Trajectories of glycaemia following acute pancreatitis: a prospective longitudinal cohort study with 24 months follow-up

Abstract

Background New-onset diabetes is the most common sequela of acute pancreatitis (AP). Yet, prospective changes in glycaemia over time have never been investigated comprehensively in this study population. The primary aim was to determine the cumulative incidence of new-onset prediabetes and new-onset diabetes after AP over 24 months of follow-up in a prospective cohort study. The secondary aim was to identify trajectories of glycaemia during follow-up and their predictors at the time of hospitalisation. Methods Patients with a prospective diagnosis of AP and no diabetes based on the American Diabetes Association criteria were followed up every 6 months up to 24 months after hospital discharge. Incidence of new-onset prediabetes/diabetes over each follow-up period was calculated. Group-based trajectory modelling was used to identify common changes in glycaemia. Multinomial regression analyses were conducted to investigate the associations between a wide array of routinely available demographic, anthropometric, laboratory, imaging, and clinical factors and membership in the trajectory groups. Results A total of 152 patients without diabetes were followed up. The cumulative incidence of new-onset prediabetes and diabetes was 20% at 6 months after hospitalisation and 43% over 24 months of follow-up (p trend \ 0.001). Three discrete trajectories of glycaemia were identified: normal-stable glycaemia (32%), moderatestable glycaemia (60%), and high-increasing glycaemia (8%). Waist circumference was a significant predictor of moderate-stable glycaemia. None of the studied predictors were significantly associated with high-increasing glycaemia.Conclusions This first prospective cohort study of changes in glycaemia (determined at structured time points in unselected AP patients) showed that at least one out of five patients develops new-onset prediabetes or diabetes at 6 months of follow-up and more than four out of ten-in the first 2 years. Changes in glycaemia after AP follow three discrete trajectories. This may inform prevention or early detection of critical changes in blood glucose metabolism following an attack of AP and, hence, reduce the burden of new-onset diabetes after acute pancreatitis.

Pathological Mechanisms in Diabetes of the Exocrine Pancreas: What’s Known and What’s to Know

“…Due to confusion with type 2 diabetes mellitus (T2DM) ( Petrov, 2017 ), it has been underestimated in clinical practice for a long time. The incidence of DEP varies with geographical distribution and etiology ( Ewald and Hardt, 2013 ; Pendharkar et al, 2017 ; Woodmansey et al, 2017 ; Bharmal et al, 2020a ), with estimated true prevalence ranging from 1 to 9% of all diabetic patients ( Hart et al, 2016 ). It has been noted that compared to other DM patients, the DEP patients present additional symptoms related to pancreatic disease, including decreased glucagon and somatostatin, pancreatic exocrine insufficiency (PEI), malabsorption of nutrients and micronutrients, severe and painful gastrointestinal symptoms, and nutritional deficiencies ( Wynne et al, 2019 ).…”

The Relationship between Abdominal Fat Phenotypes and Insulin Resistance in Non-Obese Individuals after Acute Pancreatitis

“…Initially thought to be mainly a self-resolving disease, emerging evidence has shown that individuals after AP often develop metabolic derangements after hospital discharge-in particular, new-onset prediabetes or diabetes after AP (NODAP) [1][2][3][4][5][6]. For example, a 2020 prospective longitudinal cohort study (as part of the LACERTA project) demonstrated that 43% of non-diabetic patients with AP developed NODAP within two years after hospital discharge [7]. There is a growing appreciation that NODAP is different from type 2 prediabetes or diabetes mellitus (T2DM).…”

Pancreatitis, Pancreatic Cancer, and Their Metabolic Sequelae: Projected Burden to 2050

“…Furthermore, the development of DEP is known to be influenced by a range of factors. In addition to the conventional risk factors for diabetes (e.g., central obesity) ( 29 , 30 ), recurrent episodes of AP—a pancreas-specific risk factor for DEP—( 31 ) might have differentially contributed to the incidence of DEP during the observation period.…”