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Editor,—We were interested to read the article by Challacombe et al reported a declining incidence of coeliac disease in West Somerset.1 Our observations on the incidence of coeliac disease in South Glamorgan over a 15 year period have revealed no such decline. We determined the frequency of new cases of coeliac disease from 1981 to 1995 in patients resident in South Glamorgan (1995 total population 415 900; population 14 years or younger 83 500; total live births 5700 per year). Cases of coeliac disease were ascertained from hospital activity data, pathology, dermatology, and dietetic records, general practitioner lists, and the local coeliac society.
All cases satisfied the revised ESPGAN diagnostic criteria.2 Over the three five-year periods (1981–85, 1986–90, 1991–95) the number of new cases in children younger than 14 were 8, 10, and 9, respectively—annual incidences of 2.08, 2.53, and 2.15 per 100 000. The incidence of childhood coeliac disease has therefore remained constant over the 15 year period at approximately 1 in 2500 to 1 in 3000 live births. In contrast, the incidence of adult coeliac disease has increased over the three time periods from 1.3 to 2.15 and 3.08 per 100 000. The incidence of adult dermatitis herpetiformis has remained between 0.3 and 0.43 per 100 000.
The age at diagnosis of children with coeliac disease has risen from a median of 4 years (1 to 10) between the period 1981 to 1990, to 7.6 years (1.7 to 14.9) between 1991 and 1995, whereas the age at presentation of adult patients has remained constant with a median of 49.5 years (19 to 88). From 1981–90 the predominant presenting symptoms were gastrointestinal, with 70% of the children having diarrhoea, and only three of the 18 children being anaemic. Between 1991–95 anaemia associated with vague abdominal symptoms (such as discomfort or bloating) became a more common presentation (44%) and diarrhoea was noted in only 11%.
Anaemia as the sole presenting feature remained rare at diagnosis (one of 27) compared with a figure of 25% of the adult coeliac population over the 15 year period. Two asymptomatic children were diagnosed following screening for IgA antigliadin antibodies in siblings of affected probands.
We may be missing asymptomatic cases or those that present later with symptoms such as anaemia, so the true incidence is likely to be much higher. Many adult cases are now identified from duodenal biopsies taken during upper gastrointestinal endoscopy for investigation of iron deficiency anaemia and non-specific gastrointestinal symptoms. The incidence of adult dermatitis herpetiformis, which shares the same genetic basis as coeliac disease,3 has remained stable, suggesting the increased diagnosis of adult coeliac disease primarily because of increased clinical awareness.
We consider that although the classic gastrointestinal presentation of coeliac disease may be decreasing in children, the overall incidence may not have altered, and is likely to be much higher than previously recognised once screening tests become more widely employed. It is thus vital that we remain aware of the diagnosis and how subtle its presentation may be, and screen actively for cases using IgA antigliadin antibody and antiendomysial antibody, particularly in populations at higher risk (for example, family history, Down’s syndrome, insulin dependent diabetes mellitus).
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Dr Challacombe comments:
The letter by Jenkins et al on the incidence of coeliac disease in children younger than 14 years in South Glamorgan raises some interesting questions. They have reported a constant incidence over three five-year periods (1981–85, 1986–90, 1991–95) of approximately 1:2500 to 1:3000 live births. An earlier study in West Somerset reported a declining incidence of coeliac disease between 1971–80 and 1981–92, in which the annual incidence peaked in 1974 and then decreased, and further patients were not diagnosed annually for six years between 1980 and 1992. The cumulative incidence of coeliac disease in West Somerset was 0.68 per 1000 live births during 1971–80 and 0.09 during 1981–92. The different findings could have been caused by different sampling times. A higher incidence of coeliac disease in the late 1960s and early 1970s, possibly caused by the early introduction of dietary gluten, could have been followed by a relative decline in incidence during the late 1970s and 1980s with changing infant feeding practices. These were characterised by the later introduction of dietary gluten, an increased use of baby rice and gluten free foods for weaning, and a higher incidence of initial breast feeding. The age at diagnosis of children with coeliac disease also increased in South Glamorgan and West Somerset, which could have been yet another result of delaying the introduction of dietary gluten in infancy.
Although some children still present with classic symptoms and signs of coeliac disease, others present at school age or adolescence with mild or atypical symptoms and signs. As a result, the diagnosis of coeliac disease has become more covert and difficult to recognise. The development of methods using serum IgA antibodies to gliadin and to endomysium to diagnose and follow up patients with coeliac disease has been opportune. In association with small bowel intestinal biopsy these methods will enable the true incidence of coeliac disease to be determined more precisely and will shed further light on the natural history of this disease in children and adults.