Alpha<sub>1</sub>-Antitrypsin, Serum
| Alpha1-Antitrypsin, Serum | | | |
| Number | | 001982 |
| CPT | | 82103 |
| Synonyms | | A1-Antitrypsin ; A1AT ; AAT ; Acute Phase Proteins ; Alpha1-Protease Inhibitor |
Specimen | | Serum or plasma |
| Volume | | 1 mL |
| Minimum Volume | | 0.5 mL (Note: This volume does not allow for
repeat testing.) |
| Container | | Gel-barrier tube, red-top tube, lavender-top (EDTA) or
green-top (heparin) tube |
| Collection | | Separate serum from cells. |
| Storage Instructions | | Refrigerate at 2°C to 8°C. |
| Patient Preparation | | Overnight fasting is preferred. |
| Causes for Rejection | | Chylous serum |
| Reference Interval | | 90-200 mg/dL |
| Use | | Detection of hereditary decreases in the production of alpha1-antitrypsin (AAT). Decreased or nearly absent levels of AAT can be a factor in chronic obstructive lung disease and liver disease. An increased prevalence of non-MM phenotypes is found with cryptogenic cirrhosis and with CAH. Cirrhosis in a child should raise consideration of AAT deficiency or Wilson disease. Diagnosis of inflammatory states, if elevated (eg, rheumatoid arthritis, bacterial infection, vasculitis, neoplasia). |
| Limitations | | AAT may be elevated into normal range in heterozygous deficient patients during concurrent infection, pregnancy, estrogen therapy, steroid therapy, cancer, and during postoperative periods. Homozygous deficient patients will not show such elevation. Normal AAT levels may occur in patients with liver disease who are heterozygotes. In normals, pregnancy and contraceptive medication may elevate levels. Levels are normally low at birth but rise soon thereafter. |
| Methodology | | Immunologic |
| Contraindications | | If CRP is positive, retest AAT in 10-14 days. |
| Additional Information | | Should be run when alpha1 globulin in serum protein electrophoresis is low or when two bands are seen in the alpha1 region. Heterozygous patients exhibit AAT levels which are commonly about 60% of normal. Homozygous recessive AAT patients exhibit levels at about 10% of normal. Phenotyping is desirable on patients with low values and on all patients being worked up for AAT-deficient liver disease. Most pathologic is homozygous state ZZ. An M null genotype will have phenotype as MM but low serum level. AAT is one of the alpha globulins which together are called “acute phase reactants.” These rise rapidly, but nonspecifically, in response to inflammatory insults. |
|