Abstract

Hypoglycaemia is a major factor preventing insulin-treated patients from achieving normoglycaemia. This reflects the inadequacy of current insulin treatment, which causes high insulin concentrations in the post-absorptive period. Physiological defences to hypoglycaemia include autonomic activation, which limits the fall in glucose level and causes symptoms, alerting patients to an impending episode. Many patients develop defective responses and hypoglycaemia unawareness after longstanding disease or with tight glycaemic control and are then prone to severe attacks. This may be the result of repeated hypoglycaemic episodes, which by altering cerebral glucose uptake, disturb the mechanisms that activate the central response to hypoglycaemia. Preventing further hypoglycaemia can partially reverse these defects and restore symptomatic awareness. Clinical hypoglycaemia has also been implicated in the 'dead in bed' syndrome and in chronic cognitive impairment. The problem of hypoglycaemia will eventually be solved by better insulin delivery and non-invasive glucose meters, but until then, more focused education may have a more substantial impact.

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