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Coeliac Disease

In This Article

Summary

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Epidemiology

  • Prevalence is about 1 in 100. However it is thought that only ½ of cases are actually diagnosed
  • Most common incidence is in children, and in those over 60, although it can occur at any age
  • Slightly more common in women over 60 than in men over 60
  • 30% risk for sibling, and 10% risk for first degree relatives, indicating an element of genetic susceptibility
 
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Pathology

  • It is a T-cell mediated auto-immune disease. The body has an adverse reaction to breakdown products of gluten (gliadins). This results in the production of two antibodies – anti-gliadin, and anti-endomysial. Anti endomysial antibody is the auto-immune. This attacks TGG (tissue transglutaminase) which is the enzyme responsible for gluten breakdown.
  • There is hypertrophy of crypts, and atrophy of the villi thus the overall wall thickness remains stable, but the surface area for absorption becomes greatly reduced
  • The proximal small intestine is most affected – due to the higher concentration of gluten products in this area (they get more broken down the further along the intestine they travel)
 
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Symptoms

There may just be vague symptoms present, which means it is often mistaken for IBS
  • General malaise / tiredness – often as a result of iron deficiency anaemia due to malabsorption
  • Diarrhoea – due to malabsorption
  • Nausea / vomiting
  • Bloating
  • Angular stomatitis – anaemia
  • Weight loss
  • Oral ulceration
  • Osteomalacia
 
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Investigations

  • Blood Test for anti-endomyisal antibody and/or anti tTg (anti tissue transglutaminase). Anti tTG is a newer and more sensitive specific test and should be used in preference if available. 
  • Endoscopy to take a duodenal biopsy for histological examination.  50% of those with positive antibody test may not have histological changes. These people are ‘latent Coeliacs’ and are highly likely to develop true Coeliac disease in the future.
  • Histological findings typically involve: hypertrophy of the crypts, and atrophy of the villi, giving the mucosa a flattened appearance. the overall thickness of the mucosa is not changed. There must also be an increase in the number of inflammatory cells in the lamina propria for a diagnosis to be made.
     
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Diagnosis

There are no set criteria for diagnosis, but typically you will need:

  • Evidence of malabsorption (steatorrhoea, vitamin / nutritient deficiency)
  • Villous atrophy on duodenal biopsy
  • Weight loss
  • Features resolve upon adoption of gluten free diet
 
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Complications

  • Osteopaenia – reduction in bone density – due to lack of calcium absorption
  • Osteoporosis – due to prolonged lack of calcium absorption
  • Osteomalacia– due to vitamin D / calcium malabsorption
  • Cerebellar disorders – due to problems with calcium metabolism
  • Neurological disorders – e.g. parasthesia and muscle weakness
  • Increased incidence of other auto-immune conditions
  • Increased risk of malignancy – GI lymphoma (rare) or can be oesophageal, gastric, brain or breast (these are even rarer)
 
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Treatment

This is life-long gluten free diet.
Oats do not actually cause the disease but are often prepared in factories where gluten has been used, thus these should be restricted to <30g/day
Problems with adherence are usually because people do not realise some products contain gluten
 
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More Information

Coeliac disease is caused by an intolerance of gluten. In susceptible individuals, exposure to gluten can lead to damage of the proximal small bowel. In serious cases, it can affect the whole bowel. Wheat, rye and barley all contain gluten – some people think that oats are also a problem, but this is not the case for pure oats, but there is often contamination of oats with wheat in production. This causes some confusion. These things (wheat, rye, barley) are collectively referred to as prolamin.
It is a major cause of GI malabsorption.
 
There is inflammation caused by an immune reaction. This disappears when gluten is removed from the diet, and reappears if gluten is eaten again.
 
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