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Figure 13-3. Pathophysiology of a hypoglycemic attack. The initial rapid decline in blood glucose stimulates the reflex release of epi-nephrine by the adrenal gland. As the blood glucose level continues to fall, symptoms caused by epinephrinemia merge with those caused by cerebral glucose deprivation. Reproduced with permission from Edis AJ, Ayala LA. Manual of endocrine surgery. Springer-Verlag; 1975.

mesotheliomas, leiomyosarcomas, hemangiopericy-tomas, hepatomas, and lung, gastric, and pancreatic cancer. These tumors are quite large and usually secrete incompletely processed insulin-like growth factor II (IGF-II). The incompletely processed IGF-II interacts with insulin receptors in the liver, muscle, and adipocytes, resulting in inhibition of liver glucose production and increased glucose uptake in the parenchymal tissues. The clinical diagnosis of non-islet cell tumor is made by documenting high or normal IGF-II concentrations and low levels of insulin in a hypoglycemic patient. In patients with insulinomas, proinsulin levels constitute more than 25% of the serum insulin reactivity.

When determining the cause of hypoglycemia, it is very important to determine whether the hypoglycemia occurs postprandially or with fasting. Postprandial (reactive) hypoglycemia is much more common than the fasting type. After gastrectomy, patients are prone to "reactive" or postprandial hypoglycemia; these patients may also experience diarrhea and other systemic symptoms associated with catecholamine release. In patients with insulinomas, on the other hand, symptoms almost always occur with fasting and/or after exercise.

Fasting hypoglycemia can occur owing to a variety of causes. Therefore, the low blood sugar levels in a patient with a suspected insulinoma must be dif-

Figure 13-3. Pathophysiology of a hypoglycemic attack. The initial rapid decline in blood glucose stimulates the reflex release of epi-nephrine by the adrenal gland. As the blood glucose level continues to fall, symptoms caused by epinephrinemia merge with those caused by cerebral glucose deprivation. Reproduced with permission from Edis AJ, Ayala LA. Manual of endocrine surgery. Springer-Verlag; 1975.

Table 13-1. MAJOR CAUSES OF FASTING HYPOGLYCEMIA

Postprandial (reactive hypoglycemia)

Idiopathic Fasting hypoglycemia

Conditions primarily owing to underproduction of glucose Hormone deficiencies Hypopituitarism Adrenal insufficiency Catecholamine deficiency Glucagon deficiency Enzyme defects Glucose-6-phosphatase Liver phosphorylase Pyruvate carboxylase Phosphoeno/pyruvate carboxykinase Fructose 1,6-diphosphatase

Acquired liver disease Hepatic congestion Severe hepatitis Cirrhosis Drugs Alcohol Propranolol Salicylates

Conditions primarily owing to overuse of glucose Hyperinsulinism Insulinoma Exogenous insulin Sulfonylureas

Immune disease with insulin antibodies Appropriate insulin levels Extrapancreatic tumors Cachexia with fat depletion Carnitine deficiency Carnitine acyltransferase deficiency

Adapted with permission from Jaspan JB, Polonsky KS, Foster DW, et al. Clinical features and diagnosis of islet-cell tumors. In: Moosa AR, editor.Tumors of the pancreas. Baltimore (MD): Williams and Wilkins, 1980. p. 469.

ferentiated from numerous other causes. Among them is deficient glucose production, as in the patient with cirrhosis of the liver and therefore an inability to mobilize glycogen for a glucose reserve; overuse of glucose in the fasting state (which would include insulinoma); pharmacologic and toxic agents that depress blood sugar; and late starvation when energy reserves may be exhausted. Daily hepatic production of glucose ranges from 100 to 200 g. If more than 200 g of glucose is required to offset hypoglycemic symptoms, then the patient suf fers from overuse of glucose, which is consistent with a diagnosis of insulinoma.

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