A Clinical and Histochemical Study of Celiac Disease Before and During a Gluten-Free Diet

Abstract

Summary Peroral jejunal biopsies were obtained after a 12- to 14-hr fast from 9 control patients and from 4 patients with untreated celiac disease. In the normal jejunal mucosa, lipid stained by oil red O was distributed as a fine haze in the superficial epithelial cells and as distinct droplets in the lamina propria. In untreated celiac disease, lipid droplets were limited to the superficial epithelium and to a thin band in the region of the basement membrane; none were found in the deeper portions of the lamina propria. The superficial epithelial cells of the normal jejunal mucosa were shown to contain many enzymes identifiable by histochemical techniques. The histologically abnormal superficial epithelial cells in untreated celiac disease were deficient in acid phosphatase, succinic dehydrogenase, cytochrome oxidase, lactic dehydrogenase, leucine aminopeptidase, DPN-diaphorase, and TPN-diaphorase activity. ATPase activity was markedly decreased or absent. Serial jejunal biopsies were obtained after the institution of a gluten-free diet, and 2 subjects had repeated tests of intestinal absorption. Three to five days after gluten withdrawal, lipid droplets appeared in the lamina propria, and subsequently they disappeared from the superficial cells. Coincident with this change in lipid distribution, ATPase activity returned to the superficial epithelium. The activities of the other enzymes were not appreciably changed in the immediate postgluten withdrawal period. Fecal fat excretion gradually decreased parallel with the improvement in lipid distribution. The results of this study suggest that the defect in fat absorption in celiac disease is in the intracellular metabolism or transport of lipid, rather than in the uptake of lipid by the intestinal mucosa and that this defect may be attributable to a deficiency of ATPase activity in the superficial epithelium. It is considered likely that the absorptive failure results either from a defect in the intracellular synthesis of triglycerides or from an impairment in the formation of chylomicrons. A failure of release and transport of chylomicrons out of the cell and through the interstitial space of the lamina propria would appear to be of lesser importance.