title: 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 less than .01) and steady-state exogenous glucose requirements were increased fourfold (3.6 +/- 0.6 v 0.97 +/- 0.2 mg/kg/min; P less than .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 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 micrograms/L; P less than .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.
authors.affiliation: Department of Medicine, University of the Witwatersrand Medical School, Johannesburg, South Africa.
authors.forename: J R
authors.initials: JR
authors.lastname: Wing
authors.forename: V R
authors.initials: VR
authors.lastname: Panz
authors.forename: B I
authors.initials: BI
authors.lastname: Joffe
authors.forename: W J
authors.initials: WJ
authors.lastname: Kalk
authors.forename: H C
authors.initials: HC
authors.lastname: Seftel
authors.forename: J
authors.initials: J
authors.lastname: Zapf
authors.forename: M C
authors.initials: MC
authors.lastname: Kew
mesh_terms: D001786:Blood Glucose / Q000032:analysis; D006528:Carcinoma, Hepatocellular / Q000150:complications* / Q000503:physiopathology; D005938:Glucocorticoids / Q000627:therapeutic use; D005947:Glucose / Q000502:physiology*; D013006:Growth Hormone / Q000627:therapeutic use*; D006706:Homeostasis; D006728:Hormones / Q000097:blood; D006801:Humans; D007003:Hypoglycemia / Q000209:etiology* / Q000503:physiopathology; D007262:Infusions, Intravenous; D008099:Liver / Q000503:physiopathology; D008113:Liver Neoplasms / Q000150:complications* / Q000503:physiopathology; D008297:Male
chemical_list: D001786:Blood Glucose; D005938:Glucocorticoids; D006728:Hormones; D013006:Growth Hormone; D005947:Glucose