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Vet Q. 2012;32(1):3-11. doi: 10.1080/01652176.2012.675636. Epub 2012 Apr 10.

Gluten-dependent antibodies in horses with inflammatory small bowel disease (ISBD).

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  • 1Department of Equine Sciences, Medicine Section, Faculty of Veterinary Medicine, University of Utrecht, Utrecht, the Netherlands.



Equine inflammatory small bowel disease (ISBD) is an idiopathic pathologic condition seeming to increase in prevalence.


To investigate the potential role of gluten in equine ISBD.


Antibodies known to be important in the diagnosis of human coeliac disease (CD): IgA antibodies to human recombinant and guinea pig tissue-transglutaminase (TGA), native gliadin (AGA), deamidated-gliadin-peptides (DGPA), and primate and equine endomysium (EMA) were assessed in blood samples from three different groups of horses: ISBD affected (n = 12) on a gluten-rich diet and controls either on gluten-rich (n = 22) or gluten-poor (n = 25) diets. Significant differences (p < 0.05) between groups were assessed using the Wilcoxon test.


Both ISBD-affected horses and gluten-rich controls had significantly (p < 0.0004) higher hrTGA titers than gluten-poor controls. However, ISBD horses did not show significantly increased levels of any of the CD related antibodies when compared to gluten-rich controls. Nevertheless, markedly increased antibody levels (TGA, EMA and DGPA) were found in one of the ISBD horses. The introduction of a gluten-free ration in this 14-year-old warmblood stallion resulted after 6 months in the reduction of antibody levels and clinical recovery associated with improved duodenal histopathology.


To the best of our knowledge, this is the first study assessing gluten-related antibodies in horses and results suggest a potential pathogenic role of gluten in at least some cases of equine ISBD. Clinical importance and impact for human medicine: Given serology and concurrent clinical findings, this study warrants further investigations into the immunologic basis of possible gluten-sensitive enteropathy in horses and analogy with human disease.

[PubMed - indexed for MEDLINE]
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