Older age and CNS involvement at diagnosis increase the risk of MIDi. In contrast to previous studies, higher BMI was not associated with MIDi in our population.

Larger size, microcalcifications and ill-defined margins on ultrasound demonstrate the best predictive model for malignancy in the pediatric population. Experienced pediatric radiologists demonstrate moderate inter-observer agreement in prediction of malignancy.

We report in this study the death in bed of a 14-yr-old girl with type 1 diabetes and a review of the existing literature on this topic. Diagnosed at 5 yr of age, the patient followed a relatively benign disease course. Hemoglobin A1c was 6.6-8.4%, and there were no hospital admissions apart from the one at diagnosis. Hypoglycemic episodes were not excessive or severe. At age 14 yr, the patient was found dead in bed after having been well the night before. No apparent explanation could be provided. The 'dead-in-bed' syndrome accounts for 5-6% of mortality cases in patients with type 1 diabetes, amounting to two to six cases per 10 000 patient years. Theories attempting to explain the mechanism for this syndrome include hypoglycemia or cardiac autonomic dysfunction. This case emphasizes several problems faced by clinicians: the risk for sudden death in youth with diabetes, which may compromise good glycemic control, the question of early detection of autonomic dysfunction, and the need to understand this phenomenon better and search for preventive measures.

IntroductionCoeliac disease (CD) is an autoimmune condition characterised by gluten-induced intestinal inflammation, and observed at a 5–10 fold greater prevalence in type 1 diabetes. While universal screening for CD in patients with diabetes is frequently advocated, objective data is limited as to benefits on diabetes control, bone health or quality of life related to the adoption of a gluten-free diet (GFD) in the large proportion of patients with diabetes with asymptomatic CD. The Celiac Disease and Diabetes-Dietary Intervention and Evaluation Trial (CD-DIET) study is a multicenter, randomised controlled trial to evaluate the efficacy and safety of a GFD in patients with type 1 diabetes with asymptomatic CD.Methods and analysisChildren and adults (8–45 years) with type 1 diabetes will be screened for asymptomatic CD. Eligible patients with biopsy-proven CD will be randomly assigned in a 1:1 ratio to treatment with a GFD for 1 year, or continue with a gluten-containing diet. The primary outcome will evaluate the impact of the GFD on change in glycated haemoglobin. Secondary outcomes will evaluate changes in bone mineral density, blood glucose variability and health-related quality of life between GFD-treated and the regular diet group over a 1-year period. The study was initiated in 2012 and has subsequently expanded to multiple paediatric and adult centres in Ontario, Canada.Ethics and disseminationThe findings from this study will provide high-quality evidence as to the impact of GFD treatment on glycaemic control and complications in asymptomatic children and adults with CD and type 1 diabetes.Trial registration numberNCT01566110.

To describe celiac disease (CD) screening rates and glycemic outcomes of a gluten-free diet (GFD) in patients with type 1 diabetes who are asymptomatic for CD. RESEARCH DESIGN AND METHODSAsymptomatic patients (8-45 years) were screened for CD. Biopsy-confirmed CD participants were randomized to GFD or gluten-containing diet (GCD) to assess changes in HbA 1c and continuous glucose monitoring over 12 months. RESULTSAdults had higher CD-seropositivity rates than children (6.8% [95% CI 4.9-8.2%, N 5 1,298] vs. 4.7% [95% CI 3.4-5.9%, N 5 1,089], P 5 0.035) with lower rates of prior CD screening (6.9% vs. 44.2%, P < 0.0001). Fifty-one participants were randomized to a GFD (N 5 27) or GCD (N 5 24). No HbA 1c differences were seen between the groups (10.14%, 1.5 mmol/mol; 95% CI 20.79 to 1.08; P 5 0.76), although greater postprandial glucose increases (4-h 11.5 mmol/L; 95% CI 0.4-2.7; P 5 0.014) emerged with a GFD. CONCLUSIONSCD is frequently observed in asymptomatic patients with type 1 diabetes, and clinical vigilance is warranted with initiation of a GFD.Celiac disease (CD) is an immune reaction-mediated condition triggered by gluten, a protein found in wheat, barley, and rye. CD risk is increased in patients with type 1 diabetes and is characterized by a broad spectrum of presentations, including gastrointestinal symptoms, growth alterations, and anemia, but many patients are asymptomatic (1-4).Serologic screening for CD has high sensitivity and specificity, but few reports have evaluated CD rates and the impact of treatment with a gluten-free diet (GFD) in asymptomatic CD (aCD) patients with type 1 diabetes. The Celiac Disease and Diabetes-Dietary Intervention and Evaluation Trial (CD-DIET) prospectively screened a large cohort of patients aged 8-45 years with subsequent engagement in a randomized, dietary treatment trial to evaluate changes in HbA 1c and glycemic variability.

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Our aim was to characterize clinical findings and familial associations, and to examine candidate genes for disease-causing mutations in a cohort of children suffering from primary osteoporosis without features of osteogenesis imperfecta. Patients with osteoporosis and their nuclear families were studied. Medical history was reviewed. Calcium homeostasis parameters were measured and spinal radiographs obtained. BMD was determined by DXA for patients, parents and siblings. LRP5, LRP6, and PTHLH genes were sequenced. Twenty-seven patients (14 males) from 24 families were recruited. Median age at presentation was 10.1 years (range 3.3-15.6 years). One-third of the children had at least one parent with a BMD below the expected range for age. LRP5, LRP6, and PTHLH showed no causative mutations. Four polymorphisms in LRP5 were overrepresented in patients; the minor allele frequency of Q89R, V667M, N740N, and A1330V was significantly higher than in controls. Age of onset, clinical severity, and inheritance patterns are variable in children with primary osteoporosis. Several patients had evidence suggestive of familial transmission. The underlying genetic factors remain to be elucidated.

Medication-induced diabetes (MID) is seen in children treated for acute lymphoblastic leukemia (ALL) mostly during induction, due to the use of l-asparaginase and glucocorticoids. Our objective was to assess whether MID during induction, is a risk factor for future impaired glucose tolerance (IGT), diabetes, or metabolic syndrome. Ninety survivors of pediatric ALL, ages 10 yr and older were recruited, 30 with history of MID and 60 controls. Waist/height ratio >0.5 was considered as an increased risk for central adiposity and insulin resistance. Lipid profile and an oral glucose tolerance test (OGTT) were performed. Study patients were older than controls (17.2 vs. 14.9, p < 0.05). The groups had similar sex distribution, body mass index (BMI) z-score, and Tanner staging. A waist/height ratio of >0.5 was seen in 60 and 31.7% of the study and control groups, respectively (p = 0.01). Increased frequency of IGT in the study group compared with the control group was seen (13.3 and 1%, respectively) (p = 0.07). We observed a trend toward higher proportion of patients with multiple features of metabolic syndrome in the study compared with control group (16.7 vs. 5%, p = 0.09). In conclusion, MID during induction may be an early marker for metabolic disturbances later in life. The higher rates of increased waist/height ratio, and subjects with multiple metabolic syndrome features, may predict a metabolic risk in children with history of MID. Rates of IGT were four fold higher in the study group although not statistically significant. MID may be a 'red flag' indicating the need for ongoing metabolic screening and lifestyle modifications to prevent future metabolic disease.