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Prevalence of coeliac disease in diabetic children and adolescents in Sweden
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The aim of this study was to determine the minimum prevalence of coeliac disease in a group of 459 diabetic children and adolescents. Six patients were already known to have coeliac disease. A total of 436 patients with type 1 diabetes mellitus aged 2–21 years and with age at onset at 2 months to 17 years at three paediatric departments agreed to participate in the study. All patients were tested for gliadin IgA antibodies with a commercial kit (Pharmacia Gluten IgA EIA). Later, serum was tested for reticulin IgA/IgG antibodies. Nineteen patients had elevated gliadin IgA levels (>25 AU). Eighteen underwent jejunal biopsy. Ten had total or subtotal villous atrophy. These 10 patients were reticulin IgA‐positive. Of 417 gliadin IgA‐negative patients, 408 were reticulin IgA/IgG‐negative. Of 6 reticulin IgA‐positive patients, 3 had total or subtotal villous atrophy. All 3 had become gliadin IgA‐positive at the time of biopsy. Among 3 reticulin IgG‐positive patients with IgA deficiency, 2 had total villous atrophy: 1 was not willing to be biopsied. Patients with total or subtotal villous atrophy were judged as having coeliac disease and were recommended a gluten‐free diet. Within 2 months, gliadin IgA levels were normal in patients adhering to the diet. Five patients have gone through a second jejunal biopsy to date with normal histology in all 5. The 15 newly diagnosed patients with coeliac disease plus 6 already known patients with coeliac disease and type 1 diabetes mellitus gave a minimum prevalence of coeliac disease in diabetic children and adolescents of 21/459 = 4.6%.
Title: Prevalence of coeliac disease in diabetic children and adolescents in Sweden
Description:
The aim of this study was to determine the minimum prevalence of coeliac disease in a group of 459 diabetic children and adolescents.
Six patients were already known to have coeliac disease.
A total of 436 patients with type 1 diabetes mellitus aged 2–21 years and with age at onset at 2 months to 17 years at three paediatric departments agreed to participate in the study.
All patients were tested for gliadin IgA antibodies with a commercial kit (Pharmacia Gluten IgA EIA).
Later, serum was tested for reticulin IgA/IgG antibodies.
Nineteen patients had elevated gliadin IgA levels (>25 AU).
Eighteen underwent jejunal biopsy.
Ten had total or subtotal villous atrophy.
These 10 patients were reticulin IgA‐positive.
Of 417 gliadin IgA‐negative patients, 408 were reticulin IgA/IgG‐negative.
Of 6 reticulin IgA‐positive patients, 3 had total or subtotal villous atrophy.
All 3 had become gliadin IgA‐positive at the time of biopsy.
Among 3 reticulin IgG‐positive patients with IgA deficiency, 2 had total villous atrophy: 1 was not willing to be biopsied.
Patients with total or subtotal villous atrophy were judged as having coeliac disease and were recommended a gluten‐free diet.
Within 2 months, gliadin IgA levels were normal in patients adhering to the diet.
Five patients have gone through a second jejunal biopsy to date with normal histology in all 5.
The 15 newly diagnosed patients with coeliac disease plus 6 already known patients with coeliac disease and type 1 diabetes mellitus gave a minimum prevalence of coeliac disease in diabetic children and adolescents of 21/459 = 4.
6%.
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