The Cause and Effect Relationship of Diabetes after Acute Pancreatitis

Abstract

Acute pancreatitis (AP) is an acute inflammation of the pancreas associated with high morbidity and mortality. Endocrine pancreatic insufficiency secondary to AP has drawn increasing attention in recent years. The aim of this paper is to analyze the available clinical and experimental literature to determine the cause and effect relationship of diabetes type 3c (T3cDM; pancreatogenic diabetes) after acute pancreatitis. The clinico-pathological features and management challenges of pancreatogenic diabetes overlap with other secondary causes of diabetes. A complex pathogenesis involving pancreatic exocrine insufficiency, dysfunction of insulin secretion, and insulin resistance is likely the cause of T3cDM after AP. To obtain an improved understanding of the pathophysiology of diabetes after AP, more research is now needed to understand the risk of complications related to the pancreas and diabetes in these patients.

Diagnostic Potential of Ratio Between Creatine Kinase and Amylase in Acute Pancreatitis

“…Alpha-amylase and CK are presumed to share some common biochemical properties as seen in pathological states, along with other liver enzymes such as AST, ALT and ALP ( 9 ). AP predisposition of development depends on several factors, such as hypertriglyceridemia, hypercalcemia, or some viral causes ( 15 ). AP is also associated with an increased mortality rate respectively to the severity of cases.…”

Challenges of Managing Type 3c Diabetes in the Context of Pancreatic Resection, Cancer and Trauma

“…Both exocrine and endocrine dysfunction after PP have been documented with rates as high as 35% and 40%, respectively [24]. Pre-existing hyperglycemia, elevated HbA1c, older age, female sex, and obesity are recognized as preoperative factors that impact the development of T3cDM after PP [19].…”

“…This can occur anywhere along the spectrum of disease progression from CP to PDAC [68,83,84]. Humoral aberrations and paraneoplastic phenomena, such as impaired glucose metabolism in skeletal muscle and insulin secretory capacity, have also been implicated in the development of pancreatogenic diabetes resulting from PDAC [24,85], and a recent study suggesting that PDAC-associated T3cDM is clinically distinguishable compared to patients having conventional T2DM [24]. While most research on T3cDM and pancreatic malignancy focus on PDAC, which accounts for 90% of all pancreatic cancers [86], fewer studies have been done in other pancreatic lesions, such as pancreatic neuroendocrine tumors (pNETs), intraductal papillary mucinous neoplasms (IPMNs), and mucinous cystic neoplasms.…”

“…Although diagnostic criteria have been proposed for T3cDM [7], they are not standardized and pose difficulty to implement in various clinical settings [24]. These diagnostic criteria are available and useful at present but are not absolute due to a potential overlap between different types of DM.…”

The role of CFTR in diabetes‐induced pancreatic ductal dysfunction

“…The main important message from the study is that ductal HCO 3 − secretion can serve as a protective mechanism and therefore be proposed as a potential therapeutic target for the prevention or treatment of DM. Interestingly, there is also an opposite link between pancreatic disease and DM: several studies have described a type 3c pancreatogenic diabetes secondary to pancreatic disease with up to 60.2% of adult patients after AP (Sliwinska‐Mosson et al., 2023). Therefore, there is a need for further studies in this area to fully understand the implications and potential therapeutic applications.…”