Epidemiological and experimental studies suggest that cardio-vascular risk factors could foster the development of type 2 diabetes (T2D). This could partly be mediated by pancreatic atherosclerosis resulting in pancreatic ischemia. We hypothesized that patients with T2D present with more severe atherosclerosis of pancreas-bound arteries than control patients without T2D.

We performed a case-control retrospective study comparing the abdominal computed tomography of patients with T2D and of control subjects matched for gender and for age. Forty-eight patients with T2D and 48 control subjects were included. A calcification score of the splenic artery was defined (from 0: no calcification to 3: continuous linear calcifications). It was higher in patients with T2D than in control subjects (0.6 versus 0.2, p=0.02). The mean number of pancreas-bound branches among the greater pancreatic artery, the dorsal pancreatic artery and the inferior pancreatic artery (from 0 to 3) and of visible intrapancreatic arterial subdivisions (from 0 to 2) was lower in patients with T2D than in control subjects (1.1 versus 1.7, p=0.003 and 0.7 versus 1.3, p=0.0017, respectively). Post-injection enhancement of the pancreas tended to be lower in patients with T2D than in control subjects (57 versus 68 Hounsfield units, p=0.06). None of these differences correlated with the duration of diabetes. Moreover, in control subjects, the pancreas volume was higher and the pancreas density and enhancement were lower with higher BMI. This relationship was not confirmed in patients with T2D. Thus, it could be hypothesized that more powerful factors than BMI could impact pancreas volume and density in patients with T2D. Pancreatic atherosclerosis could be one of these.

Patients with T2D present with more anomalies of the pancreatic arterial tree than control subjects. These anomalies do not correlate with the duration of diabetes, which may imply an early role of pancreatic atherosclerosis in T2D natural history.


L. Alexandre-Heymann: None. M. Barral: None. A. Dohan: None. E. Larger: None.

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