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Celiac & Non-celiac Gluten Sensitivity: Filtering facts from fiction and Faddism

Manoj Shah, MD FAAP

Chief Pediatric Gastroenterology & Nutrition at Loma Linda University School of Medicine.

Celiac disease is an auto-immune, genetically susceptible, and unique condition where gluten is the trigger that activates the auto-antigen tTG (Tissue transglutaminase.) The removal of the external trigger ie. gluten essentially eliminates the illness.

Prevalence:

It is more common in communities that ingest the gluten containing starches- wheat, rye and barley. 1 in 133 people are susceptible to it, and it is more common in females than males. In Indian populations, Punjabis are more likely to get it. Though oats do not cause gluten sensitivity, they can be cross-contaminated. Thus, the oat fields have to be afar from the wheat fields.

 

Pathogenesis:

The genetic predisposition is due to the HLA DQ2 & DQ8 genes. Exposure to the protein gluten leads to celiac disease, though it is only about 1% of the susceptible population that develops the illness. The risk factors include: Gender, infant feeding habits, enteric infections, and the gut Microbiome among others.

 

It is believed that gluten should be introduced in an infant’s diet by the age of 4-6 months. Leaving this to 12 months or more increases the susceptibility of the condition.

 

The epithelial cells of the villi in the small intestines are very tightly bound. The gut microbes distort this structure by widening the gap between the villi, thus enabling the gluten to enter the lamina propria of the gut wall. This results in villous atrophy.

 

The symptomatic celiac disease is only the tip of the ice-berg, with manifestations of mucosal lesions, which may be present in silent celiac disease too. Latent celiac disease, however, has no mucosal lesions.

In a child, the typical presentation is one where the muscle development, especially the glutei, is reduced, and the abdomen is distended.

 

Clinical Presentation:

The classic GI symptoms include: chronic or recurrent diarrhea, abdominal distention, abdominal pain, anorexia, failure to thrive and weight loss, constipation, and irritability. It has also been known to cause aggressive behavior in children.

 

Dermatitis herpetiformis with vesicular lesions can be associated with GI problems. This is due to an IgE mediated allergy. Wheat antibodies are detected in such people. Other extra-intestinal presentation also includes dental enamel hypoplasia, osteopenia, osteoporosis, short stature, delayed puberty, elevated transaminases, arthritis, and iron deficiency anemia. Neurological symptoms include epilepsy, ataxia, neuropathy and dementia. The root cause is malabsorption of nutrients.

 

The biggest group of presentation is in the non-auto immune and non-allergic individuals, who do not have true celiac disease but are gluten sensitive.

 

Diagnosis:

Serology:  Antiagliadin antibodies -(IgG and IgA);  Deamidated gliadin antibodies IgG and IgA; ttG antibodies and Endosyial antibodies-IgA

Total IgA levels are elevated.

 

Genetics: The presence of HLA-DQ2 and DQ8 genes.

Definitive diagnosis is through endoscopy and biopsy. Capsule endoscopy is a useful tool as well

 

Management:

In celiac crises, treatment with steroids and immuno-suppressive is warranted.

The gluten free food industry is a major fad in society leading to an annual industry worth $6.6 billion. 14% of the population follow this diet, but few have true celiac disease.

 

The only effective treatment of celiac disease is a gluten free diet that has to be strict and life-long. Total avoidance of wheat, rye and barley includes dietary cross mixing and contamination as well.

 

The nutritional status of a gluten free diet can be measured by; Growth parameters of height, weight and BMI; CBC with a differential count pointing to anemia and lymphopenia; albumin and transthyretin levels; zinc, magnesium, calcium, iron and selenium levels; Vitamin D, Vitamin B (Folate, Niacin, Riboflavin, & Vitamin B12.); and finally the intake of fiber.

 

Management Goals:

The goal is to avoid gluten introduction into the lamina propria of the gut wall to avoid villous atrophy.

New therapeutic agents aim to artificially bind the gluten proteins to protect the tight villous structure.

 

Other studies include the blockage of auto-immune cells, and a vaccine is being developed to make the cells that react to the antibodies more tolerant of the negative effects of the antibodies.

 

Hookworms, introduced into the intestines, have been used to desensitize the intestinal cells. Such an effect is naturally available in countries where nature is not interfered with in the provision of a boosted immune system such as in the tropical countries.

Summarized by:

Dr. Parvin D. Syal

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