Tissue Transglutaminase (tTG), IgG
Code:16023|CPT:86364|LOINC:32998-7
| Includes | t-Transglutaminase (tTG) IgG |
|---|
Analysis details
Methodology
- Enzyme immunoassay (EIA)
- Chemiluminescent immunoassay (CLIA)
Expected Turnaround Time
1 day
Special Instructions
- Avoid smoking during the 30 minutes preceding the blood draw.
How to use
The Tissue Transglutaminase (tTG), IgG test (anti‑tTG IgG; tTGA) is used to screen for, establish the diagnosis of, and monitor celiac disease/gluten‑sensitive enteropathy, particularly in individuals with selective IgA deficiency. It supports the workup of dermatitis herpetiformis and is applied to assess adherence and response to a gluten‑free diet in treated celiac disease.
Limitations
Tissue transglutaminase is the dominant autoantigen in celiac disease and is present in endothelial cells, hepatocytes, erythrocytes, and in the epithelium and submucosa of the small intestine. In genetically predisposed individuals, most often carrying HLA‑DQ2/DQ8, enzymatic deamidation of dietary gliadin by tTG increases peptide immunogenicity, promoting mucosal inflammation, villous atrophy, and consequent malabsorption. The autoimmune response in celiac disease includes antibodies to gliadin, endomysium, and tissue transglutaminase. Among these, anti‑tTG demonstrates high analytical sensitivity and specificity for celiac disease. Selective IgA deficiency occurs more commonly in patients with celiac disease; in that setting, IgA‑based serology can yield false‑negative results. Measurement of tTG IgG is therefore the preferred serologic approach in suspected IgA deficiency and should be interpreted alongside total serum IgA. Antibody titers generally mirror disease activity and decline with sustained adherence to a gluten‑free diet. A negative tTG IgG result does not exclude celiac disease; results require interpretation in conjunction with clinical findings and other serologic tests.
| Reference interval |
| ||||
|---|---|---|---|---|---|
| Indications | Workup of suspected celiac disease presenting with chronic diarrhea, recurrent vomiting, abdominal pain, pediatric growth failure, or iron‑deficiency anemia, Skin eruption consistent with dermatitis herpetiformis, Seizure disorder or peripheral neuropathy when malabsorption is suspected, Atopic dermatitis or recurrent oral aphthae/cheilitis with features suggestive of celiac disease, Clinical evidence of vitamin or nutrient deficiency (eg, osteopenia, tetany, bleeding tendency) or reproductive manifestations including menstrual irregularity or amenorrhea, infertility, or erectile dysfunction, First‑degree family history of celiac disease or other celiac disease risk factors, Known or suspected selective IgA deficiency, Follow‑up of confirmed celiac disease to monitor response to a gluten‑free diet |
Specimen Requirements
| Specimen | Serum |
|---|---|
| Container | Gold/Tiger Top (SST, Gel Separator) |
| Volume | 1 mL (min 0.5 mL) |
| Storage Instructions | Room temperature, Refrigerated, Frozen |
References
Dieterich W, Ehnis T, Bauer M, et al. Identification of tissue transglutaminase as the autoantigen of celiac disease. Nat Med. 1997 Jul;3(7):797-801. PubMed 9212111
Volta U, Molinaro N, De Franchis R, et al. Correlation between IgA antiendomysial antibodies and subtotal villous atrophy in dermatitis herpetiformis. J Clin Gastroenterol. 1992 Jun;14(4):298-301. PubMed 1607605
Dahlbom I, Olsson M, Forooz NK, Sjöholm AG, Truedsson L, Hansson T. Immunoglobulin G (IgG) anti-tissue transglutaminase antibodies used as markers for IgA-deficient celiac disease patients. Clin Diagn Lab Immunol. 2005 Feb;12(2):254-8.
Volta U, Villanacci V. Celiac disease: diagnostic criteria in progress. Cell Mol Immunol. 2011 Mar;8(2):96-102.
Armstrong D, Don-Wauchope AC, Verdu EF. Testing for gluten-related disorders in clinical practice: the role of serology in managing the spectrum of gluten sensitivity. Can J Gastroenterol. 2011 Apr;25(4):193-7.
Fauci AS, Kasper DL, Longo DL, Braunwald E, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 17th ed. New York, NY: McGraw-Hill; 2008.