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Coeliac Disease

ClearlyExplained.Com

28th April 2007

by Dr. Pradeep Bhandari M.B.B.S., M.MED

A straightforward and fast information
guide to coeliac disease from ClearlyExplained.Com

wheat free

coeliac collage

The digestive tract with bread superimposed highlights the the principles of coelic disease.

Image: composite from wikipedia and US NIH


The | What | Why | News | How | History | Future | of coeliac disease

What is coeliac disease?

Coeliac disease, also called non-tropical sprue, is an auto-immune inflammatory disorder of the small intestine caused by the sensitivity of the body to the protein ‘gluten’ that are found in many foods such as wheat, barley, rye, and sometimes oat. The symptoms include bloating, nausea, vomiting, diarrhoea with pale, bulky and smelly stool, intestinal colic, swelling of the mouth and throat, itchy skin rashes, mouth ulcers, and sometimes even serious and life-threatening anaphylactic reactions.

This life-long disease can be kept under control by strictly avoiding gluten containing foods. Swift recovery from the symptoms within weeks can occur after such a strict dietary exclusion.

Coeliac disease is more common in people of northern European decent, unlike tropical sprue, a condition that gives rise to similar symptoms due to infection of the gut, which is more common in the tropics.

A person suffering from the above mentioned symptoms should consult the doctor. The condition is diagnosed on the basis of diet history, endoscopic biopsy and detection of antibodies in the laboratory. A self-testing kit is also available these days.

 

 

Prevalance

Coeliac disease affects about 1 in 100 people in the UK and as many as 1 in 300 in other European countries. Recent studies suggest that the prevalence in America is almost similar to that in Europe. Only 10 to 20% of people with this condition are currently diagnosed.

intestines
the main parts of the digestive system highling the small intestines.

image:

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Why is coeliac disease Important or signficant?

Coeliac disease can cause considerable debility and disability. Malabsorption of nutrients can ultimately causes weight loss, anaemia, osteoporosis and infertility, and the condition is associated with an increased mortality risk due to gastrointestinal and oesophageal malignancies.

Gluten-free diet can reverse this risk in course of time, and this is also why strict dietary control is so important. Other complications include recurrent miscarriages, neurological conditions and loss of enamel in the teeth.

People with coeliac disease also have a higher incidence of other autoimmune diseases such as diabetes and thyroid diseases.  A regular follow-up is thus very important once the diagnosis is made and the condition is being effectively managed.

Complications


Coeliac disease can cause several complications if left untreated. These include: malnutrition leading to anaemia and weight loss, and stunted growth and delay in the development in children; loss of calcium and bone density can cause the sufferer to be more prone to fractures, and the softness of the bone can lead to osteomalacia in adults and rickets in children; lack of calcium absorption makes the person more prone to oxalate kidney stone; damage to the small intestine causes inability to tolerate lactose and dairy products; chances of getting cancer, especially intestinal lymphoma and bowel cancer are greater; neurological complications are common, and this includes peripheral neuropathy, epilepsy, myelopathy, cerebellar ataxia and encephalopathy, not to forget the depression that follows a constant spell of ill-health and disability. Schizophrenia has also been associated with gluten intolerance.

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News about coeliac disease

Asthma is often reported in the press, particularly in relation to new treatments.

 

Some educative websites for further information on this medical condition are:


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How does coeliac disease occur?

Coeliac disease has a strong hereditary component and it can run in families. The disease can either become apparent during infancy or may not be so until middle or old age.

In people suffering this condition, the body recognises gluten as a foreign protein (antigen) against which antibody is produced that targets the tissues in small intestine, especially the inner lining of the small intestine. This leads to defective digestion and absorption of nutrients with far reaching consequences on the over all health of the person.

Gluten is a protein universally present in wheat. Gluten is made up of different proteins, one of which is gliadin. Gliadin in gluten is what causes the immunological reaction in coeliac disease. Why gliadin causes such reaction is, however, not known yet.

Barley and rye also contain gliadin-like proteins and can cause coeliac disease in genetically-predisposed individuals. Gliadin contained in oats causes only weak inflammation in few people who are predisposed to coeliac disease. Rice and corn do not cause coeliac disease as they do not contain gliadin-like proteins.

How is coeliac disease treated?

Avoiding gluten in the diet is the only treatment for coeliac disease sufferers. This means taking full responsibility for one’s own health and making safe and healthy choices both at home and away.

In addition, supplements may be necessary to replace the deficiency in nutrients. These include iron, folate, vitamin B, vitamin D for those with low bone density, and occasionally fluids and electrolytes such as calcium, potassium and magnesium.

Additional treatment will be necessary if associated conditions such as lactose intolerance or diabetes are also present.

gluten free

 



1. Wheat-based foods are broken down in the stomach and the upper part of the small intestine called the duodenum. Gluten is broken down in the duodenum. 2. Some of the partially digested food travels to the next segment of the small intestine called the jejunum. 3. In the jejunum, structures called villi with surface-bound enzymes break food down into complex molecules the body absorbs. 4. Gluten adheres to the tips of villi where enzymes break it down into simpler molecules called peptides. Some of the peptides, called 33-MER, cannot be broken down any further. This is true for all persons whether they suffer from celiac sprue or not. 5. Absorption cells in the gut lumen absorb 33-MER peptides and pass them into the tissues of the lamina propria. Antigen presenting cells (APC), part of the body's immune system, target foreign substances in the body for response by the immune system. APC do this by binding with the foreign substance, and then send biochemical signals to white blood cells to attack. In nearly all people with celiac sprue, APC bind with 33-MER only if the APC carry a protien called DQ2. 6. Once the intestinal wall absorbs 33-MER peptides, APC in celiac sprue patients signal white blood cells to attack. The result is eventual desctruction of absorption cells and villi in the intestinal wall.

Credit: Kirk Woellert, US National Science Foundation
original source

 

 

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History of coeliac disease

First description of coeliac disease based on the characteristic stool dates back to the 2nd century AD. More had been written and published during the 17th and 18th centuries, including the acknowledgement that the prevalence of the condition is more in women and children.

Mention of the disease in lectures and journal articles had continued during the 19th centuries; however, although diet manipulation, restriction of fats and food supplements were given to those who did not tolerate normal diets, the link of bread to the causation of coeliac disease was not noted until the late 1940s by Wilem Dicke.

 

 

The pathological features of the small intestine was conclusively described and confirmed by John Paulley, a physician from Ipswich in England only in 1954. During the last 25 years, development of fibre-optic endoscopes and accurate serological tests have greatly aided in the diagnosis of this condition.

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Future of coeliac disease

Although genetic markers for coeliac disease have been identified for over three decades, there have been no successes in identifying the actual genes that cause this disorder so far. Nevertheless, certain genes have been found to be more common among individuals with coeliac disease than among individuals without the disease.

Understanding the pathogenesis of coeliac disease through researches that are ongoing may help find new treatments that do not restrict gluten containing diet. Few significant studies on this front include histological improvement and tolerance of light gluten challenge through the use of enzyme supplementation that has the possibility of widespread use in future. These enzymes are extracted from animal intestinal mucosa and have the potential to replace the enzyme deficiency in coeliac disease.

 

electrophoresis gel
image: biologyreference.com

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