Global epidemiology and holistic prevention of pancreatitis

Abstract

Knowledge of pancreatitis in the 20th century was shaped predominantly by animal data and clinical trials. Several large general population-based cohort studies and comprehensive systematic literature reviews in the 21st century have had a major effect on our understanding of pancreatitis and its sequelae. This Review provides precise and up-to-date data on the burden of acute pancreatitis, chronic pancreatitis and post-pancreatitis diabetes mellitus. Exocrine pancreatic insufficiency and altered bone metabolism following pancreatitis are also discussed. Furthermore, the article introduces a framework for the holistic prevention of pancreatitis with a view to providing guidance on strategies and intervention objectives at primary, secondary and tertiary levels. Concerted efforts by not only gastroenterologists and surgeons but also primary care physicians, endocrinologists, radiologists, pain specialists, dietitians, epidemiologists and public health specialists will be required to reduce meaningfully the burden of pancreatitis and its sequelae over the ensuing decades.

Fig. 1|. Incidence of pancreatitis in the general population.

a | Incidence of acute pancreatitis stratified by age and sex. b | Incidence of chronic pancreatitis stratified by age and sex. Data are derived from Pendharkar et al.^,.

Fig. 2 |. Frequency of transition from first episode of acute pancreatitis to chronic pancreatitis through recurrent acute pancreatitis.

Around 21% of patients suffering a first episode of acute pancreatitis will develop recurrent acute pancreatitis. Of those developing recurrent acute pancreatitis, ~36% will develop chronic pancreatitis. Data are derived from Sankaran et al..

Fig. 3 |. Diagnostic algorithm to identify individuals with PPDM.

Post-pancreatitis diabetes mellitus (PPDM) should be suspected in all adults with a history of pancreatitis who meet the diagnostic criteria for diabetes by the American Diabetes Association. Confirmed type 1 diabetes, or type 2 diabetes prior to first attack of pancreatitis, or stress hyperglycaemia during (or within 3 months after) pancreatitis rules out the diagnosis of PPDM. The 3-month threshold is applied because glycated haemoglobin (HbA_lc) level reflects average plasma glucose over the previous 8–12 weeks. The term ‘New-onset diabetes after pancreatitis’ (NODAP) is reserved for individuals with PPDM who had documented normal glucose homeostasis at baseline (as evidenced by available HbA_lc and/or fasting plasma glucose (FPG) data). The algorithm has been devised by the authors. The glycated haemoglobin HbAlc test should be performed using a method that is certified by the National Glycohaemoglobin Standardization Program (NGSP) and standardized or traceable to the Diabetes Control and Complications Trial (DCCT) reference assay. Fasting is defined as no caloric intake for at least 8 h. Autoimmune markers include islet cell autoantibodies and autoantibodies to glutamic acid decarboxylase, insulin, the tyrosine phosphatases IA-2 and IA-2b and zinc transporter antigen. The oral glucose tolerance test can also be used to diagnose diabetes, if it is deemed practical and time-efficient in a given hospital.

Fig. 4 |. Epidemiology of diabetes of the exocrine pancreas.

a | Frequency of diabetes of the exocrine pancreas in adults, b I Frequency of subtypes of diabetes of the exocrine pancreas, c | Frequency of subtypes of post-pancreatitis diabetes mellitus. Data are derived from the pooled estimates reported by Woodmansey et al. and Pendharkar et al.^–. Post-acute pancreatitis diabetes mellitus includes cases with diabetes after both first acute pancreatitis episode and recurrent acute pancreatitis.

Fig. 5 |. The holistic prevention of pancreatitis framework.

Primary, secondary and tertiary levels of prevention applied holistically to acute, recurrent acute and chronic pancreatitis and as a disease continuum. EPI, exocrine pancreatic insufficiency; PPDM, post-pancreatitis diabetes mellitus.