Differential Diagnosis of Hypoglycemia
Hypoglycemia is one of the most overdiagnosed conditions because its symptoms may be associated with many unrelated disorders. Many of the symptoms are nonspecific and relatively vague. Clinical symptoms fall into 2 broad categories known as adrenergic and neuroglucopenic. Adrenergic symptoms such as weakness, sweating, tachycardia, palpitation, and tremors are a result of increased activity of the autonomic nervous system. Neuroglucopenic symptoms such as headache, hypothermia, visual disturbances, and mental dullness are associated with a severe state of hypoglycemia. Patients with hypoglycemia experience palpitations, sweating, fatigue, and an inability to concentrate; symptoms can be relieved by eating.
Diagnosis of hypoglycemia depends upon the demonstration of Whipple's triad and includes a low plasma glucose concentration, presence of hypoglycemic symptoms, and relief of symptoms when the plasma glucose levels return to normal after ingesting food (eg, carbohydrates). All 3 criteria should be met, as some patients may have subnormal serum glucose levels and be asymptomatic, while other patients may have normal serum glucose levels but experience symptoms similar to those associated with hypoglycemia.
Patients with symptomatic fasting hypoglycemia require a thorough evaluation. It is important to consider a variety of disorders that cause symptomatic fasting hypoglycemia with and without hyperinsulinism. Conditions such as a pancreatic beta-cell tumor (eg, insulinoma) and surreptitious administration of insulin or sulfonylureas, which causes inappropriate fasting hyperinsulinism, are the most common causes of fasting hypoglycemia. Usually, these patients appear healthy between hypoglycemic episodes. The possibility of autoimmune disease (eg, antibodies to insulin) that is associated with hyperinsulinemic hypoglycemia should also be ruled out.
By contrast, patients with symptomatic fasting hypoglycemia without hyperinsulinism experience hypoglycemia associated with an illness. Usually, the clinical signs and symptoms of the major illness dominate. Some common causes of symptomatic fasting hypoglycemia without hyperinsulinism include severe hepatic dysfunction, chronic renal insufficiency, and hypercortisolism.
Factitious hypoglycemia is often diagnosed when the physician is attempting to rule out insulinoma. Whipple's triad is not of diagnostic value in detecting factitious hypoglycemia because the symptoms of Whipple's triad are the same among patients with hyperinsulinism and patients with factitious hypoglycemia.[14,15] It is difficult to differentiate factitious hypoglycemia from insulinoma because of similar clinical and biochemical findings.
Once the diagnosis of hyperinsulinemic hypoglycemia is confirmed, the next step is to differentiate the hypoglycemia due to endogenous hypersecretion of insulin from hypoglycemia due to exogenous use of insulin or oral hypoglycemic drugs. It is more difficult to diagnose insulin-induced factitious hypoglycemia in diabetic patients; approximately one third of the patients with insulin-induced factitious hypoglycemia are diabetic.
Previously, diagnosis of factitious hypoglycemia relied upon circumstantial evidence such as the patient's unauthorized possession of insulin needles and syringes. The radioimmunoassay for human C-peptide, a clinical marker of endogenous insulin secretion, can be used in the diagnosis of factitious hypoglycemia.
Medscape Pharmacotherapy. 2002;4(1) © 2002 Medscape
Cite this: Factitious Hypoglycemia - Medscape - May 09, 2002.