Epidemiology, etiopathogenesis, immune response, diagnosis, and complications of acute pancreatitis: current insights

Abstract

The pancreas is a vital organ that performs exocrine and endocrine functions essential for digestion and glucose homeostasis. Acute pancreatitis (AP) is an inflammatory disorder with a rising global incidence, particularly in countries with a low socio-demographic index (SDI). It is characterized by abdominal pain, elevated pancreatic enzymes, and imaging-confirmed pancreatic injury. The disorder is commonly linked to gallstones, alcohol consumption, and metabolic disturbances. The pathophysiology of AP involves complex interactions between oxidative stress, intracellular calcium dysregulation, and immune cell activation. Reactive oxygen and nitrogen species contribute to acinar cell injury by driving apoptosis or necrosis and amplifying inflammatory cascades. Leukocytes, including neutrophils, monocytes, macrophages, lymphocytes, and platelets, then infiltrate pancreatic tissue and produce cytokines and chemokines, thereby exacerbating tissue damage. Pancreatic stellate cells play a central role in fibrosis by modulating the deposition of the extracellular matrix and promoting persistent inflammation. AP can lead to complications such as necrosis, bacterial superinfection, pseudocyst formation, and chronic fibrosis. The long-term risk of pancreatic neoplasia is enhanced by repeated inflammatory insults and oncogenic mutations. Early prediction of severe AP is critical. Clinical tools include biochemical markers, hematological indices, scoring systems, multimarker panels, and deep learning applications. This review integrates current knowledge on oxidative stress, immune responses, and tissue remodeling in AP. It highlights the underlying mechanisms of disease progression and the potential of biomarkers and predictive models to optimize clinical management.