Celiac disease (also known as celiac sprue or gluten-sensitive enteropathy) is a chronic gastrointestinal disease in which exposure to proteins from wheat, rye, barley and possibly oats leads to abnormalities in the small intestine and consequent nutrient malabsorption (poor absorption). In wheat, such proteins are collectively known as gliadins and constitute the toxic component of gluten. Symptoms include diarrhea, general weakness, anemia and weight loss. The disease affects the mucosa of the proximal small intestine with damage gradually decreasing in severity. However, in severe cases, the lesions extend other areas of the intestines. Diagnosis of the disease is ultimately confirmed by small intestinal biopsy showing a flat mucosa that is reversed on a gluten-free diet.
A number of chronic diseases have been reported to be associeted with food hypersensitivity, including lymphocytic IBD, eosinophilic enteritis and hypereosinophilic syndrome, idiopathic colitis and gluten-sensitive enteropathy (GSE).
SIGNS
Dermatological signs include itch, which poorly responds to corticosteroid therapy, bump-like skin eruptions, hair loss, self-mutilation and secondary bacterial infections. Skin lesions most often appear on the face, neck, ears, feet and belly. Asthma, seizures, and cystitis have been associated with food hypersensitivity, but vomiting, skin lesions and diarrhea are considerably more common.
Familial GSE has been defined for Irish setters, but gluten sensitivity may affect a much wider number of dog and cat breeds. In the Irish setters the disease is seen between 4 and 7 months of age as a failure to gain weight accompanied by chronic diarrhea. In the Irish setters the gluten-sensitive enteropathy (GSE) is inherited as autosomal dominant, sex-linked recessive disorders.
Definitive diagnosis is achieved based on response to dietary trials, when the affected animal is fed a gluten-free diet and recurrence of clinical signs when the cereal-free diet is withdrawn.
The prognosis is usually good as long as the disease is not advanced. Possible mechanisms for CNS injury include potential deficiencies of calcium, magnesium, and vitamins; genetic factors; and isolated CNS vasculitis. Malabsorption may be occult, and seizures may be the predominant feature. Restricted dietary gluten may produce rapid improvement.