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The role of glucagon administration in the diagnosis and treatment of patients with tumor hypoglycemia
Author(s) -
Hoff Ana Oliveira,
VassilopoulouSellin Rena
Publication year - 1998
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/(sici)1097-0142(19980415)82:8<1585::aid-cncr22>3.0.co;2-#
Subject(s) - hypoglycemia , medicine , glucagon , insulinoma , insulin , endocrinology , gastroenterology
BACKGROUND Tumor hypoglycemia can be recurrent and severe enough to interfere with definitive antineoplastic treatment. Therefore, rapid commencement of effective therapy is essential. This is best accomplished by identifying which of the hypoglycemic processes is involved, as treatments differ. Some patients present with hypoglycemia and liver metastases; among them, only a few develop hypoglycemia as a result of a failure of hepatic glucose production. Most develop hypoglycemia as a result of an insulin‐mediated process‐either the secretion of insulin by an islet‐cell tumor or the secretion of insulin‐like growth factor‐II by an extrapancreatic tumor. Administration of glucagon can rapidly make the two groups distinguishable, thus allowing institution of therapy and prompt symptomatic control of hypoglycemia. METHODS The charts of seven patients with tumor hypoglycemia and liver metastases who had a glucagon stimulation test (serial glucose measurements after a 1 mg infusion of glucagon) as part of the workup for hypoglycemia were retrospectively reviewed. Those patients whose test revealed a rise in serum glucose of >30 mg/dL were subsequently treated as outpatients, with a continuous glucagon infusion delivered by a portable pump. RESULTS Three patients had an insulinoma and four had non‐islet cell tumor hypoglycemia (NICTH) due to hepatocellular carcinoma, colon carcinoma, meningeal sarcoma, and hemangiopericytoma, respectively. All of the patients had liver metastateses. Evaluation of these patients included a glucagon stimulation test (1 mg intravenous push), which quickly provided information about the mechanism of tumor hypoglycemia and the direction towards therapy. All patients with insulinoma responded to glucagon with a rise in blood serum glucose levels, indicating adequate glycogen stores. The four patients with NICTH had mixed responses: in two patients, the response suggested that hypoglycemia was due to an insulin‐like tumor product; glucose levels did not rise in the other two cases, indicating that hypoglycemia was due to poor hepatic glycogen reserve/liver failure. In all cases, a glycemic response to glucagon predicted good response to long term treatment with glucagon (0.06‐0.3 mg/hour, via intravenous infusion pump). CONCLUSIONS The glucagon stimulation test is a simple and fast approach that serves to clarify the etiology of hypoglycemia (diagnostic use) and guide effective long term strategies for its control (therapeutic use) in patients with neoplastic diseases and liver metastases. Cancer 1998; 82:1585‐92. © 1998 American Cancer Society.