Stephen J.LurieMD, PhD, Senior EditorIndividualAuthorPhil B.FontanarosaMD, Executive Deputy EditorIndividualAuthor
Copyright 2000 American Medical Association. All Rights Reserved.
Applicable FARS/DFARS Restrictions Apply to Government Use.2000
To the Editor: Dr Gapstur and colleagues1 observed that higher postload plasma glucose levels
were associated with an increased relative risk for pancreatic cancer in their
sample of patients, most of whom were white.
While working with a predominantly Hispanic adult patient population
during the last 6 years, I have come across 3 cases of hepatobiliary cancer
in patients with diabetes, none of whom had a history of alcoholism or hepatitis.
In recent years, there has been a reported increase in the incidence of hepatobiliary
cancer, probably related to hepatitis B and C.2
One wonders if there is a similar linkage between hepatobiliary neoplasms
and hyperglycemia, as there is between the latter and pancreatic malignancy.
Is it possible that the insulin-activated insulin-like growth factor 1 receptor3 could have a proliferative effect on disgestive
organs other than the pancreas? Because diabetes mellitus is already associated
with considerable morbidity, these newfound risks would be added incentives
for attaining glycemic control.
Kulkarni P. Relationship Between Glucose Metabolism and Pancreatic Cancer. JAMA. 2000;284(12):1512. doi:10.1001/jama.284.12.1512