Focal Pancreatic Parenchymal Atrophy and Delayed Enhancement in Early Pancreatic Ductal Adenocarcinoma: A Narrative Review of Pathologic Basis, Diagnostic Pitfalls, and Evidence Limitations.

Abstract

Early pancreatic ductal adenocarcinoma (PDAC), including carcinoma in situ (CIS)/high-grade pancreatic intraepithelial neoplasia (PanIN) and very small invasive tumors, is increasingly recognized, but the significance of pancreatic parenchymal atrophy and delayed enhancement remains unsettled. This narrative review summarizes their pathological basis, technical determinants, observer variability, differential diagnoses, and evidence limitations across computed tomography (CT), magnetic resonance imaging (MRI)/magnetic resonance cholangiopancreatography (MRCP), endoscopic ultrasonography (EUS), and regionally variable pancreatic duct-oriented cytology pathways. Parenchymal atrophy should be distinguished from ductal abnormalities such as focal main pancreatic duct stenosis and perilesional branch-duct dilation, which depend heavily on technically optimized MRCP, including high-quality two-dimensional MRCP. Atrophy is a morphologic phenotype with heterogeneous substrates, whereas delayed enhancement more often reflects fibrosis-rich or inflammatory change and is not specific for PDAC, because focal autoimmune pancreatitis may show similar delayed enhancement. Reported prevalence and diagnostic value vary according to cohort spectrum, modality, phase definition, reader blinding, cytologic verification, and hindsight bias. Current evidence supports these signs as context-dependent clues, not diagnostic thresholds or management algorithms. Prospective pathology-linked studies with standardized protocols are needed.