title: Fasting hypoglycaemia and postprandial hyperglycaemia as a prodrome of type 1 diabetes mellitus.
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.
authors: Departments of Endocrinology, Great Ormond Street Hospital for Children NHS Trust, and The Institute of Child Health, University College London, London, UK.
authors: Nayaz
authors: N
authors: Rafeullah
authors: Nicola
authors: N
authors: Cackett
authors: Khalid
authors: K
authors: Hussain
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000209:etiology*; D005215:Fasting; D005951:Glucose Tolerance Test; D006801:Humans; D006943:Hyperglycemia / Q000150:complications*; D007003:Hypoglycemia / Q000150:complications*; D049528:Insulin, Long-Acting / Q000008:administration & dosage; D008297:Male
chemical_list: D001786:Blood Glucose; D049528:Insulin, Long-Acting