Start Date
Expiration Date
Thyroglobulin with Thyroglobulin Antibodies, Tg with Tg Ab
CPT Codes
84432, 86800
Reference Test
ATLAS Test Code

Specimen Information


Gold SST


1.0 ml

Transport Info


Fasting Required?
Patient Instructions

Reference Range

Normal range: 0.0‑55.0 ng/mL
Athyroidic patient: ≤ 5.0 ng/mL

Thyroglobulin Antibodies
Normal range: 0.0‑40.0 IU/mL
% Recovery: 70‑130 %

% Recovery
Thyroglobulin antibodies are known to interfere with the measurement of thyroglobulin. Assessment of auto-antibody interference can be made by recovery studies.

Recovery of less than 70% of a sample suggests interference in the assay and the thyroglobulin result should be interpreted with caution.


Quantitative Chemiluminescent Immunoassay (CLIA)

Clinical Significance

The follow-up, but not the diagnosis, of patients with well-differentiated thyroid cancer (DTC).
Thyroglobulin is a 660,000 MW dimeric glycoprotein composed of two identical subunits. The monomeric peptide moiety is composed of 2748 amino acids, and contains 8-10% carbohydrate and iodine. The amount of iodine varies with the dietary intake of the individual. Thyroglobulin (TG) is normally synthesized and secreted by follicular cells of the thyroid gland, and its rate of synthesis is controlled by TSH. Tg and Tg mRNA is present in the serum of all euthyroid individuals. Normal serum Tg reference limits are approximately 4-40 ng/mL based on CRM-457 standardized immunoassays. The thyroid hormones thyroxine (T4) and 3,5,3’-triiodothyronine (T3) are synthesized from tyrosine residues on thyroglobulin within the thyroid epithelial cell. Thyroglobulin itself is not biologically active, and comprises about 75% of the total protein of the thyroid follicular colloid (lumen).Three factors determine serum Tg concentrations in most clinical situations: (1) thyroid cell mass; (2) physical damage to the thyroid caused by biopsy, surgery, obstructive asphyxia, hemorrhage, radioiodine administration, external irradiation, or inflammation; and (3) activation of TSH-receptors by either TSH, chorionic gonadotropin (HCG) during pregnancy, or thyroid stimulating immunoglobulins of Graves disease. With sufficiently sensitive assays, a below normal serum Tg is rarely encountered except in those patients who have had total or near-total thyroidectomy, thyroid ablation by radioiodine, or in whom TSH secretion is suppressed by exogenous thyroid hormone administration. Patients with other thyroid disorders typically have normal or high normal serum Tg concentrations, with high levels associated with autonomous thyroid function, thyroid injury, or activation of TSH receptors. For these reasons and the frequent presence of Tg autoantibodies, a serum Tg measurement seldom provides any increase in specificity in the differential diagnosis of thyroid disorders.The major clinical use of serum Tg measurements is the follow-up, but not the diagnosis, of patients with well-differentiated thyroid cancer (DTC). Serum Tg concentrations are increased in patients with both benign and DTC, and do not serve to distinguish between the two. After all cancerous thyroid tissue has been removed by surgery, radioiodine therapy, or other ablative procedures, serum Tg measurements serve as a marker in the determination of residual or recurrent metastatic tissue of thyroid origin. In this context, serum Tg measurements reflect the sum of three variables: (1) the mass of DTC remaining; (2) the ability of the remaining tumor and thyroid tissue to respond to either endogenous TSH or recombinant human TSH (rhTSH) stimulation; and (3) the intrinsic ability of the tumor to synthesize and secrete TG.The accurate measurement of serum Tg in the presence of Tg autoantibodies (TgAb) is technically challenging. TgAb interference may cause either over-estimation or under-estimation of TgAb positive sera by current methods. With competitive binding assays such as radioimmunoassays, TgAb interference generally produces over-estimated Tg results. With immunometric assays [sandwich assays], TgAb interference typically produces inappropriately low Tg results, most likely caused by endogenous Tg immune complexes that block one or more of the reagent antibodies from binding endogenous Tg.