GAD-alum may contribute to the preservation of residual insulin secretion in patients with recent-onset type 1 diabetes, although it did not change the insulin requirement. (ClinicalTrials.gov number, NCT00435981.)

SummaryGrowth during the first years of life in relation to type of feeding in infancy was retrospectively studied in an unselected population-based group of 297 children who had been diagnosed with Type i (insulin-dependent) diabetes mellitus before the age of 15 years (probands) and 792 individually-matched referent subjects. Reliable data were collected from child welfare clinics. Probands weighed slightly less at birth but their weight gain at 6, 9, 18 and 30 months of age was significantly greater (p < 0.02) than that of referent children. The weight gain of children who had never been breast-fed was more marked than that of breast-fed children; this was found for both probands and referent children. But also among exclusively breast-fed children ( > 2 months), probands gained significantly more in weight from birth up to 18 and 30 months of age than exclusively breast-fed referent children. Early weight gain appears to be a risk factor for development of Type i diabetes. The lower weight gain in breast-fed compared to non-breast-fed children may explain the protective effect of breast feeding against Type 1 diabetes observed in several studies, [Diabetologia (1994) 37: 91-94] Key words Type i (insulin-dependent) diabetes mellitus, aetiology, early growth, breast feeding.There is a close connection between insulin secretion and growth in children [1] as an adequate insulin supply is needed for normal growth. Insulin seems to have both a direct effect and an indirect effect via insulinlike growth factors [2].There have been numerous studies regarding growth in children at the time of and after the clinical onset of Type 1 (insulin-dependent) diabetes mellitus [3][4][5][6][7]. It is well known that growth is seriously impaired in Type i diabetic patients with very poor metabolic control [8]. In patients with reasonably good metabolic control varying results in growth after onset of Type 1 diabetes have been observed [3][4][5]9].A few studies have investigated growth during the first years of life in children who later develop Type 1

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%.

This study indicates that, in parallel to changes in incidence, clinical features of coeliac disease in young children have changed during the last 10 years.