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| A B C D E F G H I J K L M N O P Q R S T U V W X Y Z # |
T4 (Thyroxine) Antibody
Test Code36576
CPT Codes
83519
Preferred Specimen
1 mL serum
Minimum Volume
0.5 mL
Transport Container
Plastic screw-cap vial
Transport Temperature
Room temperature
Specimen Stability
Room temperature: 14 days
Refrigerated: 14 days
Frozen: 28 days
Refrigerated: 14 days
Frozen: 28 days
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
Gross hemolysis • Grossly lipemic • Plasma
Methodology
Radiobinding Assay (RBA)
FDA Status
This test was developed and its analytical performance characteristics have been determined by Quest Diagnostics. It has not been cleared or approved by FDA. This assay has been validated pursuant to the CLIA regulations and is used for clinical purposes.
Setup Schedule
Set up: Sun, Wed; Report available: 4-8 days
Reference Range
Negative
Clinical Significance
This test helps identify thyroxine (T4) thyroid hormone autoantibodies (THAAbs), which may interfere with T4 immunoassays in individuals with discordant serum T4 levels [1].
THAAbs may present in healthy individuals but are more common in patients with autoimmune thyroid diseases. THAAbs may affect both 1-step and 2-step immunoassays; the interference may be transient or persist for years. T4 THAAbs interfere with T4 measurements by competing with T4 antibodies used in the T4 immunoassays. When the serum T4 level is discordant with clinical manifestations or other test results (for example, elevated T4 levels with normal or elevated thyroid stimulating hormone [TSH] levels), this test may be used to determine whether T4 THAAbs is the cause of discordance [1].
Other methods of screening for interference by T4 THAAbs are polyethylene glycol precipitation and comparison against equilibrium dialysis. Anomalous T4 levels may also be caused by a range of interfering substances, such as biotin, heterophilic antibodies, and antibodies to streptavidin and ruthenium [1].
Other conditions that may result in elevated free T4 and/or free triiodothyronine levels without suppressed TSH level include thyroxine replacement therapy, familial dysalbuminemic hyperthyroxinemia, certain drugs (eg, amiodarone and heparin), nonthyroidal illness, neonatal period, TSH-secreting pituitary adenoma, resistance to thyroid hormone, and disorders of thyroid hormone transport or metabolism [2].
The results of this test should be interpreted in the context of pertinent clinical and family history and physical examination findings.
References
1. Favresse J, et al. Endocr Rev. 2018;39(5):830-850.
2. Gurnell M, et al. Clin Endocrinol (Oxf). 2011;74(6):673-678.
THAAbs may present in healthy individuals but are more common in patients with autoimmune thyroid diseases. THAAbs may affect both 1-step and 2-step immunoassays; the interference may be transient or persist for years. T4 THAAbs interfere with T4 measurements by competing with T4 antibodies used in the T4 immunoassays. When the serum T4 level is discordant with clinical manifestations or other test results (for example, elevated T4 levels with normal or elevated thyroid stimulating hormone [TSH] levels), this test may be used to determine whether T4 THAAbs is the cause of discordance [1].
Other methods of screening for interference by T4 THAAbs are polyethylene glycol precipitation and comparison against equilibrium dialysis. Anomalous T4 levels may also be caused by a range of interfering substances, such as biotin, heterophilic antibodies, and antibodies to streptavidin and ruthenium [1].
Other conditions that may result in elevated free T4 and/or free triiodothyronine levels without suppressed TSH level include thyroxine replacement therapy, familial dysalbuminemic hyperthyroxinemia, certain drugs (eg, amiodarone and heparin), nonthyroidal illness, neonatal period, TSH-secreting pituitary adenoma, resistance to thyroid hormone, and disorders of thyroid hormone transport or metabolism [2].
The results of this test should be interpreted in the context of pertinent clinical and family history and physical examination findings.
References
1. Favresse J, et al. Endocr Rev. 2018;39(5):830-850.
2. Gurnell M, et al. Clin Endocrinol (Oxf). 2011;74(6):673-678.
