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Type 1 diabetes (T1D) is a T-cell mediated autoimmune disease in which the insulin-producing beta cells are destroyed. While it is clear that full-length C-peptide, derived from proinsulin, is a major antigen in human T1D it is not clear how and why C-peptide becomes a target of the autoimmune CD4

The effect of type 1 diabetes on the developing brain is a topic of primary research interest. A variety of potential dysglycaemic insults to the brain can cause cellular and structural injury and lead to altered neuropsychological outcomes. These outcomes might be subtle in terms of cognition but appear to persist into adult life. Age and circumstance at diagnosis appear to play a substantial role in potential CNS injury. A history of diabetic ketoacidosis and chronic hyperglycaemia appear to be more injurious than previously suspected, whereas a history of severe hypoglycaemia is perhaps less injurious. Neurocognitive deficits manifest across multiple cognitive domains, including executive function and speed of information processing. Some evidence suggests that subtle brain injury might directly contribute to psychological and mental health outcomes. Impaired executive function and mental health, in turn, could affect patients' adherence and the ability to make adaptive lifestyle choices. Impaired executive functioning creates a potential feedback loop of diabetic dysglycaemia leading to brain injury, further impaired executive function and mental health, which results in suboptimal adherence, and further dysglycaemia. Clinicians dealing with patients with suboptimal glycaemic outcomes should be aware of these potential issues.

A constant supply of glucose to the brain is critical for normal cerebral metabolism. The dysglycemia of type 1 diabetes (T1D) can affect activity, survival, and function of neural cells. Clinical studies in T1D have shown impairments in brain morphology and function. The most neurotoxic milieu seems to be young age and/or diabetic ketoacidosis at onset, severe hypoglycemia under the age of 6 years followed by chronic hyperglycemia. Adverse cognitive outcomes seem to be associated with poorer mental health outcomes. It is imperative to improve outcomes by investigating the mechanisms of injury so that neuroprotective strategies independent of glycemia can be identified.

Transition is defined as the 'purposeful, planned movement of adolescents and young adults with chronic physical and medical conditions from child-centred to adult-oriented health care systems' by Blum RW, (2002). The primary goal of transition is to ensure an uninterrupted process in healthcare delivery between the paediatric and adult settings; however, losses to follow up and decreased engagement with specialist services are common during this time. The current transition literature specifically pertaining to type 1 diabetes mellitus (T1DM) is often limited by incomplete data, the absence of control data and lack of follow up data spanning both the paediatric and adult years. This paper serves to review the current transition literature base, highlighting areas which warrant further study.

To examine possible determinants of autoantibody levels at type 1 diabetes mellitus (T1DM) onset. We assessed levels of glutamic acid decarboxylase 65 islet cell antigen (GADA) and anti-insulin antibodies (IAA) in 247 incident T1DM cases presenting

The interpretation of bone density measurement in children is difficult due to a number of factors including rapid change in body size and uncertain clinical significance of bone density in children. This study asked two questions. (1) Is there a preferred bone density measurement site or type for fracture risk in children? (2) What is the best way to interpret bone density in children? This population-based case control study included 321 upper limb fracture cases and 321 class- and sex- matched randomly selected controls. Bone density at the hip, spine, and total body (including the arm) was measured by a Hologic QDR2000 densitometer (Waltham, MA) and examined as bone area (BA), bone mineral content (BMC), bone mineral density (BMD), bone mineral apparent density (BMAD), and BMC/lean mass (BMCLM). The only dual-energy X-ray absorptiometry (DXA) variables that were consistently associated with fracture risk in both boys and girls were spine BMD and BMAD for total upper limb fractures, and spine and hip BMAD for wrist and forearm fractures. No significant associations were observed for BA and BMCLM and inconsistent associations for BMC and other BMD sites. Five-yr fracture risk varied from 15–24% depending on site and gender in a child with a Z-score of -3. In the controls, all DXA variables were associated with age, height, and weight, but the weakest associations were with BMAD. In conclusion, in this study the spine BMAD had the strongest and most consistent association with upper limb fracture risk in children. The associations with age and body size imply that age specific Z-scores will be the most convenient for interpretation of DXA measures in children. Five-yr wrist and forearm fracture risk has potential as a clinical endpoint of immediate relevance.