Elsevier

The Lancet

Volume 349, Issue 9067, 14 June 1997, Pages 1755-1759
The Lancet

Seminar
Coeliac disease

https://doi.org/10.1016/S0140-6736(96)70237-4Get rights and content

Section snippets

Diagnostic criteria

The diagnostic criteria, as stated by the European Society for Paediatric Gastroenterology and Nutrition (ESPGAN) in 1970, are: small-bowel mucosal atrophy with improvement or normalisation on a gluten-free diet a deterioration of the villous morphology during intake of a gluten-containing diet. In 1990, these criteria were modified.3 The findings of characteristic small-bowel mucosal atrophy and clinical remission on a gluten-free diet are essential. In symptom-free patients, a second biopsy

Changing symptom pattern and associated disorders

Diarrhoea, weight loss, and weakness have been the classic signs of coeliac disease in adults. A severe malabsorption syndrome has been common as well. In the early 1980s, British investigators showed that the clinical features of coeliac disease have changed.7, 8 There had been by this time a shift towards milder symptoms such as indigestion in adults and recurrent abdominal pain in children. The classic symptoms and signs had become rare. Sometimes isolated iron deficiency is the only

Role of cereals

It is generally accepted that the cereals: wheat, rye, barley or their prolamines gliadin, secalin, and hordein, respectively, are the major triggering factors in coeliac disease and dermatitis herpetiformis. There is no scientific evidence that oats and its prolamin avenin is harmful to patients with coeliac disease. It has been shown that adults with coeliac disease tolerate 50 g of oats a day without clinical relapse or adverse effects on the small-bowel mucosa, and ingestion of oats does

Management

Patients with coeliac disease and dermatitis herpetiformis must adhere to the gluten-free diet permanently. In all such diets wheat starch, containing trace amounts of gliadin, is not permitted. A new issue is whether oats could be allowed. According to follow-up studies, only 50–70% of patients with coeliac disease maintain a strict gluten-free diet later in life, and poor compliance is the main reason for a poor response. Corticosteroids are rarely necessary in the treatment of coeliac

Epidemiology

The prevalence of coeliac disease has been about one in 1000 individuals. However, there are great differences between European countries.25 Recent screening studies have found a prevalence of one in 300,26, 27 and it has been suggested that the prevalence might be as high as one in 100 individuals;28 however, this finding is on the basis of the occurrence of endomysial antibodies and not on biopsy-proven cases. Nevertheless, it is clear that diagnosing symptomatic coeliac disease reveals only

Screening policy and diagnosis

A plan of action for screening and case finding for coeliac disease is shown in figure 2. Small-bowel biopsy should be the first diagnostic procedure, when clinical suspicion of coeliac disease is strong. Coeliac disease can also be detected or excluded by upper gastrointestinal endoscopy provided that biopsy specimens from distal duodenum are taken routinely. Screening for coeliac disease is recommended when the clinical symptoms are subtle, but still indicative for the disease. Screening can

Genetic, immunological, and pathogenetic aspects

The tendency of coeliac disease to run in families is well recognised.33 The disease prevalence among healthy firstdegree relatives has varied from 1 to 18%. Figure 3 shows a family where the proband was diagnosed to have coeliac disease on clinical grounds, and where biopsy samples of the healthy individuals revealed two cases of silent coeliac disease. Twin studies have also shown that the genetic component is clear. Concordance between identical twins is 70%, and may even be higher because

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