffer from bronchitis, pneumonia, or similar respiratory inflammation are likely to have falsely normal levels during acute illness. A-1 antitrypsin quantitation should be run when alpha-1 globulin in serum protein electrophoresis is low. Heterozygous recessive A1AT patients exhibit A1AT levels which are commonly about 60% of normal. Homozygous recessive A1AT patients exhibit levels at about 10% of normal. Phenotyping is desirable on patients with low values, with abnormal alpha-1 globulin migration on serum protein electrophoresis, and on all patients being worked up for A1AT deficient liver disease. The most pathologic A1AT variant is homozygous ZZ.