Abstract
OVER a century ago, in a classic paper, Samuel Gee1 provided a thorough description of the clinical features of childhood celiac sprue. However, subsequent truly seminal observations regarding celiac sprue awaited the 15 years that followed World War II. During that period, Dicke,2 a Dutch pediatrician, astutely observed that the ingestion of certain cereal grains, including wheat and rye, were harmful to children with this disease and then demonstrated, with van de Kamer and Weijers, that the alcohol-soluble, or gliadin, component of the water-insoluble protein, or gluten, moiety of wheat produced fat malabsorption in patients with celiac sprue.3 , 4 A few . . .
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