Oxyhyperglycemia is a special type of impaired glucose tolerance characterized by a rapid and transient hyperglycemia (i.e. rise in blood glucose) spike after an oral intake of glucose, the peak of this spike being high enough to cause transient, symptom free glycosuria (i.e. detectable glucose in urine), but this hyperglycemia reverses rapidly and may even go to hypoglycemia in the later phase. This sharp downstroke overshooting towards hypoglycemia distinguishes this pathologic phenomenon from the artificial hyperglycemia inducible by an intravenous bolus dose of a large amount of glucose solution. Early dumping syndrome patients usually have oxyhyperglycemia associated with any meal or OGTT.[citation needed]
The Greek root oxy means "sharp" or "pointy".[1][2] The OGTT curve in this condition appears sharp and somewhat pointy (at least relative to the other forms of hyperglycemia)- hence this name.Dorlands dictionary defines oxyhyperglycemia as:[3]
A blood level of approximately 180 mg/dL is the renal glucose threshold below which all glucose is reabsorbed from glomerular filtrate. But at blood concentrations above the renal threshold sugar starts appearing in the urine.[citation needed]Oxyhyperglycemia, like other forms of Impaired glucose tolerance has also been suggested to be a prediabetic condition[4]
Oxyhyperglycemia is most commonly caused by early dumping syndrome, but it can rarely be caused by other conditions like Graves' disease.[5] It was first described by Lawrence et al. in 1936[6][7] as often happening after gastroenterostomy. It is seen in most forms of gastrectomy, gastric bypass and gastrostomy procedures, all of which are surgical causes of dumping syndrome.[citation needed]
In early dumping syndrome, pancreatic glucagon is augmented in the early postprandial period, probably through stimulation the catecholamines involved in the generalized autonomic surge induced by the osmotic load, but at 120 min, when most of the hypoglycemias are encountered, pancreatic glucagon is no longer detectable, likely through inhibition by GLP-1.[8][9] Incretins including GLP1 and GIP also bring in the late dumping effects including the insulin rise and the reactive hypoglycemia.[10]
Most patients (or animals) with prediabetic type impaired glucose tolerance (serum glucose 140–200 mg/dL at 2 hours after OGTT) are generally not oxyhyperglycemic because:[citation needed]