Jefferson Adams is a freelance writer living in San Francisco. He has covered Health News for http://Examiner.com, and provided health and medical content for http://Sharecare.com. His work has appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate, among others.
A team of researchers recently set out to determine what factors contribute to hypertransaminasemia in patients with celiac disease.
Celiac.com 07/23/2014 - Transaminasemia develops through various pathways in patients with celiac disease. Currently, there is not much information on risk factors specifically attributable to celiac disease.
A team of researchers recently set out to determine what factors contribute to hypertransaminasemia in patients with celiac disease. The research team included B. Zanini B, R. Baschè A., Ferraresi, M.G. Pigozzi, C. Ricci, F. Lanzarotto, V. Villanacci, and A. Lanzini.
They analyzed data collected from consecutive patients referred from January 1997 through December 2009 to the celiac disease clinic at the Spedali Civili of Brescia, Italy. They then used serologic and biopsy analysis to assess the factors influencing hypertransaminasemia in 683 patients with celiac disease (group A), and 304 patients with functional gastrointestinal syndromes (group B). Both groups were about the same average age and range.
The research team detected hypertransaminasemia in 138 patients in group A (20%). Factors associated with the condition included malabsorption (odds ratio [OR], 2.22; P = .004), diarrhea (OR, 1.72; P = .005), and increasing severity of mucosal lesion (Marsh-Oberhuber class; OR, 1.46; P = .001), but not body mass index (BMI) or the blood levels of tissue-transglutaminase antibodies (tTG).
The team also detected hypertransaminasemia in 22 patients from group B (7%), which they found to be associated with the World Health Organization's BMI categories (OR, 7.9; P < .001). A total of 313 patients from group A had significantly higher levels of tTG at baseline (25.2 ± 16.9 U/L aspartate aminotransferase [AST]) than a similar bunch from group B (20.6 ± 9.9 U/L AST, P < .0001). These levels were related to BMI in group B (P = .0012), but not group A.
Patients eating gluten-free diets saw levels of AST decrease from 25.2 ± 16.9 U/L to 19.9 ± 6.6 U/L (P < .0001). This decrease was independent of the changes of duodenal histology and tTG and correlated with BMI (P = .0007). Meanwhile, the prevalence of hypertransaminasemia in gluten-free patients decreased from 13% to 4%.
These study results show that hypertransaminasemia is more common in people with celiac disease than in patients with functional gut syndromes. Also, hypertransaminasemia is related to the severity of the duodenal lesion and malabsorption, but unrelated to BMI.
By contrast, the control group, with functional gut syndromes, showed a positive correlation between the levels of AST and BMI. This relationship was restored when patients with celiac disease began to follow gluten-free diets.