The lifelong elimination of wheat, rye, and barley from the diet is the only therapy proven to be effective for treating CD.2 The gluten threshold for causing intestinal mucosal damage is estimated to be 10 mg to 50 mg, or approximately 1/150 to 1/30 of a slice of bread.1,21 Initiation of a gluten-free diet results in the reduction of serologic markers and resolution of the abnormal GI histology.2 Adherence to a gluten-free diet is difficult, and patients with CD are at risk of frequent inadvertent exposure to gluten as a contaminant of other commonly used substitutes, such as oats. Additional gluten-containing grains that should be avoided include semolina, kamut, spelt, triticale, and malt. Patients are advised to use alternative grains and starches (Table 2).
Most alternative grains are not fortified with B vitamins, and testing for folic acid; vitamins B6, B12, A, D, E, and K; and iron and calcium should be performed.2 Any deficiencies should be corrected. Up to 30% of patients will fail to experience clinical or histologic improvement on a gluten-free diet.22 Most often, these patients have been unable to adhere to the diet because of known or inadvertent exposure. If dietary noncompliance is excluded, the confidence of the original diagnosis should be reassessed. There are other causes of villous atrophy, and intercurrent illnesses can occur.
There is also interest in developing treatment involving nondietary alternatives, such as recombinant enzymes that could digest gliadin in the stomach or proximal small intestine.23 These therapies are not yet available, but patients may be interested in information about them (Table 3).