Risk of Diabetes Mellitus After First-attack Acute Pancreatitis

A National Population-Based Study

Hsiu-Nien Shen MD, PhD; Chun-Chieh Yang, MD; Ya-Hui Chang, MSc; Chin-Li Lu, MS; Chung-Yi Li, PhD


Am J Gastroenterol. 2015;110(12):1698-1706. 

In This Article

Abstract and Introduction


Objectives: Population-based data on the risk of diabetes mellitus onset after acute pancreatitis (AP) are lacking. We assessed the incidence of diabetes in AP survivors compared with matched controls.

Methods: The study cohort, drawn from Taiwan National Health Insurance claims data, included 2,966 first-attack AP patients and 11,864 non-AP general controls individually matched on age and sex, with an AP/non-AP ratio of 1:4. Incidence rate was estimated under Poisson assumption. Relative risks of diabetes were indicated by hazard ratios (HRs) estimated from Cox proportional hazard regression models with a partitioning of time at 3 months to account for proportionality.

Results: In the first partition of time (<3 months), the incidences of diabetes were 60.8 and 8.0 per 1,000 person-years in AP and control groups, respectively; representing a covariate-adjusted HR of 5.90 (95% confidence interval (CI) 3.37–10.34). In the second partition (≥3 months), the incidences of diabetes were 22.5 and 6.7 per 1,000 person-years in AP and control groups, respectively (adjusted HR 2.54, 95% CI 2.13–3.04). In the second partition, the risk of diabetes was greater in men than in women (HR 3.21 vs. 1.58, P=0.0004). When the analyses were stratified by severity of AP, the results for mild AP were similar to those for all AP.

Conclusions: The risk of diabetes increases by twofold after AP; therefore, a long-term screening is necessary to evaluate diabetes after an attack regardless of severity. Further research should be conducted to develop cost-effective follow-up strategies, and to elucidate the underlying mechanisms of the relationship between diabetes and AP.


Diabetes mellitus (DM) may occur after acute pancreatitis (AP). One mechanism of DM development after AP involves the loss of islet cells because of severe pancreatic necrosis; if subsequent surgery is performed, the β-cell area may be reduced to a critical threshold that induces the development of DM.[1] In previous reports,[2–4] DM commonly occurs (28 to 100%) after a patient undergoes pancreatic surgery for severe AP.[2–4] When patients with severe AP are treated conservatively, the frequency of new-onset DM decreases (6.2–15.7%).[5–7] These observations suggest that DM after AP is largely caused by pancreatic resection, not by pancreatitis.[2] However, a recent meta-analysis of 24 prospective studies on patients with first-episode AP but without pancreatic surgery shows that the pooled prevalence of newly diagnosed DM is 15% within 1 year and 40% at 5 years after AP.[8] Moreover, other studies suggest that endocrine pancreatic function may recover completely after AP regardless of severity,[5,6] and that the incidence of DM after AP "is similar to the reported values for the general population".[9] Therefore, without a population-based control, whether and to what extent AP increases the risk of DM remains unknown.

After an episode of AP, glucose intolerance caused by an impaired β-cell function and insulin resistance[7,9] is commonly observed (>30%), even in mild cases.[10] For this reason, some researchers proposed that the "determination of plasma glucose levels should be included in the follow-up of all patients with AP"[11] despite the lack of epidemiological evidence on the increased risk of DM. Evidence should be documented, especially for patients with mild AP because these patients constitute approximately 80% of all AP cases[12,13] and are not subjected to regular follow-up after the attack. Therefore, we conducted this population-based matched cohort study to assess the overall and age- and sex-specific incidence rates and relative risks of DM after AP on the basis of the AP severity.