Blood glucose concentration and risk of pancreatic cancer: systematic review and dose-response meta-analysis

Abstract

Objective To evaluate potential linear and non-linear dose-response relations between blood glucose and risk of pancreatic cancer.Design Systematic review and dose-response meta-analysis of prospective observational studies.Data sources Search of PubMed, Scopus, and related reviews before 30 November 2013 without language restriction.Eligibility criteria Prospective studies evaluating the association between blood glucose concentration and pancreatic cancer. Retrospective and cross sectional studies excluded to avoid reverse causality.Data extraction and synthesis Two reviewers independently extracted relevant information and assessed study quality with the Newcastle-Ottawa scale. Random effects dose-response meta-analysis was conducted to assess potential linear and non-linear dose-response relations.Results Nine studies were included for analysis, with a total of 2408 patients with pancreatic cancer. There was a strong linear dose-response association between fasting blood glucose concentration and the rate of pancreatic cancer across the range of prediabetes and diabetes. No non-linear association was detected. The pooled rate ratio of pancreatic cancer per 0.56 mmol/L (10 mg/dL) increase in fasting blood glucose was 1.14 (95% confidence interval 1.06 to 1.22; P<0.001) without significant heterogeneity. Sensitivity analysis excluding blood glucose categories in the range of diabetes showed similar results (pooled rate ratio per 0.56 mmol/L increase in fasting blood glucose was 1.15, 95% confidence interval 1.05 to 1.27; P=0.003), strengthening the association between prediabetes and pancreatic cancer.Conclusions Every 0.56 mmol/L increase in fasting blood glucose is associated with a 14% increase in the rate of pancreatic cancer. As prediabetes can be improved or even reversed through lifestyle changes, early detection of prediabetes coupled with lifestyle changes could represent a viable strategy to curb the increasing incidence of pancreatic cancer.

Validation of N-glycan markers that improve the performance of CA19-9 in pancreatic cancer

“…Evidence has suggested that high glucose and type 2 diabetes might be risk factors for PC [35]. In our study, we also noted that blood glucose concentrations in PC groups were higher than control groups.…”

A clinical prediction model to assess risk for pancreatic cancer among patients with new-onset diabetes.

“…This hypothesis was supported by a meta-analysis demonstrating a linear increase of 14% in pancreatic cancer risk with every 0.56mmol/L increase in fasting blood glucose levels. 24 Because of the high incidence of diabetes mellitus in the general population and the lack of a low-risk and low-cost PDA screening test, conducting mass PDA screening in all patients with new-onset diabetes mellitus is not feasible. Nevertheless, targeted screening for PDA (e.g., using endoscopic ultrasound [EUS]) may be feasible if diabetic individuals at the highest risk for PDA-associated diabetes could be identified.…”

Hereditary Pancreatic Cancer

“…Due to one of the functions of the pancreas in regulating glucose metabolism, diabetes is a common presenting finding for pancreatic cancer. In one dose-response metaanalysis of prospective observational studies, it was shown that every 0.56 mmol/L increase in fasting blood glucose is associated with a 14% increase in the rate of pancreatic cancer [54]. This roughly translates to around a 0.35% change in the Hemoglobin A1C (HgbA1C).…”