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Coeliac disease: dispelling the myths

Harold Hin
Member of the Medical Committee for the Coeliac Society

Although the coeliac iceberg has been a well-recognised phenomenon over the last few decades,  new research evidence has increased our understanding and dispelled a number of long-accepted assumptions engraved in textbooks. This article highlights some of the more interesting recent developments in the field.

Advances in immunology have provided evidence that coeliac disease (CD) is an autoimmune disorder triggered by an external antigen (gluten) in genetically predisposed individuals. However, the glutens found in wheat, rye, barley and oats are all different and consequently have varying toxicity levels, the most antigenic being wheat gluten (gliadin) and the least toxic being oat gluten (avenin).
Contrary to previous belief, new evidence shows that oats can be tolerated by coeliac sufferers,(1) although difficulty in ensuring the purity of commercial oats from contamination from other grain during milling and transport remains a major problem. Consequently, advice about the safety of oats remains controversial.
In the 1960s, gastroenterologists used to say "all that is flat isn't coeliac". While this is still true today, we also now realise that "all that is coeliac isn't flat". Electron-microscope scanning reveals that the typical flat mucosa is in fact the endstage lesion of T-cell-dependent immune reactivity that progresses through several stages - from normal villi with increased intraepithelial lymphocytes as the earliest indication of sensitisation, to the totally flat mucosa at the other end of the spectrum.(2) Furthermore, the degree and length of mucosal changes are dependent on the amount of gluten ingested, although this does not always correlate with clinical symptoms.

Clinical manifestations
Coeliac Society prevalence figures show that there is a definite shift from paediatric presentations to the adult and the elderly. Indeed, there are now twice as many adults over the age of 65 years joining the society compared with children. This changing pattern of presentation may be because of changes in weaning guidelines in infants and the wider recognition of the protean manifestations of CD with the advent of reliable serological tests. More than 50% of patients with CD have iron-deficiency anaemia at diagnosis. The anaemia is of variable severity, intermittent and often overlooked in general practice as being dietary in origin.(3) Guidelines published last year from the Primary Care Society for Gastroenterology(4) advise GPs to consider CD in patients presenting with:

  • Iron- or folate-deficiency anaemia (regardless of severity).
  • A feeling of being "tired all the time", or chronic fatigue.
  • Unexplained diarrhoea.

This is particularly the case if the patient also has:

  • A family history of CD.
  • Type 1 diabetes.
  • Autoimmune thyroid disease.
  • Osteoporosis.
  • Infertility.
  • An unexplained neurological disorder.

Other less well known associations are: recurrent miscarriages; Down's syndrome; short stature; dental enamel hypoplasia; abnormal liver function tests (raised transaminases); and unexplained macrocytosis.
GPs should beware of persistent or intermittent iron- deficiency anaemia - it is the most common presentation of CD.

Endomysial antibody (EMA) is the initial screening test of choice. It is extremely reliable, although false-negatives do occur, especially in those under the age of 2 years. As it is an IgA antibody, false-negative results will also be seen in the 2% of the population that are IgA-deficient. For this reason, an IgA reading is always obtained in conjunction with EMA.
Diagnosis should always be confirmed by intestinal biopsy, which remains the gold standard. It is important that the patient remains on a gluten-containing diet at the time of serological testing and biopsy.

The malignant complications of coeliac disease have been known for many years, and there is good evidence of a protective effect of a strict gluten-free diet in reducing the risks. Enteropathy-associated T-cell lymphoma (EATL) should be suspected in cases of weight loss, lethargy and diarrhoea in a previously well coeliac patient. A high index of suspicion is required as the onset of deterioration can be insidious.
The non-malignant complications are those of bone and calcium metabolism (osteoporosis), neurological and psychiatric disorders (cerebellar ataxia and depression) and reproductive disorders (infertility, impotence and recurrent miscarriages).

The treatment of coeliac disease involves a lifelong exclusion of gluten from the diet. Rice and maize can be eaten, as can other natural food such as vegetables, fruit, fish, eggs and meat. A wide range of palatable gluten-free products that guarantee the absence of toxic amounts of gluten are specifically manufactured for coeliac patients and can be prescribed.
There are many pitfalls for the unwary as there are many sources of hidden gluten as a result of inadequate food labelling and contamination. Compliance is as low as 47% in some published series. A reliable way of checking compliance is repeating the endomysial antibody test at each clinic visit. Yearly follow-up by a dietitian with an interest in coeliac disease is therefore important.
The Coeliac Society publishes a regularly updated handbook listing allowable food.

The future
Recent publications by Anderson(5) and Arentz-Hansen(6) look extremely promising. These two studies, which use different methods of identification, suggest that a single peptide on the a-gliadin chain may be the offending epitope responsible for initiating T-cell reactivity in coeliac disease. If true, it may be possible to:

  • Induce immunological tolerance to gluten by feeding individuals with antigenic peptides.
  • Modify the peptides by way of molecular engineering and administer them systemically (the vaccine approach).
  • Genetically modify gluten in the food chain to remove or mutate the offending peptide.

It may be some years before any of the above become reality, but in the meantime, as primary care practitioners, we must be aware of our crucial role in diagnosis and follow-up of this eminently treatable condition.


  1. Srinivasan U, Leonard N, Jones E, et al. Absence of oats toxicity in adult coeliac disease. BMJ 1996;313:1300-1.
  2. Maki M, Collin P. Coeliac disease. Lancet 1997;349:1755-9.
  3. Hin H, Bird AG, Fisher P, Mahy N, Jewell D. Coeliac disease in primary care: case finding study. BMJ 1999;318:164-7.
  4. Primary Care Society for Gastroenterology. Decision points in the management of adult coeliac disease in primary care. Oxford: Primary Care Society for Gastroenterology; 2000.
  5. Anderson RP, Degano P, Godkin AJ, Jewell DP, Hill AVS. In vivo antigen challenge in celiac disease identifies a single transglutaminase- modified peptide as the dominant a-gliadin T-cell epitope. Nat Med 2000;6:337-2.
  6. Arenz-Hansen, Körner R, Molberg Ø, et al. The intestinal T-cell response to a-gliadin in adult celiac disease is focused on a single de-aminated glutamine targeted by tissue transglutaminase. J Exp Med 2000;191:603-12.

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