Bidirectional Relationship Between Diabetes and Acute Pancreatitis

Abstract

The proposed bidirectional relationship between acute pancreatitis (AP) and diabetes has never been examined with the same source of data. Furthermore, the effects of disease severity on this relationship have not been fully evaluated. The present study employed the findings from a single database to measure the strength of the association between AP and diabetes.Findings from 1 million National Health Insurance beneficiaries were utilized. Two cohort studies with this database were selected to evaluate the linkage between diabetes and AP. The first cohort analysis addressed the risk of AP among diabetic patients and was comprised of 42,080 diabetic patients and 672,146 unexposed subjects. The second cohort analysis considered the risk of diabetes among patients with AP and enrolled 3187 patients with AP and 709259 unexposed subjects. All adult beneficiaries were followed from January 1, 2005 to December 31, 2012 to identify outcomes of interest. Cox regression models were applied to compare hazards adjusted for potential confounders.For the first cohort, the adjusted hazard ratio (HR) of AP was significantly increased by the presence of diabetes (1.72; 95% confidence interval [CI], 1.52–1.96). In diabetic patients with a history of hyperglycemic crisis episodes (HCEs), the HR was even higher (6.32; 95% CI, 4.54–8.81). For the second cohort, the adjusted HR of diabetes in patients with AP was increased compared to the general population (2.15; 95% CI, 1.92–2.41). For patients with severe AP, the HR was also higher (2.22; 95% CI, 1.50–3.29) but did not differ significantly from that for patients with nonsevere AP.The 2 cohort studies provided evidence for the bidirectional relationship between diabetes and AP. Moreover, diabetic patients with history of HCEs may be associated with higher risk of AP.

Nomogram for predicting diabetes mellitus after the first attack of acute pancreatitis

“…However, we can establish an i ndirect correlation through obesity, alcohol intake, and abnormal glucose 32–34. With the increase of BMI, the risk of developing DM increased proportionally on our nomogram, as previous literature studies 24,35,36. Lipid metabolism (including LDL-C) had connection with alcohol consumption, and increased alcohol consumption (>200 g/week) was associated with increased LDL and triglycerides 34,37,38.…”

“…This result challenged the widely accepted view that pancreatic injury is temporary, and that endocrine pancreatic function recovers fully after AP regardless of severity 4–6. DM can occur after AP 3,7–9, but there remains no consensus regarding the extent of the risk following AP.…”

Acute Pancreatitis Induced by Diabetic Ketoacidosis with Major Hypertriglyceridemia: Report of Four Cases

“…As far as the physiological side is concerned, there is a bidirectional relationship between dysglycemia and pancreatitis [4]. Acute pancreatitis could induce a beta cell dysfunction and transient insulin deficiency, and it could also increase insulin resistance due to systemic inflammation [5].…”

The Role of Gut–brain Axis in Regulating Glucose Metabolism After Acute Pancreatitis

“… 16 , 17 , 18 Further, this estimate is based on the studies focused on new onset diabetes after chronic pancreatitis and pancreatic cancer, but not acute pancreatitis (AP). Given the recently emerged evidence from clinical and population-based studies of a high incidence of diabetes after AP (regardless of the magnitude of macroscopic mechanical destruction of the pancreas) 19 , 20 , 21 , 22 and taking into account that AP is the most frequent disease of the pancreas, 23 it is very likely that the relative contribution of diabetes associated with diseases of the exocrine pancreas has actually been underestimated in the literature.…”