Celiac disease (CD) is a chronic immune-mediated gluten-dependent enteropathy induced by ingestion of gluten-containing products, characterized by intestinal malabsorption and subtotal or total atrophy of intestinal villi, which improves after gluten-free diet (GFD). Untreated patients affected by the classic form of CD are at high risk of malnutrition, but an impairment of nutritional status is frequently reported also in patients with the subclinical form of the disease. Strict adherence to a GFD greatly improves nutritional status, inducing an increase in fat and bone compartments, but does not completely normalize body composition. A lack of improvement in nutritional status may identify incomplete adherence to GFD treatment. Evidence has shown lower body weights and lower fat mass and fat-free mass contents in CD patients. Untreated CD patients oxidize more carbohydrates as energy substrate compared to treated subjects. In addition, circulating ghrelin concentration was reduced after GFD treatment as a possible consequence of body composition improvement, while leptin did not correlate with the changes in body composition and substrate oxidation in patients with CD. A significant correlation was reported between ghrelin and the degree of severity of intestinal mucosal lesions. CD patients might show an alteration in lipid metabolism, i.e. low serum total and high- density lipoprotein-cholesterol as a consequence of lipid malabsorption and decreased intake. In conclusion, weight loss and nutritional deficiencies are relevant clinical features in CD. Thus, an early and accurate evaluation of nutritional status and energy metabolism represents a fundamental tool in the management of CD patients.
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