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Spontaneous hypoglycemia in adults is of two principal types: fasting and postprandial. Symptoms begin at plasma glucose levels in the range of 60 mg/dL (3.3 mmol/L) and impairment of brain function at approximately 50 mg/dL (2.8 mmol/L). Fasting hypoglycemia is often subacute or chronic and usually presents with neuroglycopenia as its principal manifestation; postprandial hypoglycemia is relatively acute and is often heralded by symptoms of neurogenic autonomic discharge (sweating, palpitations, anxiety, tremulousness).


Fasting hypoglycemia may occur in certain endocrine disorders, such as hypopituitarism, Addison disease, or myxedema; in disorders related to liver malfunction, such as acute alcoholism or liver failure; and in instances of ESKD, particularly in patients requiring dialysis (Table 27–11). These conditions are usually obvious, with hypoglycemia being only a secondary feature. When fasting hypoglycemia is a primary manifestation developing in adults without apparent endocrine disorders or inborn metabolic diseases from childhood, the principal diagnostic possibilities include (1) hyperinsulinism, due to either pancreatic B cell tumors or iatrogenic or surreptitious administration of insulin or sulfonylurea; and (2) hypoglycemia due to extrapancreatic tumors.

Table 27–11.Common causes of hypoglycemia in adults.1

Postprandial (reactive) hypoglycemia may occur after GI surgery and is particularly associated with the dumping syndrome after gastrectomy and Roux-en-Y gastric bypass surgery. Occult diabetes very occasionally presents with postprandial hypoglycemia.

Alcohol-related hypoglycemia is due to hepatic glycogen depletion combined with alcohol-mediated inhibition of gluconeogenesis. It is most common in malnourished individuals with excessive alcohol intake but can occur in anyone who is unable to ingest food after an acute alcoholic episode followed by gastritis and vomiting.

Immunopathologic hypoglycemia is an extremely rare condition in which anti-insulin antibodies or antibodies to insulin receptors develop spontaneously. In the former case, the mechanism appears to relate to increasing dissociation of insulin from circulating pools of bound insulin. When antibodies to insulin receptors are found, most patients do not have hypoglycemia but rather severe insulin-resistant diabetes and acanthosis nigricans. However, during the course of the disease in these patients, certain anti-insulin receptor antibodies with agonist activity mimicking insulin action may develop, producing severe hypoglycemia.

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