Enzymatic Patterns of Pancreatic Involvement in Celiac Disease: Pathophysiology, Diagnosis, and Clinical Significance

Celiac disease (CD) is a systemic immune-mediated disorder that extends beyond its classic intestinal manifestations to affect multiple organ systems, including the exocrine pancreas. While the association between CD and endocrine pancreatic disorders is well established, exocrine pancreatic involvement remains underappreciated despite its significant clinical implications. This review provides a comprehensive examination of pancreatic enzyme alterations in CD, focusing on three key biomarkers: serum amylase, serum lipase, and fecal elastase-1.The pathophysiological mechanisms linking intestinal injury to pancreatic dysfunction involve impaired enteroendocrine hormone secretion, inflammatory and mechanical obstruction of pancreatic drainage, and immune-mediated pancreatic injury. Hyperamylasemia in CD predominantly reflects macroamylasemia rather than true pancreatic inflammation, occurring through the formation of amylase-immunoglobulin complexes. Hyperlipasemia, detected in approximately twenty percent of untreated patients, typically presents as mild elevations that normalize with gluten-free diet (GFD) adherence. Reduced fecal elastase-1 levels indicate functional exocrine pancreatic insufficiency secondary to villous atrophy and impaired pancreatic stimulation, rather than structural pancreatic disease.Recognition of these enzyme patterns is essential for accurate diagnosis and appropriate clinical management. Most pancreatic abnormalities in CD are reversible with strict GFD adherence, emphasizing the functional rather than structural nature of pancreatic involvement in this condition.