Fasting hypoglycaemia and postprandial hyperglycaemia as a prodrome of type 1 diabetes mellitus.
Overview
abstract
The pathophysiology of type 1 diabetes mellitus (DM) involves the selective autoimmune destruction of the pancreatic beta-cells [Pihoker et al.: Diabetes 2005;54(suppl 2):S52-S61]. The onset of type 1 DM is characterised by hyperglycaemia. Islet cell antibody (ICA), anti-insulin, anti-glutamic acid decarboxylase and the antibody against tyrosine phosphatase-like protein known as ICA-512 (IA-2) usually appear before the clinical onset of DM and are markers of the autoimmune process. Hypoglycaemia in type 1 DM is a common complication and a result of the interaction between excess insulin administration and a compromised glucose counterregulatory hormonal response [Cryer: Endocrinol Metab Clin North Am 2010;39:641-654]. Spontaneous fasting hypoglycaemia alternating with hyperglycaemia prior to the onset of antibody-positive type 1 DM has not been described before.
