Gluten - sensitive enteropathy
The condition is characterized by abnormal jejunal mucosa that improves
morphologically when treated with gluten free diet. Gluten is a protein
that can be found in cereals, wheat, barley and oats. It is rare
in Africans and Asians and affects mainly in Northern Europe.
Gluten is a high molecular weight compound that contains alpha-Gliadin
which is injurious to the small intestine. An immune reaction occurs against
alpha-Gliadin leading to the intestinal injury.
The mucosa of the proximal small bowel is predominantly affected with
damage decreasing in severity towards the ileum as the gluten is digested
into smaller non-toxic fragments.
Clinical picture (symptoms and signs)
The disease may present at any age., but peaks in adults at 20-40 years
and may occur in infancy after weaning.
Symptoms are those of small bowel disease with malabsorption. There
diarrhea or steatorrhea, abdominal pain, weight loss and nutritional
deficiencies. There may be evidence of
anemia and malnutrition.
There is an increased incidence of autoimmune disease including thyroid
disease and insulin dependent diabetes as well as inflammatory bowel disease,
chronic liver disease and fibrosing alveolitis.
Jujenal biopsy may reveal subtotal villous atrophy. Endomysial antibodies
(IgA) is the investigation of choice since it has more sensitivity and
specificity than the anti-Gliadin antibodies (IgA, IgG). IgA and
IgG anti-Gliadin antibodies may be associated with false negative and
false positive results. False-positives are possible as other gastrointestinal
disorders are known to induce circulating antigliadin antibody, mainly
Crohn disease, food protein intolerance, and postinfection malabsorption.
A gluten free diet usually produces rapid clinical and morphological
improvement. Replacement therapy (dietary deficiency) may be required.
Corticosteroids and immunosuppression with cyclosporin for cases showing
resistance to gluten free diet.
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