The processes of chronic pancreatitis include chronic inflammation and fibrosis with loss of parenchymal cells of the exocrine and endocrine pancreas. These processes lead to irreversible and debilitating exocrine and endocrine insufficiency and a severe chronic pain syndrome. Although elucidation of the mechanisms underlying chronic pancreatitis are incomplete, considerable progress has been made in our understanding of the fibrosis process as a result of identification and characterisation of pancreatic stellate cells (PSCs) starting in 1997.^1–3 Studies with these cells suggest that they play a key role in chronic pancreatitis in a manner analogous to hepatic stellate cells and hepatic fibrosis^4,5

In common with liver fibrosis and hepatic stellate cells there is increasing evidence demonstrating a central role for PSCs in pancreatic fibrosis and chronic pancreatitis. In the normal pancreas, quiescent PSCs are identified using antibodies to desmin, a cytoskeletal protein and specific PSC marker.¹ They are present in the periacinar space with long cytoplasmic processes encircling the base of the acinus. Similar to hepatic stellate cells in their quiescent state, PSCs store significant amounts of vitamin A as lipid droplets in their cytoplasm.

There is general acceptance that during …