Reactive Hypoglycemia (Postprandial Hypoglycemia) – A Lurking Fear
Reactive Hypoglycemia……. A lurking fear
Reactive hypoglycemia or its synonym Post prandial hypoglycemia in otherwise normoglycemic individuals, though not taken too well, is not an unexpected finding in routine Blood Glucose Estimation in Clinical Labs of repute. Though diagnostic labs always have a relook in these reports of comparative low post prandial glucose levels before releasing it to clients or clinicians but then the labs are mentally prepared to answer volley of queries not only from patients/individuals but also from ambitious medical practitioners.
Maintenance of plasma glucose concentration within narrow bounds is essential for health. Lower levels of blood glucose relates to a pathological condition, popularly termed as hypoglycemia, which is a dangerous condition as brain for which primary source of energy substrate is only glucose tends to be vulnerable because it can not utilize circulating fatty acids as energy source as evident in other tissues.
Hypoglycemia can be classified as Postprandial (reactive ) or fasting. Low glucose levels occurring in response to and as a follow up after meals is what we call it Reactive(PP) hypoglycemia. Levels of PP glucose falling below fasting could be marginal or more but than any levels falling below 2.5 mmol/litre (45 mg/dl) can lead to adverse effects producing recognizable symptoms which may be autonomic or neuroglycopenic but these are unlikely to surface on levels above 2.8 mmol/l (50mg/dl). It is commonly thought that fasting hypoglycemia is a serious condition with most likely etiopathology of insulinoma whereas reactive hypoglycemia is invariably a benign disorder.
However yet another type of hypoglycemia is drug induced which can be encountered in patients of diabetes mellitus who are either on insulin or oral hypoglycemics. Besides in normoglycemics drugs like alcohol, salicylates,B-blockers and pentamidine can lead to PP hypoglycemia.
Early/pre diabetes can be considered to occur in patients who are suffering from reactive hypoglycemias.
The most common cause of reactive hypoglycemia is Alimentary hyperinsulism. More often such patients have either undergone gastrectomy, pyloroplasty or vagotomy. Hypoglycemia in such patients occur anytime within 1 -2.30 hrs after food/ glucose intake. The reason attributed is excessive and early serum insulin response presumably due to rapid gastric emptying and brisk absorption of glucose thereby depleting glucose more than provide in meals. This feature can also be observed in patients without prior surgery.
Hormone deficiencies viz. growth hormone can also lead to reactive hypoglycemia. Besides glucagons deficiency and enzymes like fructose-1,6-diphosphatase deficiency or genetic derangements such as heredity fructose intolerance can lead to reactive hypoglycemias. Liver diseases may also contribute to pp hypoglycemia by affecting neoglucogenesis. Galactose intolerance ,a metabolic disorder, is also responsible for hypoglycemias. Renal glycosuria is yet another factor for causing postprandial reactive hypoglycemia
Overall high insulin sensitivity is tipped to be the most important cause for reactive hypoglycemias. The most usual cause of increased insulin response is most often assumed to be insulin resistance related hyperinsulinemia.
Under circumstances quoted above it is observed that glucose levels fall more rapidly than insulin thereby resulting in insulin-glucose imbalance and eventually leading to hypoglycemias.
The phenomena of reactive hypoglycemia was observed by Harris in 1924 who reported five cases of hypoglycemia following meals and the term was coined by him. He postulated that reactive hypoglycemia was some kind counterpart of diabetes mellitus resulting due to hyperinsulinism or dysinsulinism. It was a debatable question and finally in third international conference/symposium on hypoglycemia held in Rome on 22/23 sept’1986 a consensus statement was released that it was an overdiagnosed entity but than there was no doubt that some patients exhibit postprandial symptoms suggesting hypoglycemia in everyday life and if these symptoms are accompanied by blood glucose levels of 2.5mmol/litre than the diagnosis of postprandial or reactive hypoglycemia may be correct.
Symptoms of reactive hypoglycemia, unless PP glucose level is < 45mg/dl , may not be acknowledged by patient at all. However the most common symptoms are as listed below. Patient may suffer with one or all of them.
Hunger, nervousness, anxiety, perspiration , cold sweat, confusion, dizziness , sleepiness, light headedness or weakness.
Interestingly hyperinsulinemia is responsible for enhancing epinephrine, norepinepherine and cortisol secretion in response to hypoglycemia which collectively are involved in producing postprandial adrenergic syndrome.
Once it has been observed that PP levels of glucose are low , if not insisted upon for repeat, Oral Glucose Tolerance Test (OGTT) is advised after 10hrs of fasting observing all diet/ drugs and alcohol limitations. Since plasma glucose levels in healthy persons may be usually below 2.8 mmol/litre without any specific symptoms therefore OGTT has not been considered as a choice investigation though surely it still remains as first line investigation . Interestingly reactive hypoglycemia is quite a normal occurrence after OGTT whether or not individual suffers with hypoglycemia after meals in everyday life.
Therefore it is imperative to state that glucose tolerance test alone is not fully reliable means of establishing diagnosis of reactive hypoglycemia. It is suggested that no doubt the test should be carried out but than it must be combined with insulin response( Insulin Glucose tolerance) test. And glucose levels must be correlated with symptoms of hypoglycemia. Additional tests like C-peptide and proinsulin can also be advised.
Finally the reactive hypoglycemia, a functional disorder, suffered from apt approach in past as a result of inadequate knowledge regarding its mechanism but now as more facts are being revealed, is now considered to be a “non disease” by most Physicians.
A positive and well reasoned approach by clinicians and pathologists will definitely allay all lurking fears from mind of our patients. It is definitely not a lab error.
