Hypoglycemia in hepatocellular carcinoma: Failure of short-term growth hormone administration to reduce enhanced glucose requirements

Abstract

The mechanism of tumor-associated hypoglycemia was investigated in 10 (six hypoglycemic and four normoglycemic) southern African blacks with hepatocellular carcinoma. The mean basal blood glucose concentration was significantly lower (2.4 ± 0.1 v 3.6 ± 0.2 mmol/L; P < .01) and steady-state exogenous glucose requirements were increased fourfold (3.6 ± 0.6 v 0.97 ± 0.2 mg/kg/min; P < .01) in the hypoglycemic compared with the normoglycemic patients. Plasma insulin and C-peptide levels were suppressed to the lower limit of sensitivity of each of the assays in both groups of patients. The concentrations of insulin-like growth factors (IGF) I and II were lower (19 ± 1.6 v 25 ± 4.6 ng/L) and higher (230 ± 42 v 173 ± 40 ng/L), respectively, in the hypoglycemic patients, although the differences were not statistically significant. Of the counterregulatory hormones measured, only the growth hormone (GH) concentration was significantly lower in the hypoglycemic patients (0.9 ± 0.2 v 18.6 ± 5.6 μg/L; P < .01). Correction of the plasma GH level into the high-normal physiological range in two hypoglycemic patients failed to reduce steady-state exogenous glucose requirements. However, the glucose requirements were reduced from 2.6 to 1.1 mg/kg/min in the same two patients when “acromegalic” plasma concentrations of GH were achieved. We conclude that steady-state glucose requirements are increased in black patients with hypoglycemia complicating hepatocellular carcinoma, and that short-term correction of the associated hyposomatotropism fails to reduce the enhanced requirements.