In the presence of vegetative adrenergic symptoms postprandial hypoglycemia should only be considered if biochemical hypoglycemia does occur within 2-4 hours after intake of a standardized testmeal (rich in carbohydrates) during laboratory test conditions, e.g. as compared to a testmeal rich in proteins.
Postprandial hypoglycemia typically may occur after a carbohydrate rich meal, thus also classified as "alimentary hypoglycemia". This is in contrast to fasting hypoglycemia or spontaneous hypoglycemia in insulinoma.
Eventually patients with an insulinoma may experience hypoglycemia within 3-6 hours after an oral glucose load or a meal (depending upon the insulin secretion pattern of the tumor). The hypoglycemia cannot be efficiently counterregulated, fasting needs to be withdrawn.
Patients with postprandial hypoglycemia are able to counterregulate hypoglycemia adaequately and thus return to the normal range of blood glucose levels .
postprandial hypoglycemia and " d i a b e t e s " ?
Very often we face the erroneus notion, postprandial or meal-associated hypoglycemia mistakingly be seen as "an early sign" of diabetes mellitus ???
It is true that real hypoglycemia after a meal may occur early in the development of type II diabetes. However, this is caused by untimely delayed and therefore increased insulin secretion when elevated hyperglycemic blood glucose levels have been detected early-postprandially (so called right-shift of the insulin secretion curve).
Typically, co-existence of hyperglycemia and hypoglycemia is found but not hypoglycemia alone. The HbA1c may be normal, too.
postprandial hypoglycemia and
Non-insulinoma pncreatogenic hypoglycemia-syndrome (NIPHS)
postprandial hypoglycemia together with clearly neuroglycopenic symptoms may be a challenging issue if caused by non-insulinoma pancreatogenic hypoglycemia-syndrome / NIPHS (= islet cell hyperplasia, rarely hypertrophy ).
According to J.Service (Mayo Clinic Rochester MN) this is probably the correct terminus for rare islet cell hyperplasia or nesidioblastosis in adults.
The oral glucose tolerance test (OGTT) does not allow the diagnosis of postprandial hypoglycemia, since the "meal" is not physiological and the availibility of glucose in the gastrointestinal tract of short duration. Glucose tolerance testing is suitable for screening purposes.
The term "reactive" or "functional" hypoglycemia is outdated and should not be used.
Adrenergic Postprandial Syndrome - APS
Despite normal concentrations of blood glucose patients face unspecific symptoms (sweating, tremor, palpitations, anxiety, nausea) caused through autonomic adrenergic counterregulation. The adrenergic tone elicits the symptoms and simultaneously avoids hypoglycemia through biochemical mechanisms (action of epinephrine / adrenaline; see "Gluco-Homeostasis".
APS represents a reactive or functional dysregulation of the autonomic nervous system and should not be classified as "hypoglycemia". Terms like "pseudohypoglycemia" or even "non-hypoglycemia" should be avoided, since they do not address the virtual presence of discomfort reported by these patients.
The biochemically defined cutoff for hypoglycemia as tolerated in the brain is 2.8 mmol/l (50 mg/dl). A counterregulatory response (epinephrine/adrenaline and glucagon) is triggered at higher blood glucose levels in the range of > 60 mg/dl (cutoff 3.1-3.3 mmol/l). Glucagon does not cause symptoms, but epinephrine does.
The early dumping-syndrome does occur within 30 minutes in 10-15% of patients after resective gastric surgery. These are orthostatic hemodynamic symptoms induced secondary to a rise in intestinal osmotic pressure due to a rapid emptying of the osmotically active gastric content. Symptoms are characterized as adrenergic symptoms, in addition patients experience nausea, intestinal rumors, fullness, falling blood pressure with tachycardia/bradycardia.
Causes are: catecholamines, serotonin, vasoactive kinines; intraluminal pressure. Eventually and depending upon the carbohydrate content transient hyperglycemia may even be seen.
The late dumping-syndrome is identical with true postprandial hypoglycemia in patients after gastric surgery caused by an imbalance of postprandial hyperinsulinemia and availability of carbohydrates.
It may occur in patients with dysfunction of intestinal motility without prior gastric surgery. Increase of the intestinal passage and contractions are mediated by the secretion of intestinal hormones / peptides (cholecystokinine - CCK, gastrin, motilin, neurotensin (?), substance P).
Causes of postprandial hypoglycemia: 1. Increased insulin secretion (triggered through increased glucagon-like peptide 1 - secretion ("early responder") 2.
Rapid gastric emptying (after gastric surgery):
a. stimulation of insulin secretion
b. stimulation of GLP-1-secretion, GIP (gastric insulinotropic polypeptide)
3. Renal glucosuria 4. Increased insulin sensitivity (increased non-oxidative glucose metabolism) 5. Decreased insulin sensitivity ("insulin resistance") with initially decreased insulin response, thereafter right-shifted increased insulin response ("late responder"). 6. Decreased glucagon secretion / glucagon resistance (hyposensitivity of glucagon receptors) ?
Literature postprandial hypoglycemia: 1. Hogan MJ, Service FJ, Sharbrough FW, Gerich JE. Oral glucose tolerance test compared with a mixed meal in the diagnosis of reactive hypoglycemia. Mayo Clin Proc 58:1983, 491-496 2. Gastineau CF. Is reactive hypoglycemia a clinical entity? Mayo Clin Proc 58:1983, 545-549 3. Lefebvre PJ, Andreani D, Marks V, Creutzfeldt W. Statement on postprandial or reactive hypoglycemia. Diabetes Care 11: 1988, 439 4. Brun JF, Fedou C, Mercier J. Postprandial reactive hypoglycemia. Diabetes & Metabolism 26:2000, 337-351