Abstract

Celiac disease is characterized by gluten-induced villous atrophy of the upper small intestine, which can result in a severe malabsorption and hypocholesterolemia. In the present study, cholesterol metabolism was investigated by measuring fecal neutral sterol and bile acid excretion in 24 patients with celiac disease of varying severity before and after a gluten-free diet and cholestyramine treatment. The mean fecal bile acid output was normal, modestly increased values being found in the most severe cases only. Thus, the presence of ileal dysfunction was infrequent. The fecal neutral sterol excretion was markedly increased and was positively correlated with fecal fat and serum triglycerides, and negatively with the jejunal villous height and the serum cholesterol level. The lower the latter, the higher was cholesterol elimination in feces and the higher was cholesterol synthesis. On a gluten-free diet, fecal steroid excretion was normalized. On a fat-rich diet, cholestyramine further increased fecal fat but had no effect on fecal neutral sterols. Serum cholesterol was further decreased as the result of an increase in fecal bile acids. This increment was lowest in cases with the most severe steatorrhea, but elimination of dietary fat did not consistently improve fecal bile acid response to cholestyramine, indicating that the poor response in severe cases was not solely due to interference of fatty acids with cholestyramine. It can be concluded that the mucosal damage of the upper small intestine causes a proportionate cholesterol malabsorption, which is apparently the main reason for hypocholesterolemia in gluten enteropathy. The mechanism of hypertriglyceridemia found in severe cases with celiac disease requires further exploration.

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