Non-islet cell tumor-induced hypoglycemia
NICTH should be considered in patients presenting with tumor of mesenchymal origin and hypoglycemia.
Hypoinsulinemic hypoglycemia with low IGF1** is a strong biochemical evidence of NICTH.
IGF2:IGF1*ratio of more than 10is a complementary investigation in the absence of an assay facility for IGF2.
Type A NICTH is characterized by high tumor utilization of glucose in poorly nourished patients with depleted glycogen stores and defective gluconeogenesis. This type of NICTH is often seen during the late stages of HCC when tumor burden is large and hepatic destruction is extensive .
In type B NICTH, there is increased tumor secretion of incompletely processed IGF-2 (pro-IGF-2), which is poorly metabolized due to defective hepatocytes in cirrhosis. This defective pro-IGF-2 is smaller, crosses the capillary membranes easier, and stimulates more insulin receptors throughout the body than normal IGF-2. This occurs early in liver disease and is characterized by overwhelming tissue glucose uptake and severe, persistent hypoglycemia.