Post Date: July 15, 2011
Research team identifies diagnostic marker for nonresponsive celiac disease
The presence of transglutaminase 2-specific autoantibodies in the small-bowel mucosa is specific to celiac disease.
Phoenix, Arizona—Healthcare practitioners often ask the question “Why?” when a patient with celiac disease does not respond to a gluten-free diet (GFD). Understanding the reasons behind the patient’s nonresponse is important because of the serious complications that can occur when the GFD does not work. Part of the process of answering this question includes ensuring that the patient does not have another condition that may be causing the problems in the absence of gluten.
Seeking to find a diagnostic marker that can differentiate celiac disease from other nonceliac-related enteropathies, a Finish research team examined the presence of small-bowel mucosal transglutaminase 2 (TG2)-specific autoantibodies in three groups of patients: 27 patients who were nonresponsive to a GFD diet, 28 patients who were responsive to a GFD diet, and 10 patients who had a nonceliac-related enteropathy, such as Crohn’s disease. They also studied other potential markers, such as the levels of serum autoantibodies, CD3+, and CD30+, as well as HLA-type.
After conducting the tests, the researchers found that small-bowel mucosal TG2-specific autoantibodies better distinguished nonresponsive celiac disease from nonceliac-related enteropathies than the other markers. Specifically, all but one of the patients with celiac disease (both responsive and nonresponsive) had small-bowel mucosal TG2-specific autoantibodies, while all controls without celiac disease did not have them.
The team concluded that small-bowel mucosal TG2-specific autoantibodies “offer a valuable tool in the differential diagnostics of seronegative enteropathies, enabling the design of appropriate therapeutic strategies.”
Koskinen O, Lindfors K, Collin P, et al. Intestinal transglutaminase 2 specific antibody deposits in non-responsive coeliac disease. Dig Liver Dis. 2010 Oct;42(10):692-697