scholarly journals Anti-tissue transglutaminase antibodies in the follow-up of adult coeliac disease

2009 ◽  
Vol 30 (3) ◽  
pp. 236-244 ◽  
Author(s):  
C. R. DIPPER ◽  
S. MAITRA ◽  
R. THOMAS ◽  
C. A. LAMB ◽  
A. P. C. MCLEAN-TOOKE ◽  
...  
Keyword(s):  
Coeliac Disease ◽  
Tissue Transglutaminase ◽  
Tissue Transglutaminase Antibodies

A comparative study of tissue transglutaminase antibodies and endomysium antibody immunofluorescence in routine clinical laboratory practice

2003 ◽  
Vol 40 (4) ◽  
pp. 411-416 ◽  
Author(s):  
David Sinclair ◽  
Callum B Pearce ◽  
Michael S. L. Saas ◽  
David Poller
Keyword(s):  
Guinea Pig ◽  
Coeliac Disease ◽  
Clinical Laboratory ◽  
Tissue Transglutaminase ◽  
Iga Deficiency ◽  
Complete Agreement ◽  
Tissue Transglutaminase Antibodies ◽  
Routine Clinical Laboratory ◽  
Endomysium Antibodies ◽  
Human Source

Background: The demand for screening for coeliac disease has grown rapidly over the last few years. Laboratories depending on immunofluorescence assays are faced with an increasing workload using a labour-intensive test, and an alternative to this test has been sought. This study compares tissue transglutaminase (TTG) and endomysium antibodies (EMA) in a routine clinical laboratory situation. Methods: An immunofluorescence IgA EMA test was compared with a guinea pig TTG antibody ELISA for 816 unselected requests for gut antibody screening. Discrepant results were investigated more fully using a variety of human source TTG antigen kits. Results: Guinea pig TTG ELISA and EMA assays showed agreement for 93·6% of samples. Four samples were misclassified and 48 samples gave false positive TTG results. Study of 46 EMA samples (this group included 39 of the 'discrepant' negative EMA/positive guinea pig TTG group) using three different human purified and/or recombinant TTG sources showed that 42 patients had no TTG antibodies using human sources, three were misclassified and one patient had negative EMA and positive TTG results that could not be readily explained. Further study of 32 EMA positive samples showed almost complete agreement between the human source TTG kits. Conclusions: We can recommend the replacement of EMA with ELISA for TTG antibodies for the routine screening for coeliac disease, but all positive TTG antibodies should still be followed up with IgA EMA and samples should be screened for IgA deficiency.

IgA class anti-endomysial and anti-tissue transglutaminase antibodies in relation to duodenal mucosa changes in coeliac disease

Pathology ◽  
2003 ◽  
Vol 35 (1) ◽  
pp. 56-60 ◽  
Author(s):  
Lorete Maria da Silva Kotze ◽  
Shirley Ramos da Rosa Utiyama ◽  
Renato Mitsunori Nisihara ◽  
Vanessa Ferreira de Camargo ◽  
Sergio Ossamu Ioshii
Keyword(s):  
Coeliac Disease ◽  
Tissue Transglutaminase ◽  
Duodenal Mucosa ◽  
Tissue Transglutaminase Antibodies

Anti-Tissue Transglutaminase Antibodies in Patients with Abnormal Liver Tests: Is It Always Coeliac Disease?

2005 ◽  
Vol 100 (11) ◽  
pp. 2472-2477 ◽  
Author(s):  
Oreste Lo Iacono ◽  
Salvatore Petta ◽  
Giovanna Venezia ◽  
Vito Di Marco ◽  
Giuseppe Tarantino ◽  
...  
Keyword(s):  
Coeliac Disease ◽  
Tissue Transglutaminase ◽  
Tissue Transglutaminase Antibodies ◽  
Liver Tests

An Attempt of Specific Desensitising Treatment with Gliadin in Celiac Disease

2005 ◽  
Vol 18 (4) ◽  
pp. 709-714 ◽  
Author(s):  
G. Patriarca ◽  
N. Pogna ◽  
G. Cammarota ◽  
D. Schiavino ◽  
C. Lombardo ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Tissue Transglutaminase ◽  
Clinical Manifestations ◽  
Current Treatment ◽  
Gluten Free Diet ◽  
Gluten Free ◽  
Dietary Regimen ◽  
New Approach ◽  
Tissue Transglutaminase Antibodies

Gluten-free diet is the current treatment of celiac disease. We decided to verify the occurrence of histological and serological modification and/or clinical manifestations during a gradual and progressive introduction of gliadin in the diet and if it may induce a tolerance to food, as it occurs in allergic patients. We studied the case of a celiac woman with complete clinical and histological remittance after 10 years of gluten free diet. She took increasing daily doses of gliadin, reaching the final dose of 9 g of gliadin (15 g of gluten) in 6 months. Then she started a free dietary regimen. During the 15-month follow-up period esophago-gastro-duodenoscopy showed normal Kerckring folds and villi. Anti-gliadin, anti-endomysium and anti-tissue-transglutaminase antibodies, as well as the haematological and biochemical parameters remained normal. Our results represent a new approach in the research concerning celiac disease, and could provide a future line of study for its management.

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