Explains gluten-free diets and allergy free food lists

Data shows that celiac disease is probably more common than is known.

A multicenter study, involving 36 centers from 22 countries, found that the average celiac incidence was one case in every 1,000 live births. Greco L, Maki M, Di Donato F, et al. Epidemiology of celiac disease in Europe and the Mediterranean area.

A summary report on the multicenter study by the European Society of Pediatric Gastroenterology and Nutrition. Auricchio S, Visakorpi JK, eds. Common food intolerances 1: epidemiology of coeliac disease. New York: Karger, 1992:14.

The predicted rate of celiac disease in newborns is one case in every 300. Greco L, Di Donato F, Ansaldi N, et al. Analysis of incidents trends--an example from the Italian cohort. In: Auricchio S, Visakorpi JK, eds. Common food intolerances 1: epidemiology of coeliac disease. New York: Karger, 1992:25.

In one study among blood donors, the prevalence of celiac disease was found to be as high as one in 266. Hed J, Lieden G, Ottosson E, Strom M, Walan A, Groth O, et al. IgA anti-gliadin antibodies and jejunal mucosal lesions in healthy blood donors [Letter]. Lancet 1986;2(8500):215.

To determine the prevalence of celiac disease in the United States, 2,000 healthy blood donors were screened for IgA and IgG antigliadin antibodies. Subjects with elevated levels were tested for antiendomysial antibodies. The prevalence of elevated antiendomysial antibody levels in healthy blood donors was found to be 1 in 250. The authors of the study conclude that data suggest that celiac disease may be greatly underdiagnosed and is relatively common in this country. Horvath K, Hill ID, Fasano A, Hammed A, Magazzu G. Endomysium antibodies in blood donors predicts a high prevalence of celiac disease in the USA. Digestive Disease Week and the 96th annual meeting of the American Gastroenterological Association [Abstracts]. Gastroenterology 1996; 110(4 Suppl):A1-1591.

The incidence of celiac disease in relatives of celiac patients is significantly greater than the incidence in the control population. The prevalence of celiac disease is approximately 10 percent in near relatives. MacDonald WC, Dobbins WO, Rubin CE. Studies of the familial nature of celiac sprue using biopsy of the small intestine. N Engl J Med1965;272:448-56.

In patients with celiac disease, the immune system is abnormally activated by gluten, specifically the gliadin portion of wheat protein, and prolamines (insoluble proteins) in rye, barley and oats. de Ritis G, Auricchio S, Jones HW, Lew EJ, Bernardin JE, Kasarda DD. In vitro (organ culture) studies of the toxicity of specific A-gliadin peptides in celiac disease. Gastroenterology 1988;94:41-9.

Celiac disease is a genetic, immunologically mediated, small intestine enteropathy in which mucosal villi are destroyed by cellular and humoral-mediated immunologic reactions to gliadin protein. The loss of functioning villi limits the ability of the small intestine to absorb nutrients, thus adversely affecting all systems of the body. Doniach I, Shiner M. Duodenal and jejunal biopsies II. Histology. Gastroenterology 1957;33:71-86.

When people genetically predisposed to celiac disease do not ingest gluten, they have no manifest illness. Delaying ingestion of gluten products through breast feeding or dietary habits may change or delay the onset of disease. Maki M, Holm K. Incidence and prevalence of coeliac disease in Tampere. Coeliac disease is not disappearing. Acta Paediatr Scand 1990;79:980-2.

In a study of 212 patients with dermatitis herpetiformis who were managed over a period of 25 years with a gluten-free diet, several benefits of dietary therapy were found, including (1) the patients' need for medication was reduced or abolished, (2) the enteropathy resolved and (3) patients experienced a feeling of well-being after beginning the diet. Garioch JJ, Lewis HM, Sargent SA, Leonard JN, Fry L. 25 years' experience of a gluten-free diet in the treatment of dermatitis herpetiformis. Br J Dermatol 1994;131:541-5.

Malabsorption should be suspected in any patient with weight loss and diarrhea, and the signs and symptoms of specific vitamin or nutritional deficiencies. The latter include visual disturbances, neuropathy, anemia, osteopenic bone disease, tetany, hemorrhagic diathesis or infertility. In celiac disease, the clinical symptoms are determined by the severity and the proximal-to-distal extent of the intestinal lesions. Symptoms often manifest in childhood and then disappear, only to recur in adulthood. Mason RE, Giannella RA. Malabsorption. In: Rakel RE, ed. Conn's Current therapy 1995: latest approved methods of treatment for the practicing physician. Philadelphia: Saunders, 1995:450-3.

A national survey of 1,937 members of the Canadian Celiac Association addressed the issue of previous missed diagnosis of celiac disease. Of 686 patients with biopsy-proven celiac disease, 299 (43 percent) had previously been given the following incomplete or missed diagnoses: anemia, 47; stress, 45; nervous condition, 41; irritable bowel syndrome, 34; gastric ulcer, 23; food allergy, 19; colitis, 13; menstrual problems, 13; edema, 9; gallstones, 9; diverticulitis, 6; dermatitis herpetiformis, 4 and other, 36. Vogelsang H, Genser D, Wyatt J, Lochs H, Ferenci P, Granditsch G, et al. Screening for celiac disease: a prospective study on the value of noninvasive tests. Am J Gastroenterol 1995;90:394-8. In one study, 102 patients examined for nonspecific abdominal symptoms underwent small intestine biopsy. In this group, 49 patients were ultimately diagnosed with celiac disease. Report of Working Group of European Society of Paediatric Gastroenterology and Nutrition. Revised criteria for diagnosis of coeliac disease. Arch Dis Child 1990;65:909-11.