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What is Gluten and Dairy Intolerance? What is the difference between an allergy and intolerance/sensitivity. Latest medical research. Open to the public.
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TOPIC: Gluten Sensitivty Enteropathy More Common Than You Think

Gluten Sensitivty Enteropathy More Common Than You Think 27 Jul 2008 14:48 #533

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Gluten Sensitivity Enteropathy, More Common than You Think.

DAVID A. NELSEN, JR., M.D., M.S., University of Arkansas for Medical Sciences, Little Rock, Arkansas

Gluten-sensitive enteropathy or, as it is more commonly called, celiac disease, is an autoimmune inflammatory disease of the small intestine that is precipitated by the ingestion of gluten, a component of wheat protein, in genetically susceptible persons. Exclusion of dietary gluten results in healing of the mucosa, resolution of the malabsorptive state, and reversal of most, if not all, effects of celiac disease. Recent studies in the United States suggest that the prevalence of celiac disease is approximately one case per 250 persons. Gluten-sensitive enteropathy commonly manifests as "silent" celiac disease (i.e., minimal or no symptoms). Serologic tests for antibodies against endomysium, transglutaminase, and gliadin identify most patients with the disease. Serologic testing should be considered in patients who are at increased genetic risk for gluten-sensitive enteropathy (i.e., family history of celiac disease or personal history of type I diabetes) and in patients who have chronic diarrhea, unexplained anemia, chronic fatigue, or unexplained weight loss. Early diagnosis and management are important to forestall serious consequences of malabsorption, such as osteoporosis and anemia. (Am Fam Physician 2002;66:2259-66,2269-70. Copyright© 2002 American Academy of Family Physicians.)

Although celiac disease was formally described late in the 19th century, treatment remained empiric until the middle of the 20th century when patients were noted to improve dramatically after wheat was removed from their diet. With the development of small-bowel biopsy techniques, the small intestine was identified as the target organ. Disease causality was established when the characteristic features of villous flat tening, crypt hyperplasia, and increased intraepithelial lymphocytes (Figure 1)[/i] were shown to normalize after the institution of a gluten-free diet.1
 
In the mid-1960s, an enteropathy strikingly similar to celiac disease was identified in patients with dermatitis herpetiformis. Subsequently, this skin disorder was shown to be a manifestation of gluten-sensitive enteropathy. In the mid-1960s, adult celiac disease was also noted to be associated with numerous neuro logic disorders, including epilepsy, cerebral calcifications, and peripheral neuropathy.1

Recent population studies indicate that celiac disease is more common than was previously thought. Some patients with gluten-sensitive enteropathy have minimal or no symptoms and are unlikely to be referred to a gastroenterologist unless the disease is considered. Hence, family physicians need to be familiar with the diagnosis and management of gluten-sensitive enteropathy.


Fewer than 10 percent of adults with gluten-sensitive enteropathy present with dermatitis herpetiformis.


Pathophysiology 

Ingested protein does not normally provoke an immune response. This phenomenon is termed "oral tolerance." Patients who exhibit true allergy to an ingested protein (e.g., milk or soy protein) have a typical IgE-mediated response consisting of urticaria, angioedema, and bronchoreactivity.

The autoimmunity in gluten-sensitive enteropathy involves plasma cells that produce IgA and IgG; there is little or no IgE involvement. Current theory suggests that ingested alpha-gliadin (a component of the gluten protein) and related peptides bind with tissue transglutaminase (a ubiquitous intracellular enzyme) in enterocytes. The alpha-gliadin is rich in glutamine; transglutaminase deamidates glutamine residues, forming glutamic acid. Deamidation enhances the immunogenicity of alpha-gliadin by creating epitopes that are recognized as foreign by host cell­mediated immunity.2

Plasma cells produce IgA and IgG that are directed against a variety of antigens, including transglutaminase, endomysium, gliadin, and reticulin. Locally elaborated lymphokines attract inflammatory cells.3 This intense local inflammatory reaction produces the villous flattening characteristic of gluten-sensitive enteropathy. Malabsorption of micronutrients (e.g., vitamins and minerals) and macronutrients (e.g., protein, carbohydrate, fat) follows. Small-bowel involvement is most prominent proximally and may be "patchy," especially in patients with "silent" celiac disease (i.e., minimal or no symptoms) and those with dermatitis herpetiformis.

Approximately 95 percent of patients with celiac disease exhibit specific Human Leukocyte Antigen (HLA) class II alleles DQA1*0501 and DQB1*0201.4 Patients with type 1 diabetes, autoimmune thyroid disease,5 Sjögren's syndrome, primary biliary cirrhosis, Addison's disease, systemic lupus erythematosus, selective IgA deficiency, and alopecia areata may also exhibit similar genotypes and are at risk for gluten-sensitive enteropathy (Table 1).[/i] Because many persons have these genotypes and only a few develop gluten-sensitive enteropathy, investigators have hypothesized that other genes or cofactors may be involved.1 

 
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