Diabetes: glycaemic control in type 1


The term diabetes mellitus encompasses a group of disorders characterised by chronic hyperglycaemia with disturbances of carbohydrate, fat, and protein metabolism resulting from defects of insulin secretion, insulin action, or both. The WHO definition now recognises diabetes as a progressive disorder of glucose metabolism in which individuals may move between normoglycaemia, impaired glucose tolerance or impaired fasting glycaemia, and frank hyperglycaemia. Type 1 diabetes occurs when destruction of the pancreatic islet beta cells, usually attributable to an autoimmune process, causes the pancreas to produce too little insulin or none at all. Markers of autoimmune destruction (autoantibodies to islet cells, autoantibodies to insulin, or autoantibodies to both islet cells and insulin, and to glutamic acid decarboxylase) can be found in 85% to 90% of people with type 1 diabetes when hyperglycaemia is first detected.[1] The definition of type 1 diabetes also includes beta-cell destruction, in people prone to ketoacidosis, for which no specific cause can be found. However, it excludes those forms of beta-cell destruction for which a specific cause can be found (e.g., cystic fibrosis, pancreatitis, pancreatic cancer).[2] Type 2 diabetes results from defects in both insulin secretion and insulin action. Type 2 diabetes is not covered in this review. Population: For the purpose of this review, we have included adolescents and adults with type 1 diabetes, but have excluded pregnant women and people who are acutely unwell: for example, after surgery or MI.

Latest citations

Earlier intensified insulin treatment of Type 1 diabetes and its association with long-term macrovascular and renal complications. ( 02 June 2016 )

Integrated sensor-augmented pump therapy systems [the MiniMed(R) Paradigm Veo system and the Vibe and G4(R) PLATINUM CGM (continuous glucose monitoring) system] for managing blood glucose levels in type 1 diabetes: a systematic review and economic evaluation. ( 26 April 2016 )