Celiac

Celiac Disease. A disturbance of the lower gastroiatestiaal tract, celiac disease is a chronic disease characterized by loss of appetite and weight, depression and irritabiUty, and diarrhea frequendy followed by constipation (35). One of the more disturbiag features of ceHac disease is the large, frothy, foul-smelling stools. The disease may develop ia childhood or later ia life. Frequendy, the patients who develop the disease ia adulthood report having had some of the symptoms duting childhood. 

In addition to blood, certain types of specimens are submitted to the Pediatric laboratory which would not be commonly seen elsewhere. An example of this is sweat for analysis of chloride. The process of obtaining the sweat by iontophoresis usually falls to the personnel of the Laboratory of Neonatology (17). Stool for analysis of lipids and trypsin is more commonly submitted to the Laboratory of Neonatology than to the laboratory which services the adult population. The reason for this is that one is screening for certain intestinal diseases characteristic of infants and newborns which are rare in adults. Such conditions would be celiac disease, cystic fibrosis and others. 

Proteinaceous phytochemicals can contain toxic epitopes that elicit defense responses for example gliaden and glutein peptides which cause celiac disease and other mucosal disorders (Tighe and Ciclitira, 1995 Van de Wal et al, 1999). The mucosal inflammation caused by feeding carnivorous Atlantic salmon diets with soybean meal decreases rates of nutrient absorption (Nordrum et al, 2000), whereas the detrimental influence of such diets is much less pronounced when fed to omnivorous fish, such as catfish and tilapia. 

Noninfectious causes of acute diarrhea include drugs and toxins (Table 18-3), laxative abuse, food intolerance, irritable bowel syndrome (IBS), inflammatory bowel disease, ischemic bowel disease, lactase deficiency, Whipple s disease, pernicious anemia, diabetes mellitus, malabsorption, fecal impaction, diverticulosis, and celiac sprue. 

Since there is no true excretion of iron from the body, iron-deficiency anemia occurs mostly because of inadequate absorption of iron or excess blood loss. Inadequate absorption may occur in patients who have congenital or acquired intestinal diseases, such as inflammatory bowel disease, celiac disease, or bowel resection. Achlorhydria and diets poor in iron also may contribute to poor absorption of iron. In contrast, iron deficiency also may occur in patients who exhibit a higher rate of iron loss from the body. This is manifested in... 

Illy With or without involvement of splenic, hilar, celiac, or portal nodes. 

There are a variety of other disease states whose influence on drug absorption has been reported, including cystic fibrosis, villous atrophy, celiac disease, diverticulosis, and Crohn s disease. The results of these studies are frequently divergent, and therefore general statements cannot be made. A thorough discussion of these findings is beyond the scope of this... 

Humans given zinc supplements should be aware of possible complications (Fosmire 1990). Low intakes of 100 to 300 mg of zinc daily in excess of the recommended dietary allowance of 15 mg Zn daily may produce induced copper deficiency, impaired immune function, and disrupted blood lipid profiles. Patients treated with zinc supplements (150 mg daily) to control sickle cell anemia and nonresponsive celiac disease developed a severe copper deficiency in 13 to 23 months normal copper status was restored by cessation of zinc supplements and increased dietary copper (Fosmire 1990). 

This chapter reviewed current research pertaining to selected environmental agents and autoimmune diseases (Table 25.3). Other infectious agents (e.g., parvovirus, varicella), occupational exposures (e.g., mercury), dietary factors (dietary supplements, nutrients such as antioxidants, and specific proteins in wheat and other grains implicated in celiac disease), and stress have been the focus of additional research that was not included in this review. 

Berger (B8, B9) showed that both normal and celiac children form antibodies to a number of food proteins. These antibodies did not cause any deleterious effect in most of these individuals, but it is claimed that they have a different form in celiac children, in whom some antigens may assume a damaging role. In the celiac child certain cereals such as wheat gliadin have been shown to cause a reduction in... 

B8. Berger, E., Antibodies against various foods in infantile enteritis with special reference to antibodies in children with celiac disease. Bibliotheca. Paediat., Suppl. Ann. Paediat. No. 64, 213-221 (1957). 

C8. Collins-Williams, C., and Ebbs, J. H., Use of protein skin tests in celiac syndrome. Ann. Allergy 12, 237-240 (1954). 

G4. Gerrard, J. W., Marko, A. M., and Buchan, D., Glutamic acid derivatives in juvenile and adult celiac disease, 1. Plasma glutamic acid levels after a gliadin tolerance test. Can. Med. Assoc. J. 83, 1321-1323 (1960). 

K6. Krainick, H. G., The injurious effect of gliadin in celiac disease and its probable causes. Neue Forsch. Getreideeiweiss, GetreidestUrke u. Getreideenzyme, Ber. Getreidechemiker-Tagung, Detmold 1958 120-131 (Pub. 1959) Chem. Abstr. 54, 2552c (1960). 

K8. Krainick, H. G., Debatin, F., Gautier, E., Tobler, R., and Velasco, J. A., Additional research on the injurious effect of wheat flour in celiac disease. I. Acute gliadin reaction (gliadin shock). Helv. Paediat. Acta 13, 432-454 (1958). 

R8. Rubin, C. E., Brandborg, L. L., Phelps, P. C., and Taylor, H. C., Jr., Studies of celiac disease. I. The apparent identical and specific nature of the duodenal and proximal jejunal lesion in celiac disease and idiopathic sprue. Gastroenterology 38, 28-49 (1960). 

R12. Rubin, C. E., Celiac disease and idiopathic sprue. Some reflections on reversibility, gluten and the intestine. Gastroenterology 39, 260-261 (1960). 

T3. Thompson, M. W., Heredity, maternal age, and birth order in etiology of celiac disease. Am. J. Human Genet. 3, 159 (1951). 

Zl. Zetterqvist, H., and Hendrix, T. R., A preliminary note on an ultrastructural abnormality of the intestinal epithelium in adult celiac disease. Bull. Johns Hopkins Hosp. 106, 240-249 (1960). 

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