Celiac Disease and Malabsorption

Any disease that affects nutrient digestion or small bowel function or that compromises bowel circulation or motility may result in a malabsorption syndrome, which includes systemic vascular, infectious, and neoplastic diseases ( Fig. 65.1 ). This chapter and others in this section discuss common intestinal diseases that cause malabsorption disorders.

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Malabsorption and Celiac Disease: Primary and Secondary Malabsorption.

Gluten enteropathy, or celiac disease, is a malabsorption syndrome that results from gluten-sensitive damage to the intestinal microvilli and villi, producing an abnormal villous architecture and resulting in malabsorption. This disease process exemplifies the classic signs and symptoms of malabsorption disorders. When a person with gluten enteropathy ingests gluten, the epithelium becomes damaged, the cellular maturation of epithelial cells of the villus becomes disturbed, the small bowel mucosa becomes inflamed, and mild villous atrophy to total loss of villi results in atrophic-looking mucosa.

Understanding this classic disease entity leads to an understanding of small bowel function and all its possible diseases. Almost all manifestations of abnormal digestion and absorption and all systemic manifestations, from skin disorders to malignancy, are associated with celiac disease.

Samuel Gee first described celiac disease in 1888 as “celiac affliction,” later publicized by Herter in 1908. Finally, in 1950, Dicke and colleagues found that removing wheat from the diet caused the signs and symptoms to disappear. “Celiac disease” should be used only when gluten is demonstrated to be the cause. Some persons have “refractory sprue,” in which gluten removal does not reverse the disease. Other names associated with this disorder include “idiopathic steatorrhea” and “celiac sprue.”

Celiac disease occurs worldwide, affecting an estimated 1% of the world's population. Ireland has the highest incidence, but recently, a high incidence has been reported in Italy. Gluten enteropathy appears primarily in Europe, North and South America, East Asia, and Australia.

When glutens from wheat, rye, and barley are presented to the intestinal mucosa, they react to form gliadins, which can cause the damage. Genetic studies show that a person must have alleles that encode for HLA-DQ2 or HLA-DQ8 proteins. However, many persons have DQ2 or DQ8 human lymphocyte antigen (HLA) gene expression and do not have celiac disease. Patients with celiac disease appear to be able to tolerate oats, which contain some of the biochemical products present in the other grains. Along with oats, patients tolerate rice, corn, sorghum, and millet without intestinal villous damage.

Clinical Picture

Fig. 65.2 demonstrates all possible presentations and signs/symptoms associated with celiac disease and severe malabsorption. The cardinal presentation of weight loss associated with steatorrhea is seen only occasionally. The clinician should check for celiac disease in the current environment of plentiful food when a patient experiences anemia, osteoporosis, unexplained diarrhea, or any vitamin deficiency, even if weight loss is not apparent. With the availability of numerous serologic tests, latent celiac disease has become more apparent in patients with such conditions as occult anemia, osteoporosis, and some associated malignancies.