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Susan M. Gapstur, PhD; Peter H. Gann, MD, ScD; William Lowe, MD; Kiang Liu, PhD; Laura Colangelo, MS; Alan Dyer, PhD

JAMA. 2000;283:2552-2558.

Context  Previous studies reported an increased risk of pancreatic cancer among persons with diabetes. Few data exist, however, on the association of postload plasma glucose concentration with pancreatic cancer, which could provide insight into the role of abnormal glucose metabolism in the etiology of pancreatic cancer.

Objective  To determine the independent association between postload plasma glucose concentration and risk of pancreatic cancer mortality among persons without self-reported diabetes.

Design  Prospective cohort study.

Setting and Participants  Employees of 84 Chicago-area organizations, with an average age of 40 years at baseline, were screened from 1963 to 1973 and followed up for an average of 25 years. A total of 96 men and 43 women died of pancreatic cancer among 20,475 men and 15,183 women, respectively.

Main Outcome Measures  Relationship of pancreatic cancer mortality with postload plasma glucose levels.

Results  Compared with a postload plasma glucose level of 6.6 mmol/L (119 mg/dL) or less and after adjusting for age, race, cigarette smoking, and body mass index, the relative risks (95% confidence intervals) of pancreatic cancer mortality were 1.65 (1.05-2.60) for postload plasma glucose levels between 6.7 (120) and 8.8 (159) mmol/L (mg/dL); 1.60 (0.95-2.70) for levels between 8.9 (160) and 11.0 (199); and 2.15 (1.22-3.80) for levels of 11.1 (200) or more; P for trend=.01. An association appeared to be stronger for men than women. Estimates were only slightly lower after excluding 11 men and 2 women who died of pancreatic cancer during the first 5 years of follow-up. In men only, higher body mass index and serum uric acid concentration also were independently associated with an elevated risk of pancreatic cancer mortality.

Conclusion  These results suggest that factors associated with abnormal glucose metabolism may play an important role in the etiology of pancreatic cancer.

Author Affiliations: Department of Preventive Medicine, Northwestern University Medical School (Drs Gapstur, Gann, Liu, and Dyer, and Ms Colangelo); The Robert H. Lurie Comprehensive Cancer Center (Drs Gapstur and Gann); Department of Medicine, Center for Endocrinology, Metabolism and Molecular Medicine, Northwestern University Medical School, and Veterans Affairs Chicago Health Care System, Lakeside Division (Dr Lowe), Chicago, Ill.

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