Insights into skeletal muscle size after pancreatitis

Abstract

Background and Aims: Pancreatitis often progresses from the first episode of acute pancreatitis (FAP), to recurrent episodes of acute pancreatitis (RAP), and then to chronic pancreatitis (CP), as a continuum. It may cause harmful sequelae, such as diabetes after pancreatitis. Skeletal muscle size has been comprehensively studied in the context of several diseases but not in relation to pancreatitis. The first aim of this thesis was to investigate the differences in skeletal muscle size between healthy controls and pancreatitis patients according to the progression of the disease. The second aim was to investigate the associations between skeletal muscle size and diabetes status in individuals after pancreatitis. Materials and Methods: This thesis included two cross-sectional studies, which encompassed individuals after pancreatitis and healthy controls. All participants underwent abdominal magnetic resonance scans, and Psoas muscle volume (PMV), skeletal muscle, visceral, intra-pancreatic, and intra-hepatic fat deposition were measured using previously published protocols. Information on tobacco smoking, alcohol consumption, and physical activity status was acquired using a comprehensive standardised questionnaire. Serum levels of cytokines (including leptin) were measured. Statistical analyses included the creation of additive models, followed by multivariate analyses, and the adoption of linear regression models. Results: A total of 153 individuals were analysed. A significant downward trend in PMV was observed between FAP, RAP, CP and healthy controls in all adjusted models (p = .047, .005, .004, and < .001). Leptin was significantly directly associated with PMV in all models. PMV was significantly reduced in the diabetes group compared with healthy controls (β = -30.0, p = .034 in the most adjusted model). The Matsuda index of insulin sensitivity was significantly directly associated with PMV. Skeletal muscle fat deposition (SMFD) was significantly inversely associated with PMV. Conclusions: A progressive reduction in PMV was observed in individuals after pancreatitis. Individuals with diabetes after pancreatitis also showed a decrease in PMV. At least in part, three factors may explain this: Chronic inflammation (demonstrated by serum leptin levels), reduced insulin sensitivity, and increased SMFD. Adoption of modern imaging modalities and advancements in data processing capabilities have the potential to improve the outcomes of pancreatitis and its sequelae in the future.