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.

OBJECTIVE: New-onset diabetes is an important sequela of acute pancreatitis, but there are no biomarkers to differentiate it from the much more common type 2 diabetes. The objective was to investigate whether postprandial circulating levels of gut hormones can serve this purpose. METHODS: This was a case-control study nested into a prospective longitudinal cohort study that included 42 insulin-naive cases with new-onset prediabetes/diabetes after acute pancreatitis (NODAP) and prediabetes/diabetes followed by acute pancreatitis (T2D-AP), sex matched with 21 healthy controls. All individuals underwent a standardized mixed-meal test, and blood samples were assayed for gut hormones (glucose-dependent insulinotropic peptide, glucagon-like peptide-1, oxyntomodulin, and peptide YY). Analysis of variance and linear regression analysis were conducted in unadjusted and adjusted models (accounting for age, homeostatic model assessment of β-cell function, and magnetic resonance imaging–derived body fat composition). RESULTS: Oxyntomodulin levels were significantly lower in NODAP compared with T2D-AP and healthy controls (P = 0.027 and P = 0.001, respectively, in the most adjusted model). Glucagon-like peptide-1 and peptide YY were significantly lower in NODAP compared with T2D-AP (P = 0.001 and P = 0.014, respectively, in the most adjusted model) but not compared with healthy controls (P = 1.000 and P = 0.265, respectively, in the most adjusted model). Glucose-dependent insulinotropic peptide levels were not significantly different between NODAP and T2D-AP. DISCUSSION: Oxyntomodulin is a promising biomarker to guide the differential diagnosis of new-onset diabetes after acute pancreatitis. However, external validation studies are warranted before it can be recommended for routine use in clinical practice.

Objectives Tobacco smoking and alcohol consumption are established risk factors for pancreatitis. This study investigated the associations between tobacco smoking/alcohol consumption in people after an attack of pancreatitis and intrapancreatic fat deposition (IPFD), intrahepatic fat deposition (IHFD), and skeletal muscle (SMFD) fat deposition. Methods In this cross-sectional study, magnetic resonance imaging was used to quantify IPFD, IHFD, and SMFD by 2 independent raters. A validated questionnaire was used to determine tobacco smoking and alcohol consumption. Results A total of 119 individuals after an attack of pancreatitis were included. Average tobacco smoking contributed most to variance in IPFD (R 2 = 6.5%) and least to variance in SMFD (R 2 = 0.4%). Average alcohol consumption contributed most to variance in variance in IPFD (R 2 = 2.8%) and least to IHFD (R 2 = 1.1%). Packs/day contributed more than years of smoking to variance in IPFD (R 2 = 4.9 and 0.2%, correspondingly), whereas years of drinking contributed more than average daily alcohol consumption (R 2 = 3.9 and 3.2%, correspondingly). Conclusions Tobacco smoking and alcohol consumption contributed more to variance in IPFD than IHFD and SMFD. Smoking contributed more than drinking to variance in IPFD. The daily amount of tobacco smoked appeared to be more important than years of smoking for IPFD.

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