IV. The Gliadin Antibody Test
Background
Gliadin reactivity and intolerance is a genetically determined enteropathy, and a non IgE mediated response. The permanent intolerance to the gliadin, a group of proteins present in the grain of many cereals, shows a wide variation in its prevalence across population pools. The apparent incidence of celiac disease among newborns tested in Ireland, Austria and Sweden is respectively, 1/300, 1/1000, 1/8500, with about a two fold bias in females. The true occurrence of gliadin intolerance appears much higher since the latent and subclinical stages present minor symptoms in otherwise healthy individuals. Many of these individuals are rarely diagnosed with gliadin intolerance, nevertheless, they incur gradual tissue damage. Clinical Presentation The damaging effect of gliadin is mediated by a tetrapeptide which causes a mucosal inflammatory reaction. Endoscopic introduction of gluten into the human lumen demonstrates a local inflammation reaction followed by a gradual spread of the reaction to the more distal parts of the tract. Products of inflammation then leak into the general circulation and upregulate the pituitary release of ACTH, which in turn stimulates cortisol production. In adults with latent manifestation, the ongoing consumption of the offending grains becomes a chronic tissue insult and a challenge to the adrenal cortex. The cumulative effect of microtrauma eventually presents itself most commonly as: · Generalized fatigue or weakness ·Pain in the bones · Recurrent loose stool · Skin problems · Oligospermia

Clinical Presentation (continued) Other associated clinical manifestations include: · IgA deficit in the gut · Osteoporosis · Autoimmune diseases TExamples: Type I diabetes, Hashimoto's thyroiditis, Myxoedema, Grave's disease, scleroderma Tchronic discoid lupus, chronic hepatitis, and Sjogrens syndrome. · Psoriasis · Schizophrenia Diagnosis of Gliadin Intolerance In celiacs, the use of Gliadin antibody measurement has recently been included in the diagnostic procedure and monitoring protocols of the European Society of Pediatric Gastroenterology and Nutrition (ESPGAN). The diagnostic sensitivity (90-100%) and specificity (95-100%) of the gliadin antibody screen are generally regarded as good. Clinical Utilization The Salivary IgA antigliadin antibody test offered by Diagnos-Techs allows discrimination between celiac disease and other types of inflammatory bowel conditions. The test has adequate sensitivity to detect gliadin intolerance in the latent-subclinical stage. The test can also be used to monitor compliance in gliadin free diets, since many individuals consume wheat products unintentionally. Following the avoidance of gluten, the salivary IgA levels return to control levels. The ease of collection makes this test suitable for infants and children as well as adults.

References Selected Bibliography for Gliadin Antibody 1. Al-Bayaty, H.F. et al. Salivary and serum antibody to gliadin in the diagnosis of celiac disease. J. Oral-Pathol. Med. 18:578-581 (1989). 2. Arnason, J.A. et al. Do adults with high gliadin antibody concentrations have subclinical gluten intolerance. 3. Corazza, G. et al. Gliadin immune reactivity is associated with overt and Latent Enteropathy in relatives of celiac patient. Gastroenterol. 103:1517- 1522 (1992). 4. Grodzinsky, E. et al. High Prevalence of Celiac disease in healthy adults revealed by gliadin antibodies. Ann. Allergy. 69:66-70 (1992). 5. Hakeem, V. et al. Salivary IgA antigliadin antibody as a marker for celiac disease. Arch Dis. childhood. 67:724-727 (1992). 6. Lindh, E. et al. Screening for antibodies against gliadin in patients with osteoporosis. J. Int. Med. 231:403-406 (1992). 7. Michaelsson, G. et al. Patients with psoriasis often have increased serum levels of IgA antibodies to gliadin. Br. J. Dermatol. 129:667-673 (1993). 8. Reichert, K., Landmark, Johan. Specific IgA antibody increases in schizophrenia. Bid. psychiatry. 37:410-413 (1995).


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