Published online Jun 21, 2020. doi: 10.3748/wjg.v26.i23.3260
Peer-review started: January 22, 2020
First decision: February 27, 2020
Revised: March 29, 2020
Accepted: May 15, 2020
Article in press: May 15, 2020
Published online: June 21, 2020
Pancreatic endocrine insufficiency after acute pancreatitis (AP) has drawn increasing attention in recent years.
In recent years, we discovered another complication with an increasing frequency after AP onset, namely, pancreatic endocrine insufficiency. DM is associated with a heavy burden on the society due to related disabilities and high costs. Therefore, it is important to determine the incidence rate, risk factors, treatment, and outcome of pancreatic endocrine insufficiency after AP onset, which remain unclear. Hence, in this study, we conducted a long-term follow-up investigation to assess the potential risk factors for and incidence of pancreatic endocrine insufficiency after AP onset.
The aim of the present study was to assess the impact of risk factors on the development of pancreatic endocrine insufficiency after AP.
This was a long-term follow-up retrospective observational study with patient data collected from the AP database of the First Affiliated Hospital of Nanchang University; it was conducted from January 1, 2012 to December 30, 2018. A total of 361 AP patients agreed to be followed after discharge. Pancreatic endocrine function was assessed by the fasting blood glucose level and an oral glucose tolerance test. All tests were performed at the First Affiliated Hospital of Nanchang University. One-way analysis of variance, Kolmogorov-Smirnov test, Cox regression, and univariate Cox regression analysis were used in this study.
The morbidity of DM and IGT in patients with pancreatic necrosis was significantly higher than that in the non-pancreatic necrosis patients (χ2 = 4.152, P = 0.001). According to the CT images, the area of pancreatic necrosis was divided into three subgroups on the basis of the extent of pancreatic necrosis: Necrotic area < 30%, necrotic area 30%-50%, and necrotic area > 50%. The morbidity of DM and IGT showed a significant difference between patients with different extents of pancreatic necrosis (P = 0.001).
The results of multivariate Cox regression analysis showed that the severity of AP and pancreatic necrosis were independent risk factors for pancreatic endocrine insufficiency in AP patients and that the area of pancreatic necrosis was related to pancreatic endocrine function.
This study is the first to explore the association between AP and endocrine insufficiency in such a long follow-up time from 3 mo to 7 years. We confirmed that pancreatic necrosis and the severity of AP are independent risk factors for pancreatic endocrine insufficiency after AP. Meanwhile, we proposed that the area of pancreatic necrosis can affect pancreatic endocrine function after AP and high blood glucose recovers to normal levels as the disease of AP improves in this study. Our result will provide some guidance on the clinical practice in the future.
In the future, pancreatic endocrine function should be further evaluated with HbA1c and C-peptide. This study found that pancreatic endocrine insufficiency recovers over time, but we did not determine which time point is associated with the highest incidence of pancreatic endocrine insufficiency. An RCT will be needed to evaluate the time point, and we should not only pay attention to the pancreatic endocrine insufficiency, but also the exocrine pancreatic insufficiency.