Alison Odey

Coeliac disease is a disorder of the small intestine caused by an autoimmune response to wheat gluten and to similar proteins found in barley, rye and oats.

The disease eliciting factor is the gluten molecule, or more specifically its alcohol-soluble fraction, gliadin. It causes damage to the small intestine which prevents the body taking up many of the nutrients that it needs from food.

The condition is widely misdiagnosed or goes unrecognised. By definition the disease is characterised by gastrointestinal complications but many people present with out any GI symptoms.

A diagnosis is made by blood screening for either antigliadin or endomysial and transglutaminase antibodies. This preliminary diagnosis is then confirmed by biopsy.

The anti-gliadin test identifies an immune response to gluten, while
the anti-endomysial and transglutaminase screening identifies an auto-immune activity.
The distinction needs to be drawn between coeliac disease and gluten sensitivity as this may not necessarily manifest as CD in the classical sense. Also someone who has been avoiding gluten in there diet would test negative to CD blood screening.

Coeliac disease has a clear genetic predisposition. There is a 10% prevalence of the disease among first degree relatives.

Classic presentation would be diarrhoea, exaggerated weight loss, enteropathy with crypts in the intestinal villi.
Elevated anti-gliadin or endomysial and transglutaminase anti-bodies. Often the patient is thin, pale/anaemic, pot bellied with abdominal discomfort, feeling unwell and fatigued.

This can be difficult to determine in a young child who may just present as being a little pale, listless, irritable with a tendency to loose bowel motions and a slightly bloated tummy.

An important associated disorder of coeliac disease is Dermatitis Herpeiformis, which
manifests in the form of an intensely itchy skin rash distinguished by the formation of small papules or blisters. These lesions are often symmetrically distributed over the elbows, knees, buttocks, scalp, neck, shoulders or sacral regions.
There is evidence that the changes in the intestinal mucosa and immunological findings are the same as those found in coeliac disease. However it is not a condition for self diagnosis as these lesions can be confused with many other conditions.

Treatment is usually complete abstinence from gluten containing cereals (use rice instead) and improvement can often be seen within 2-3 weeks.
If this proves to be successful, the additional use of carefully designed supplements, which include probiotic cultures and proteases,can make the management of this condition attainable without being overly
restrictive.

There has been some debate over whether oats can be tolerated by people diagnosed with CD. It appears that the gluten in wheat is likely to be more problematic than the gluten in oats, but is best assessed on an individual basis.

It is also likely that the gluten in wheat varieties used to make pasta is less reactive than the gluten in wheat varieties used to make bread.