Studies using finger-prick blood sampling during spontaneous symptomatic episodes have shown that only a very small proportion of sufferers from the postprandial syndrome have hypoglycemia at the relevant time. Of those who do, a substantial proportion have an identifiable cause for it. The commonest is partial gastrectomy and rapid gastric emptying from any cause, in the West, and the autoimmune insulin syndrome in the Far East, i.e., Japan. Other more rare causes include insulinoma, the newly described condition of noninsulinoma pancreatogenic hypoglycemia, and abnormalities of GLP-1 secretion.
In some people reactive hypoglycemia occurs only in response to a specific dietary indiscretion: for example, ingestion of large amounts of gin (alcohol) and tonic (sugar and quinine) on an empty stomach. A hard core of subjects remains for whom no satisfactory pathogenic mechanism can be identified. Only in them is it justified to describe them as suffering from (idiopathic or functional) reactive hypoglycemia (Figure 2).
Because of their short duration and modest severity, acute spontaneous neuroglycopenic episodes require no specific treatment beyond ingestion of a rapidly assimilable form of carbohydrate (e.g., a lump of sugar), exactly as for iatrogenic hypoglycemia.
There is no evidence that this ever produces rebound hypoglycemia and should it do so the grounds for making a diagnosis of essential reactive hypoglyce-mia should be reviewed.
Dietary prevention of reactive hypoglycemia, whether of the 'idiopathic', alimentary variety, or secondary to some other disease, is based on the premise that it is caused by imbalance between the timing and amount of insulin secreted in response to the ingestion of a meal and disposal of the glucose derived from it. Evidence for this supposition is small and disputed but provides the best explanation for the apparent breakdown in glucose homeostasis in patients with idiopathic reactive hypoglycemia.
Frequent small meals containing only modest amounts of sugars (glucose and sucrose) and refined starches but rich in poorly absorbed complex carbohydrates and containing dietary fiber have replaced the diets rich in proteins (and fats) previously advocated, but evidence of their unique efficacy is lacking. Avoidance of drinks rich in sucrose or glucose, especially with alcohol, may be helpful in subjects who are highly susceptible to this combination. There is no evidence that confectionery eaten in moderation is uniquely detrimental, though excessive use should be discouraged on general health grounds.
The long-term outcome of such dietary advice in patients in whom strict criteria for diagnosis were adopted are not available and most published studies on the subject have drawn attention to the need for supplementary pharmacological methods in order to achieve a satisfactory therapeutic outcome.
Pharmaceutical agents that have been used include guar, acarbose, and miglitol, all of which slow glucose absorption and decrease the insulinemic response to food, while others including phenytoin and propranolol do not. Paradoxically, diazoxide, which inhibits insulin secretion by direct action, has not been found effective except in patients with proven endogenous hyperinsulinism.
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